PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
9863172-1	1996	AIM: To observe the effect of captopril (Cap) on intracellular pH (pHi) in aortic smooth muscle cells (ASMC).	asmc	103-107	glucose-6-phosphate isomerase	Rattus norvegicus	67-70
9863172-2	1996	METHODS: Cultured ASMC derived from rat and rabbit aortae were loaded with the fluorescent dye BCECF and pHi was determined using digital image processing method.	asmc	18-22	glucose-6-phosphate isomerase	Oryctolagus cuniculus	105-108
9863172-4	1996	Oral Cap decreased pHi (7.11 +/- 0.26, P < 0.05) and exaggerated pHi response to angiotensin II (Ang-II, 0.1 mumol.L-1) in ASMC of SHR rats vs WKY rats (0.14 +/- 0.05 vs 0.21 +/- 0.05 pH units, P < 0.01).	asmc	126-130	glucose-6-phosphate isomerase	Rattus norvegicus	68-71
9863172-4	1996	Oral Cap decreased pHi (7.11 +/- 0.26, P < 0.05) and exaggerated pHi response to angiotensin II (Ang-II, 0.1 mumol.L-1) in ASMC of SHR rats vs WKY rats (0.14 +/- 0.05 vs 0.21 +/- 0.05 pH units, P < 0.01).	asmc	126-130	angiotensinogen	Rattus norvegicus	84-98
9863172-4	1996	Oral Cap decreased pHi (7.11 +/- 0.26, P < 0.05) and exaggerated pHi response to angiotensin II (Ang-II, 0.1 mumol.L-1) in ASMC of SHR rats vs WKY rats (0.14 +/- 0.05 vs 0.21 +/- 0.05 pH units, P < 0.01).	asmc	126-130	angiotensinogen	Rattus norvegicus	100-106
8663449-7	1996	Although APEG-1 was expressed highly in differentiated ASMC in vivo, its expression was quickly down-regulated and disappeared in dedifferentiated ASMC in culture.	asmc	55-59	striated muscle enriched protein kinase	Rattus norvegicus	9-15
8663449-7	1996	Although APEG-1 was expressed highly in differentiated ASMC in vivo, its expression was quickly down-regulated and disappeared in dedifferentiated ASMC in culture.	asmc	147-151	striated muscle enriched protein kinase	Rattus norvegicus	9-15
8663449-8	1996	In vivo, APEG-1 mRNA levels decreased by more than 80% in response to vascular injury as ASMC changed from a quiescent to a proliferative phenotype.	asmc	89-93	striated muscle enriched protein kinase	Rattus norvegicus	9-15
9772664-4	1996	KCl-, norepinephrine (NE)-, and angiotensin II (Ang)-induced [Ca2+]i increases were enhanced in ASMC of SHR vs WKY (220 +/- 6, 212 +/- 8, and 215 +/- 14 vs 199 +/- 6, 202 +/- 7, and 195 +/- 7 nmol.L-1, respectively).	asmc	96-100	angiotensinogen	Rattus norvegicus	32-46
9772664-4	1996	KCl-, norepinephrine (NE)-, and angiotensin II (Ang)-induced [Ca2+]i increases were enhanced in ASMC of SHR vs WKY (220 +/- 6, 212 +/- 8, and 215 +/- 14 vs 199 +/- 6, 202 +/- 7, and 195 +/- 7 nmol.L-1, respectively).	asmc	96-100	angiotensinogen	Rattus norvegicus	48-51
9772664-6	1996	Cap and Ena inhibited KCl-, NE-, and Ang-increased [Ca2+]i in ASMC of SHR (210 +/- 7, 194 +/- 6, and 201 +/- 6 nmol.L-1, respectively).	asmc	62-66	angiotensinogen	Rattus norvegicus	37-40
7973817-4	1994	The extent of heat shock protein 70 messenger RNA accumulated in ASMC was higher in SHR than in WKY rats when the cells were heated by immersing the culture bottles in 42 degrees C water bath for 15 min and allowed to recover at 37 degrees C for 2 h. In contrast with WKY rats, the Bam HI restricted bepatic DNA showed that a fragment about 5.6 kb was lost in heat shock protein 70 gene from hepatic DNA of SHR.	asmc	65-69	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	14-35
7656389-2	1995	The changes in cAMP, ANG II and CaM contents in ASMC were also studied.	asmc	48-52	cathelicidin antimicrobial peptide	Rattus norvegicus	15-19
7656389-7	1995	In addition, ANG II content in ASMC had a direct bearing on blood pressure, showing a marked difference between prehypertensive and hypertensive SHR.	asmc	31-35	angiogenin	Rattus norvegicus	13-16
7656389-8	1995	The disturbance of transmembrane Ca2+ transport in ASMC of hypertensive rats appears to be related to genetic defect and the changes of cAMP contents might play a role in membrane Ca2+ transport in ASMC during the development of hypertension.	asmc	51-55	cathelicidin antimicrobial peptide	Rattus norvegicus	136-140
7656389-8	1995	The disturbance of transmembrane Ca2+ transport in ASMC of hypertensive rats appears to be related to genetic defect and the changes of cAMP contents might play a role in membrane Ca2+ transport in ASMC during the development of hypertension.	asmc	198-202	cathelicidin antimicrobial peptide	Rattus norvegicus	136-140
8169847-5	1994	In addition, the effects of vasodilator-derived NO on Angiotensin-II (Ang-II)-induced ASMC growth and contraction were studied.	asmc	86-90	angiotensinogen	Homo sapiens	54-68
7911451-7	1994	Higher cyclic GMP production with CNP than with ANP was observed in cultured ASMC from Wistar-Kyoto (WKY) rats.	asmc	77-81	natriuretic peptide C	Rattus norvegicus	34-37
8169847-5	1994	In addition, the effects of vasodilator-derived NO on Angiotensin-II (Ang-II)-induced ASMC growth and contraction were studied.	asmc	86-90	angiotensinogen	Homo sapiens	70-76
8169847-10	1994	Furthermore, NO generated from SNAP (10(-6) M) inhibited Ang-II (10(-6) M)-induced ASMC contraction.	asmc	83-87	angiotensinogen	Homo sapiens	57-63
2163216-5	1990	Plasma from rats injected with ANF inhibited the Na pump activity (18 +/- 4%, n = 4 experiments) in ASMC compared with plasma obtained from rats injected with the vehicle.	asmc	100-104	natriuretic peptide A	Rattus norvegicus	31-34
1450393-6	1992	In addition, immunocytochemistry showed positive ANF staining in cultured ASMC of both strains.	asmc	74-78	natriuretic peptide A	Rattus norvegicus	49-52
1450393-7	1992	The results suggest that ANF can be synthesized and secreted by cultured ASMC from rats.	asmc	73-77	natriuretic peptide A	Rattus norvegicus	25-28
35157180-5	2022	Furthermore, miR-1278 promoted ASMC proliferation, in which TGF-beta1 played an important role by regulating the SHP-1/STAT3 signaling pathway.	asmc	31-35	microRNA 1278	Homo sapiens	13-21
33590796-9	2021	Conclusion LncRNA NEAT1 played a pivotal role in ASMC inflammation and exerted its function through the miR-139/JAK3/STAT5 signaling network.	asmc	49-53	nuclear paraspeckle assembly transcript 1	Homo sapiens	18-23
33590796-9	2021	Conclusion LncRNA NEAT1 played a pivotal role in ASMC inflammation and exerted its function through the miR-139/JAK3/STAT5 signaling network.	asmc	49-53	microRNA 139	Homo sapiens	104-111
33590796-9	2021	Conclusion LncRNA NEAT1 played a pivotal role in ASMC inflammation and exerted its function through the miR-139/JAK3/STAT5 signaling network.	asmc	49-53	Janus kinase 3	Homo sapiens	112-116
33590796-9	2021	Conclusion LncRNA NEAT1 played a pivotal role in ASMC inflammation and exerted its function through the miR-139/JAK3/STAT5 signaling network.	asmc	49-53	signal transducer and activator of transcription 5A	Homo sapiens	117-122
34102715-18	2021	Conclusion: VDR gene silencing could promote ASMC proliferation and the underlying mechanism may involve the activation of NF-kappaB signaling pathway.	asmc	45-49	vitamin D receptor	Rattus norvegicus	12-15
35134593-11	2022	These data suggest that PGE2 inhibits CCh-induced Ca2+ oscillations in murine ASMC via stimulation of EP2Rs and a mechanism involving activation of PKA and EPAC.	asmc	78-82	Rap guanine nucleotide exchange factor (GEF) 3	Mus musculus	156-160
35157180-5	2022	Furthermore, miR-1278 promoted ASMC proliferation, in which TGF-beta1 played an important role by regulating the SHP-1/STAT3 signaling pathway.	asmc	31-35	transforming growth factor, beta 1	Mus musculus	60-69
35157180-5	2022	Furthermore, miR-1278 promoted ASMC proliferation, in which TGF-beta1 played an important role by regulating the SHP-1/STAT3 signaling pathway.	asmc	31-35	protein tyrosine phosphatase, non-receptor type 6	Mus musculus	113-118
35157180-5	2022	Furthermore, miR-1278 promoted ASMC proliferation, in which TGF-beta1 played an important role by regulating the SHP-1/STAT3 signaling pathway.	asmc	31-35	signal transducer and activator of transcription 3	Mus musculus	119-124
35396910-13	2022	In conclusion, ANRIL indirectly up-regulates CCND1 expression by targeting miR-98-5p to promote ASMC proliferation, migration and ECM deposition, thus facilitating the pathogenesis of asthma.	asmc	96-100	CDKN2B antisense RNA 1	Homo sapiens	15-20
35396910-13	2022	In conclusion, ANRIL indirectly up-regulates CCND1 expression by targeting miR-98-5p to promote ASMC proliferation, migration and ECM deposition, thus facilitating the pathogenesis of asthma.	asmc	96-100	cyclin D1	Homo sapiens	45-50
35396910-13	2022	In conclusion, ANRIL indirectly up-regulates CCND1 expression by targeting miR-98-5p to promote ASMC proliferation, migration and ECM deposition, thus facilitating the pathogenesis of asthma.	asmc	96-100	microRNA 98	Homo sapiens	75-81
33542087-6	2021	Inhibition of Rac1 by EHT1864 showed that Rac1 signalling controlled human aSMC proliferation induced by mitogenic stimuli through the signal transducer and activator of transcription 3 (STAT3) signalling pathway.	asmc	75-79	Rac family small GTPase 1	Homo sapiens	14-18
3141056-12	1988	The ASMC obtained after the injection produced TGIF in vitro in the absence of OK-432; the preinjection ASMC showed no such production.	asmc	4-8	interleukin 10	Homo sapiens	47-51
3141056-13	1988	A positive correlation was found between TGIF-producing activity by ASMC and the effect of OK-432 injection on ascites volume.	asmc	68-72	interleukin 10	Homo sapiens	41-45
33675818-15	2021	CONCLUSION: Epithelial cell-derived HSP70 and HSP90 improve the function of epithelial cells, but block ASMC remodeling.	asmc	104-108	heat shock protein family A (Hsp70) member 4	Homo sapiens	36-41
33675818-15	2021	CONCLUSION: Epithelial cell-derived HSP70 and HSP90 improve the function of epithelial cells, but block ASMC remodeling.	asmc	104-108	heat shock protein 90 alpha family class A member 1	Homo sapiens	46-51
33542087-6	2021	Inhibition of Rac1 by EHT1864 showed that Rac1 signalling controlled human aSMC proliferation induced by mitogenic stimuli through the signal transducer and activator of transcription 3 (STAT3) signalling pathway.	asmc	75-79	Rac family small GTPase 1	Homo sapiens	42-46
33542087-6	2021	Inhibition of Rac1 by EHT1864 showed that Rac1 signalling controlled human aSMC proliferation induced by mitogenic stimuli through the signal transducer and activator of transcription 3 (STAT3) signalling pathway.	asmc	75-79	signal transducer and activator of transcription 3	Homo sapiens	135-185
33542087-6	2021	Inhibition of Rac1 by EHT1864 showed that Rac1 signalling controlled human aSMC proliferation induced by mitogenic stimuli through the signal transducer and activator of transcription 3 (STAT3) signalling pathway.	asmc	75-79	signal transducer and activator of transcription 3	Homo sapiens	187-192
33542087-10	2021	CONCLUSION: This study demonstrates that Rac1 is overactive in the airways of patients with severe asthma and is essential for aSMC proliferation.	asmc	127-131	Rac family small GTPase 1	Homo sapiens	41-45
29999407-4	2018	Pretreatment of cells with S1PR2 antagonist JTE013, S1PR3 antagonist CAY10444, or ROCK inhibitor Y27632 blocked S1P-induced alterations of YAP, FOXM1, cyclin D1, and ASMC proliferation, migration, and contraction.	asmc	166-170	sphingosine-1-phosphate receptor 2	Homo sapiens	27-32
33191679-8	2021	Secondly, ASMC autophagy was increased in the OVA-challenged models.	asmc	10-14	serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene	Mus musculus	46-49
33191679-10	2021	Thirdly, MIF can induce ASMC autophagy in vitro.	asmc	24-28	macrophage migration inhibitory factor (glycosylation-inhibiting factor)	Mus musculus	9-12
33191679-11	2021	Moreover, the cellular source of MIF which promoted ASMC autophagy was macrophages.	asmc	52-56	macrophage migration inhibitory factor (glycosylation-inhibiting factor)	Mus musculus	33-36
33191679-12	2021	Finally, MIF promoted ASMC autophagy in a CD74-dependent manner.	asmc	22-26	macrophage migration inhibitory factor (glycosylation-inhibiting factor)	Mus musculus	9-12
33191679-12	2021	Finally, MIF promoted ASMC autophagy in a CD74-dependent manner.	asmc	22-26	CD74 antigen (invariant polypeptide of major histocompatibility complex, class II antigen-associated)	Mus musculus	42-46
33191679-13	2021	CONCLUSIONS: MIF can increase asthmatic airway remodeling by enhancing ASMC autophagy.	asmc	71-75	macrophage migration inhibitory factor (glycosylation-inhibiting factor)	Mus musculus	13-16
33223504-10	2020	Conclusively, lncRNA PVT1-miR-15a-5p/miR-29c-3p-PI3K-Akt-mTOR axis was implicated in ozone-induced asthma development by promoting ASMC proliferation and Th1/Th2 imbalance.	asmc	131-135	Pvt1 oncogene	Mus musculus	21-25
33223504-10	2020	Conclusively, lncRNA PVT1-miR-15a-5p/miR-29c-3p-PI3K-Akt-mTOR axis was implicated in ozone-induced asthma development by promoting ASMC proliferation and Th1/Th2 imbalance.	asmc	131-135	thymoma viral proto-oncogene 1	Mus musculus	53-56
33223504-10	2020	Conclusively, lncRNA PVT1-miR-15a-5p/miR-29c-3p-PI3K-Akt-mTOR axis was implicated in ozone-induced asthma development by promoting ASMC proliferation and Th1/Th2 imbalance.	asmc	131-135	mechanistic target of rapamycin kinase	Mus musculus	57-61
33182705-7	2020	Treatment of ASMC with either AGEs or S100B at concentrations detected in T2D patients increased markers of inflammation and apoptosis.	asmc	13-17	S100 calcium binding protein B	Homo sapiens	38-43
30317624-9	2019	These results indicated that Drp1 may function as a key factor in asthma airway remodeling by mediating ASMC proliferation and cell cycle acceleration through an effect on mitochondrial metabolic disturbance.	asmc	104-108	dynamin 1 like	Homo sapiens	29-33
30690080-11	2019	AM did not affect the secretion of IL-6 or IL-8 by EC but stimulated the secretion of IL-6 by ASMC.	asmc	94-98	interleukin 6	Homo sapiens	86-90
30988708-4	2019	In addition, the influence of let-7a on ASMC apoptosis was detected using flow cytometry and a caspase-3/7 activity assay.	asmc	40-44	caspase 3	Homo sapiens	95-104
30290314-3	2018	Therefore, we designed this study to explore whether TRPM7 is involved in TGF-beta1-induced ASMC proliferation.	asmc	92-96	transient receptor potential cation channel, subfamily M, member 7	Mus musculus	53-58
30290314-3	2018	Therefore, we designed this study to explore whether TRPM7 is involved in TGF-beta1-induced ASMC proliferation.	asmc	92-96	transforming growth factor, beta 1	Mus musculus	74-83
30290314-8	2018	MTT and flow cytometry were applied to evaluate the effects of TRPM7 knockdown on ASMC proliferation and apoptosis.	asmc	82-86	transient receptor potential cation channel, subfamily M, member 7	Mus musculus	63-68
33413331-12	2021	In vitro study showed that rhynchophylline suppressed ASMC autophagy through suppressing the activation of JAK2/STAT3 signal.	asmc	54-58	Janus kinase 2	Mus musculus	107-111
33413331-12	2021	In vitro study showed that rhynchophylline suppressed ASMC autophagy through suppressing the activation of JAK2/STAT3 signal.	asmc	54-58	signal transducer and activator of transcription 3	Mus musculus	112-117
32583575-3	2020	In this study, the regulatory effects of microRNA-620 (miR-620) on ASMC proliferation and apoptosis in response to transforming growth factor beta1 (TGF-beta1) stimulation was investigated.	asmc	67-71	microRNA 620	Homo sapiens	41-53
32583575-3	2020	In this study, the regulatory effects of microRNA-620 (miR-620) on ASMC proliferation and apoptosis in response to transforming growth factor beta1 (TGF-beta1) stimulation was investigated.	asmc	67-71	microRNA 620	Homo sapiens	55-62
32583575-3	2020	In this study, the regulatory effects of microRNA-620 (miR-620) on ASMC proliferation and apoptosis in response to transforming growth factor beta1 (TGF-beta1) stimulation was investigated.	asmc	67-71	transforming growth factor beta 1	Homo sapiens	115-147
32583575-3	2020	In this study, the regulatory effects of microRNA-620 (miR-620) on ASMC proliferation and apoptosis in response to transforming growth factor beta1 (TGF-beta1) stimulation was investigated.	asmc	67-71	transforming growth factor beta 1	Homo sapiens	149-158
32583575-8	2020	Moreover, knocking down miR-620 alone efficiently reduced the phosphorylation of protein kinase B (AKT), decreased TGF-beta1-induced proliferation and promoted apoptosis in ASMCs, whereas downregulation of PTEN in miR-620 inhibitor-transfected cells restored the activation of AKT, increased TGF-beta1-triggered proliferation, and partially inhibited ASMC apoptosis.	asmc	173-177	microRNA 620	Homo sapiens	24-31
31435973-9	2019	These findings suggest that esculetin might exert its inhibitory effect on PDGF-induced ASMC phenotype switching through inhibition of PI3K/Akt pathway.	asmc	88-92	AKT serine/threonine kinase 1	Homo sapiens	140-143
30781615-6	2019	Reduced PTEN expression correlated with enhanced PI3K signaling, which upregulated ASMC remodeling.	asmc	83-87	phosphatase and tensin homolog	Homo sapiens	8-12
30781615-9	2019	IgE induced ASMC remodeling was significantly reduced by inhibition of mTOR or STAT3.	asmc	12-16	mechanistic target of rapamycin kinase	Homo sapiens	71-75
30781615-9	2019	IgE induced ASMC remodeling was significantly reduced by inhibition of mTOR or STAT3.	asmc	12-16	signal transducer and activator of transcription 3	Homo sapiens	79-84
30781615-10	2019	In conclusion, non-immune IgE alone is sufficient for stimulated ASMC remodeling by upregulating microRNA-21-5p.	asmc	65-69	microRNA 215	Homo sapiens	97-111
29760303-15	2018	CONCLUSIONS: The result suggests that miR-140-3p regulates ASMC function via targeting C-Myb and BCL-2 in the process of ISR in PAD.	asmc	59-63	microRNA 140	Homo sapiens	38-45
29760303-15	2018	CONCLUSIONS: The result suggests that miR-140-3p regulates ASMC function via targeting C-Myb and BCL-2 in the process of ISR in PAD.	asmc	59-63	MYB proto-oncogene, transcription factor	Homo sapiens	87-92
29760303-15	2018	CONCLUSIONS: The result suggests that miR-140-3p regulates ASMC function via targeting C-Myb and BCL-2 in the process of ISR in PAD.	asmc	59-63	BCL2 apoptosis regulator	Homo sapiens	97-102
29999407-5	2018	In addition, prior silencing of YAP or FOXM1 with siRNA reversed the effect of S1P on ASMC functions.	asmc	86-90	Yes1 associated transcriptional regulator	Homo sapiens	32-35
29999407-5	2018	In addition, prior silencing of YAP or FOXM1 with siRNA reversed the effect of S1P on ASMC functions.	asmc	86-90	forkhead box M1	Homo sapiens	39-44
29999407-6	2018	Taken together, our study indicates that S1P stimulates ASMC proliferation, migration, and contraction by binding to S1PR2/3 and modulating ROCK/YAP/FOXM1 axis and suggests that targeting this pathway might have potential value in the management of asthma.	asmc	56-60	sphingosine-1-phosphate receptor 2	Homo sapiens	117-122
29999407-6	2018	Taken together, our study indicates that S1P stimulates ASMC proliferation, migration, and contraction by binding to S1PR2/3 and modulating ROCK/YAP/FOXM1 axis and suggests that targeting this pathway might have potential value in the management of asthma.	asmc	56-60	Yes1 associated transcriptional regulator	Homo sapiens	145-148
29999407-6	2018	Taken together, our study indicates that S1P stimulates ASMC proliferation, migration, and contraction by binding to S1PR2/3 and modulating ROCK/YAP/FOXM1 axis and suggests that targeting this pathway might have potential value in the management of asthma.	asmc	56-60	forkhead box M1	Homo sapiens	149-154
29155102-3	2018	OBJECTIVE: The objective of this study was to identify the role of Rac1 in aSMC contraction and to investigate its involvement in AHR associated with allergic asthma.	asmc	75-79	Rac family small GTPase 1	Mus musculus	67-71
29999407-3	2018	S1P induced yes-associated protein (YAP) dephosphorylation and nuclear localization via the S1PR2/3/Rho-associated protein kinase (ROCK) pathway, and this in turn increased forkhead box M1 (FOXM1) and cyclin D1 expression leading to ASMC proliferation, migration, and contraction.	asmc	233-237	Yes1 associated transcriptional regulator	Homo sapiens	36-39
29999407-3	2018	S1P induced yes-associated protein (YAP) dephosphorylation and nuclear localization via the S1PR2/3/Rho-associated protein kinase (ROCK) pathway, and this in turn increased forkhead box M1 (FOXM1) and cyclin D1 expression leading to ASMC proliferation, migration, and contraction.	asmc	233-237	sphingosine-1-phosphate receptor 2	Homo sapiens	92-99
29775222-4	2018	The purpose of the present study was to investigate the functional role and potential molecular mechanism of ABCA1 in platelet derived growth factor (PDGF)-induced primary rat ASMC proliferation and migration.	asmc	176-180	ATP binding cassette subfamily A member 1	Rattus norvegicus	109-114
29775222-4	2018	The purpose of the present study was to investigate the functional role and potential molecular mechanism of ABCA1 in platelet derived growth factor (PDGF)-induced primary rat ASMC proliferation and migration.	asmc	176-180	myotrophin	Rattus norvegicus	135-148
29775222-6	2018	Overexpression of ABCA1 strikingly suppressed PDGF-induced ASMC proliferation accompanied by a decrease in the expression of PCAN stimulated by PDGF.	asmc	59-63	ATP binding cassette subfamily A member 1	Rattus norvegicus	18-23
30132829-7	2018	Preincubation of rat ASMCs with pioglitazone, a PPAR-gamma activator, blocked TGF-beta1-induced activation of Smad2/3 and its downstream targets changes of miR-21, PTEN, Akt, FOXO1, and cyclin D1, resulting in the inhibition of rat ASMC proliferation.	asmc	21-25	peroxisome proliferator-activated receptor gamma	Rattus norvegicus	48-58
29665364-7	2018	Taken together, these data demonstrated that casticin inhibits PDGF-induced human ASMC proliferation and migration through suppressing the activation of ERK1/2 and NF-kappaB signaling pathways.	asmc	82-86	mitogen-activated protein kinase 3	Homo sapiens	153-159
28851074-2	2018	In the present study, we found that an enhanced expression of MIF promoted ASMC proliferation, increased the population of cells in the S/G2 phase, downregulated P21 expression, and upregulated cyclin D1, cyclin D3, and Cdk6 expression.	asmc	75-79	macrophage migration inhibitory factor	Rattus norvegicus	62-65
30233858-10	2018	Conclusions: NK1R antagonists may suppress ASMC migration in a rat model of airway remodelling by inhibiting tubulin expression, indicating a new potential target for the treatment and control of chronic asthma.	asmc	43-47	tachykinin receptor 1	Rattus norvegicus	13-17
29337379-8	2018	However IL-17A had no direct effect on HMVEC-L function but it enhanced endothelial tube formation and cell migration through the production of angiogenic factors by NHBE and ASMC.	asmc	175-179	interleukin 17A	Homo sapiens	8-14
29414651-7	2018	Besides, preincubation with TNF-alpha led to a higher expression of CD38 protein and increased intracellular calcium in ASMC of the HFD-fed mice.	asmc	120-124	tumor necrosis factor	Mus musculus	28-37
29207148-8	2018	In conclusion, the present study demonstrated for the first time that PF inhibited ASMC growth and migration induced by PDGF-BB, and that this effect may be partly due to inhibition of the PI3K/Akt signaling pathway.	asmc	83-87	AKT serine/threonine kinase 1	Homo sapiens	194-197
30076719-5	2018	Both gain- and loss-of-function studies were performed to study the role of miR-638 in ASMC proliferation and migration.	asmc	87-91	microRNA 638	Homo sapiens	76-83
30076719-6	2018	We found that adenovirus-mediated miR-638 overexpression markedly inhibits ASMC proliferation and migration, while ablation of miR-638 by anti-miR-638 markedly increases cell proliferation and migration, as determined by WST-8 proliferation and scratch wound assays.	asmc	75-79	microRNA 638	Homo sapiens	34-41
30076719-9	2018	Together, our study provides the first in vitro evidence highlighting the antiproliferative and antimigratory roles of miR-638 in human ASMC remodeling and suggests that targeted overexpression of miR-638 in ASMCs may provide a novel therapeutic strategy for preventing ASM hyperplasia associated with asthma.	asmc	136-140	microRNA 638	Homo sapiens	197-204
30132829-6	2018	Our study further showed that loss of FOXO1 increased cyclin D1 expression, leading to rat ASMC proliferation.	asmc	91-95	forkhead box O1	Rattus norvegicus	38-43
30132829-6	2018	Our study further showed that loss of FOXO1 increased cyclin D1 expression, leading to rat ASMC proliferation.	asmc	91-95	cyclin D1	Rattus norvegicus	54-63
30132829-7	2018	Preincubation of rat ASMCs with pioglitazone, a PPAR-gamma activator, blocked TGF-beta1-induced activation of Smad2/3 and its downstream targets changes of miR-21, PTEN, Akt, FOXO1, and cyclin D1, resulting in the inhibition of rat ASMC proliferation.	asmc	21-25	transforming growth factor, beta 1	Rattus norvegicus	78-87
30132829-7	2018	Preincubation of rat ASMCs with pioglitazone, a PPAR-gamma activator, blocked TGF-beta1-induced activation of Smad2/3 and its downstream targets changes of miR-21, PTEN, Akt, FOXO1, and cyclin D1, resulting in the inhibition of rat ASMC proliferation.	asmc	21-25	SMAD family member 2	Rattus norvegicus	110-117
30132829-7	2018	Preincubation of rat ASMCs with pioglitazone, a PPAR-gamma activator, blocked TGF-beta1-induced activation of Smad2/3 and its downstream targets changes of miR-21, PTEN, Akt, FOXO1, and cyclin D1, resulting in the inhibition of rat ASMC proliferation.	asmc	21-25	microRNA 21	Rattus norvegicus	156-162
30132829-7	2018	Preincubation of rat ASMCs with pioglitazone, a PPAR-gamma activator, blocked TGF-beta1-induced activation of Smad2/3 and its downstream targets changes of miR-21, PTEN, Akt, FOXO1, and cyclin D1, resulting in the inhibition of rat ASMC proliferation.	asmc	21-25	phosphatase and tensin homolog	Rattus norvegicus	164-168
30132829-7	2018	Preincubation of rat ASMCs with pioglitazone, a PPAR-gamma activator, blocked TGF-beta1-induced activation of Smad2/3 and its downstream targets changes of miR-21, PTEN, Akt, FOXO1, and cyclin D1, resulting in the inhibition of rat ASMC proliferation.	asmc	21-25	AKT serine/threonine kinase 1	Rattus norvegicus	170-173
30132829-7	2018	Preincubation of rat ASMCs with pioglitazone, a PPAR-gamma activator, blocked TGF-beta1-induced activation of Smad2/3 and its downstream targets changes of miR-21, PTEN, Akt, FOXO1, and cyclin D1, resulting in the inhibition of rat ASMC proliferation.	asmc	21-25	forkhead box O1	Rattus norvegicus	175-180
30132829-7	2018	Preincubation of rat ASMCs with pioglitazone, a PPAR-gamma activator, blocked TGF-beta1-induced activation of Smad2/3 and its downstream targets changes of miR-21, PTEN, Akt, FOXO1, and cyclin D1, resulting in the inhibition of rat ASMC proliferation.	asmc	21-25	cyclin D1	Rattus norvegicus	186-195
28802903-1	2017	AIMS: Canonical transient receptor potential channel-3 (TRPC3)-encoded Ca2+-permeable nonselective cation channel (NSCC) has been proven to be an important native constitutively active channel in airway smooth muscle cell (ASMC), which plays significant roles in physiological and pathological conditions by controlling Ca2+ homeostasis in ASMC.	asmc	223-227	transient receptor potential cation channel, subfamily C, member 3	Mus musculus	16-54
28924004-6	2017	These observations identify ASMC-derived FGF2b as a factor needed for LMC formation by CD4 T cells, affecting intercellular communication.	asmc	28-32	CD4 molecule	Homo sapiens	87-90
28901394-15	2017	Thus, to the best of our knowledge, this is the first study to report that the expression level of ATP5b was markedly increased in lung tissue samples of an asthma model compared with the tissue samples from normal lungs, which promoted ASMC proliferation and contributed to airway remodeling.	asmc	237-241	ATP synthase F1 subunit beta	Homo sapiens	99-104
30423573-13	2018	CONCLUSION: The overexpression of miR-200a may downregulate FOXC1, thereby inhibiting the activation of the PI3K/AKT signaling pathway and ultimately suppressing ASMC proliferation and airway remodeling in asthmatic mice.	asmc	162-166	microRNA 200a	Mus musculus	34-42
30423573-13	2018	CONCLUSION: The overexpression of miR-200a may downregulate FOXC1, thereby inhibiting the activation of the PI3K/AKT signaling pathway and ultimately suppressing ASMC proliferation and airway remodeling in asthmatic mice.	asmc	162-166	forkhead box C1	Mus musculus	60-65
29191950-7	2017	Inhibition of glycolysis and glutamine depletion attenuated TGF-beta/FBS-stimulated growth of COPD ASMCs.Changes in glycolysis, glutamine and fatty acid metabolism may lead to increased biosynthesis and redox balance, supporting COPD ASMC growth.	asmc	99-103	transforming growth factor beta 1	Homo sapiens	60-68
28802903-4	2017	Here, we investigated the role of TRPC3 in ACh-induced ASMC proliferation.	asmc	55-59	transient receptor potential cation channel, subfamily C, member 3	Mus musculus	34-39
28802903-6	2017	Small interfering RNA (siRNA) technology was used to confirm the contribution of TRPC3 to ACh-induced ASMC proliferation.	asmc	102-106	transient receptor potential cation channel, subfamily C, member 3	Mus musculus	81-86
28802903-7	2017	KEY FINDINGS: TRPC3 blocker Gd3+, antibody or siRNA largely inhibited ACh-induced up-regulation of TRPC3 protein, enhancement of NSCC currents, resting [Ca2+]i and KCl-induced changes in [Ca2+]i, eventually inhibiting ACh-induced ASMC proliferation.	asmc	230-234	transient receptor potential cation channel, subfamily C, member 3	Mus musculus	14-19
28802903-8	2017	SIGNIFICANCE: Our data suggested ACh could induce ASMC proliferation, and TRPC3 may be involved in ACh-induced ASMC proliferation that occurs with airway remodeling.	asmc	111-115	transient receptor potential cation channel, subfamily C, member 3	Mus musculus	74-79
28802903-1	2017	AIMS: Canonical transient receptor potential channel-3 (TRPC3)-encoded Ca2+-permeable nonselective cation channel (NSCC) has been proven to be an important native constitutively active channel in airway smooth muscle cell (ASMC), which plays significant roles in physiological and pathological conditions by controlling Ca2+ homeostasis in ASMC.	asmc	223-227	transient receptor potential cation channel, subfamily C, member 3	Mus musculus	56-61
28802903-1	2017	AIMS: Canonical transient receptor potential channel-3 (TRPC3)-encoded Ca2+-permeable nonselective cation channel (NSCC) has been proven to be an important native constitutively active channel in airway smooth muscle cell (ASMC), which plays significant roles in physiological and pathological conditions by controlling Ca2+ homeostasis in ASMC.	asmc	340-344	transient receptor potential cation channel, subfamily C, member 3	Mus musculus	16-54
28802903-1	2017	AIMS: Canonical transient receptor potential channel-3 (TRPC3)-encoded Ca2+-permeable nonselective cation channel (NSCC) has been proven to be an important native constitutively active channel in airway smooth muscle cell (ASMC), which plays significant roles in physiological and pathological conditions by controlling Ca2+ homeostasis in ASMC.	asmc	340-344	transient receptor potential cation channel, subfamily C, member 3	Mus musculus	56-61
28387977-3	2017	Fibroblast growth factor 10-positive (FGF10+ ) cells, originally residing in the submesothelial mesenchyme, contribute to ASMC formation in the distal lung.	asmc	122-126	fibroblast growth factor 10	Mus musculus	0-27
28387977-3	2017	Fibroblast growth factor 10-positive (FGF10+ ) cells, originally residing in the submesothelial mesenchyme, contribute to ASMC formation in the distal lung.	asmc	122-126	fibroblast growth factor 10	Mus musculus	38-43
27377672-4	2016	We hypothesized that TRPC3 is important in LPS-induced airway remodeling by regulating ASMC proliferation.	asmc	87-91	transient receptor potential cation channel, subfamily C, member 3	Mus musculus	21-26
27746262-7	2016	To determine the underlying mechanisms responsible for these effects, we used TNF-alpha-stimulated BECs and TGF-beta1-challenged human ASMCs to explore the impacts of CAPE on pro-inflammatory proteins and ASMC proliferation.	asmc	135-139	transforming growth factor beta 1	Homo sapiens	108-117
27484035-7	2017	Finally, the lncRNA plasmacytoma variant translocation 1 (PVT1) was inhibited by transfection of primary ASMCs with small interfering RNAs, and the effect on ASMC phenotype was examined.	asmc	105-109	Pvt1 oncogene	Homo sapiens	20-56
27484035-7	2017	Finally, the lncRNA plasmacytoma variant translocation 1 (PVT1) was inhibited by transfection of primary ASMCs with small interfering RNAs, and the effect on ASMC phenotype was examined.	asmc	105-109	Pvt1 oncogene	Homo sapiens	58-62
27377672-9	2016	These results demonstrated that TRPC3-mediated Ca(2+) entry contributed to LPS-induced ASMC proliferation and identified TRPC3 as a possible key target in airway remodeling intervention.	asmc	87-91	transient receptor potential cation channel, subfamily C, member 3	Mus musculus	32-37
27236325-8	2016	Icilin and menthol, agonists for TRPM8 and TRPA1, inhibited ASMC proliferation and migration induced by fetal bovine serum (FBS) or platelet-derived growth factor (PDGF).	asmc	60-64	transient receptor potential cation channel, subfamily M, member 8	Rattus norvegicus	33-38
27236325-8	2016	Icilin and menthol, agonists for TRPM8 and TRPA1, inhibited ASMC proliferation and migration induced by fetal bovine serum (FBS) or platelet-derived growth factor (PDGF).	asmc	60-64	transient receptor potential cation channel, subfamily A, member 1	Rattus norvegicus	43-48
26920052-4	2016	We found that exogenous S100A8 protein significantly inhibited PDGF-induced ASMC migration.	asmc	76-80	S100 calcium binding protein A8	Homo sapiens	24-30
27297409-11	2016	The expression of Wnt-5a, TGF-beta1, collagen, and fibronectin genes in ASMC was significantly higher after 24 h of co-culture with eosinophils from asthmatic subjects, while co-culture of ASMC with eosinophils from healthy subjects increased only TGF-beta1 and fibronectin gene expression.	asmc	72-76	Wnt family member 5A	Homo sapiens	18-24
27297409-11	2016	The expression of Wnt-5a, TGF-beta1, collagen, and fibronectin genes in ASMC was significantly higher after 24 h of co-culture with eosinophils from asthmatic subjects, while co-culture of ASMC with eosinophils from healthy subjects increased only TGF-beta1 and fibronectin gene expression.	asmc	72-76	transforming growth factor beta 1	Homo sapiens	26-35
27297409-11	2016	The expression of Wnt-5a, TGF-beta1, collagen, and fibronectin genes in ASMC was significantly higher after 24 h of co-culture with eosinophils from asthmatic subjects, while co-culture of ASMC with eosinophils from healthy subjects increased only TGF-beta1 and fibronectin gene expression.	asmc	72-76	fibronectin 1	Homo sapiens	51-62
27297409-11	2016	The expression of Wnt-5a, TGF-beta1, collagen, and fibronectin genes in ASMC was significantly higher after 24 h of co-culture with eosinophils from asthmatic subjects, while co-culture of ASMC with eosinophils from healthy subjects increased only TGF-beta1 and fibronectin gene expression.	asmc	72-76	transforming growth factor beta 1	Homo sapiens	248-257
27297409-11	2016	The expression of Wnt-5a, TGF-beta1, collagen, and fibronectin genes in ASMC was significantly higher after 24 h of co-culture with eosinophils from asthmatic subjects, while co-culture of ASMC with eosinophils from healthy subjects increased only TGF-beta1 and fibronectin gene expression.	asmc	72-76	fibronectin 1	Homo sapiens	262-273
27297409-11	2016	The expression of Wnt-5a, TGF-beta1, collagen, and fibronectin genes in ASMC was significantly higher after 24 h of co-culture with eosinophils from asthmatic subjects, while co-culture of ASMC with eosinophils from healthy subjects increased only TGF-beta1 and fibronectin gene expression.	asmc	189-193	Wnt family member 5A	Homo sapiens	18-24
27297409-11	2016	The expression of Wnt-5a, TGF-beta1, collagen, and fibronectin genes in ASMC was significantly higher after 24 h of co-culture with eosinophils from asthmatic subjects, while co-culture of ASMC with eosinophils from healthy subjects increased only TGF-beta1 and fibronectin gene expression.	asmc	189-193	fibronectin 1	Homo sapiens	51-62
26181301-12	2016	Modulation of ASMC phenotypes by methylated PDE4D oligonucleotides can reverse the aberrant ASMC functions to normal phenotypes.	asmc	14-18	phosphodiesterase 4D	Homo sapiens	44-49
26181301-12	2016	Modulation of ASMC phenotypes by methylated PDE4D oligonucleotides can reverse the aberrant ASMC functions to normal phenotypes.	asmc	92-96	phosphodiesterase 4D	Homo sapiens	44-49
26722444-5	2015	We found that apigenin inhibited transforming growth factor-beta1 (TGF-beta1)-induced ASMC proliferation.	asmc	86-90	transforming growth factor, beta 1	Mus musculus	67-76
26181301-5	2016	In this study, we aimed to examine the relationship between epigenetic regulation of PDE4D and ASMC phenotypes.	asmc	95-99	phosphodiesterase 4D	Homo sapiens	85-90
26575887-5	2015	With NK-1R inhibitor WIN62577 treatment, the changes in the migration of ASMC were measured by transwell chambers.	asmc	73-77	tachykinin receptor 1	Rattus norvegicus	5-10
26575887-6	2015	RESULTS: NK-1R in ASMC was expressed mainly in the cytoplasm and cell membrane in the airway remodeling group, and the mRNA expression of NK-1R was higher than the normal control group (P<0.01).	asmc	18-22	tachykinin receptor 1	Rattus norvegicus	9-14
26575887-9	2015	CONCLUSIONS: NK-1R may affect airway remodeling possibly through promoting the migration ability of ASMC in rats with asthma.	asmc	100-104	tachykinin receptor 1	Rattus norvegicus	13-18
25874477-5	2015	We investigate the implications of RyR sensitization on Ca(2+) dynamics in ASMC using a combination of mathematical modeling and experiments with mouse precision-cut lung slices.	asmc	75-79	ryanodine receptor 1, skeletal muscle	Mus musculus	35-38
25874477-10	2015	These results suggest that RyR sensitization could play a role in ASMC proliferation (by inducing slow Ca(2+) oscillations) and in airway hyperresponsiveness (by inducing greater mean [Ca(2+)]i for similar levels of contractile agonist).	asmc	66-70	ryanodine receptor 1, skeletal muscle	Mus musculus	27-30
25411910-2	2015	OBJECTIVES: We investigated whether there was a defect in the actions of the glucocorticoid receptor (GR) underlying the ability of CS to suppress the inflammatory response in ASMC of patients with SA.	asmc	176-180	nuclear receptor subfamily 3 group C member 1	Homo sapiens	77-100
26332463-3	2015	OBJECTIVE: We postulate that IgE contained in serum of allergic asthma patients, in the absence of allergens, stimulates ASMC remodeling activities and can be prevented by anti-IgE antibodies.	asmc	121-125	immunoglobulin heavy constant epsilon	Homo sapiens	29-32
26332463-3	2015	OBJECTIVE: We postulate that IgE contained in serum of allergic asthma patients, in the absence of allergens, stimulates ASMC remodeling activities and can be prevented by anti-IgE antibodies.	asmc	121-125	immunoglobulin heavy constant epsilon	Homo sapiens	177-180
26332463-9	2015	CONCLUSION AND CLINICAL RELEVANCE: Our data provides experimental evidence that the beneficial effect of Omalizumab on airway wall remodeling and improved lung function may be due to its direct action on IgE bound ASMC.	asmc	214-218	immunoglobulin heavy constant epsilon	Homo sapiens	204-207
25411910-2	2015	OBJECTIVES: We investigated whether there was a defect in the actions of the glucocorticoid receptor (GR) underlying the ability of CS to suppress the inflammatory response in ASMC of patients with SA.	asmc	176-180	nuclear receptor subfamily 3 group C member 1	Homo sapiens	102-104
25447441-7	2015	RESULTS: Triptolide significantly inhibited TGF-beta1-induced ASMC proliferation (P<0.05).	asmc	62-66	transforming growth factor, beta 1	Rattus norvegicus	44-53
25411910-4	2015	MEASUREMENTS AND MAIN RESULTS: GR expression in ASMC from SA and N-SA was reduced compared with that from healthy subjects by 49% (P < 0.01).	asmc	48-52	nuclear receptor subfamily 3 group C member 1	Homo sapiens	31-33
25411910-6	2015	Tumor necrosis factor (TNF)-alpha induced greater nuclear factor (NF)-kappaB (p65) mRNA expression in ASMC from subjects with SA (5.6- vs. 2.0-fold; P < 0.01), whereas baseline and TNF-alpha-induced nuclear translocation and dexamethasone-mediated suppression of p65 expression were similar between groups.	asmc	102-106	tumor necrosis factor	Homo sapiens	0-33
25411910-6	2015	Tumor necrosis factor (TNF)-alpha induced greater nuclear factor (NF)-kappaB (p65) mRNA expression in ASMC from subjects with SA (5.6- vs. 2.0-fold; P < 0.01), whereas baseline and TNF-alpha-induced nuclear translocation and dexamethasone-mediated suppression of p65 expression were similar between groups.	asmc	102-106	nuclear factor kappa B subunit 1	Homo sapiens	50-76
25411910-6	2015	Tumor necrosis factor (TNF)-alpha induced greater nuclear factor (NF)-kappaB (p65) mRNA expression in ASMC from subjects with SA (5.6- vs. 2.0-fold; P < 0.01), whereas baseline and TNF-alpha-induced nuclear translocation and dexamethasone-mediated suppression of p65 expression were similar between groups.	asmc	102-106	RELA proto-oncogene, NF-kB subunit	Homo sapiens	78-81
25411910-6	2015	Tumor necrosis factor (TNF)-alpha induced greater nuclear factor (NF)-kappaB (p65) mRNA expression in ASMC from subjects with SA (5.6- vs. 2.0-fold; P < 0.01), whereas baseline and TNF-alpha-induced nuclear translocation and dexamethasone-mediated suppression of p65 expression were similar between groups.	asmc	102-106	tumor necrosis factor	Homo sapiens	184-193
25411910-6	2015	Tumor necrosis factor (TNF)-alpha induced greater nuclear factor (NF)-kappaB (p65) mRNA expression in ASMC from subjects with SA (5.6- vs. 2.0-fold; P < 0.01), whereas baseline and TNF-alpha-induced nuclear translocation and dexamethasone-mediated suppression of p65 expression were similar between groups.	asmc	102-106	RELA proto-oncogene, NF-kB subunit	Homo sapiens	266-269
25267491-10	2014	RESULTS: Triptolide significantly inhibited TGF-beta1 induced ASMC proliferation and migration (p<0.05).	asmc	62-66	transforming growth factor, beta 1	Rattus norvegicus	44-53
26151666-8	2015	MiR-138 controls ASMC proliferation through directly inhibiting the phosphoinositide 3-kinase (PI3K) pathway.	asmc	17-21	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	68-93
25255717-5	2014	ASMC-associated cytokines/chemokines implicated in asthma (TGF-beta1, eotaxin, IL-6 and IL-8) were measured in co-culture or transwell culture of ASMC + FC by ELISA.	asmc	0-4	transforming growth factor beta 1	Homo sapiens	59-68
25255717-7	2014	Cytokine secretion was measured in the transwell culture of ASMC + FC, where NF-kappaB-p65 or ERK1/2 in ASMC was silenced by siRNA.	asmc	60-64	RELA proto-oncogene, NF-kB subunit	Homo sapiens	87-90
25255717-7	2014	Cytokine secretion was measured in the transwell culture of ASMC + FC, where NF-kappaB-p65 or ERK1/2 in ASMC was silenced by siRNA.	asmc	60-64	mitogen-activated protein kinase 3	Homo sapiens	94-100
25255717-7	2014	Cytokine secretion was measured in the transwell culture of ASMC + FC, where NF-kappaB-p65 or ERK1/2 in ASMC was silenced by siRNA.	asmc	104-108	mitogen-activated protein kinase 3	Homo sapiens	94-100
25255717-8	2014	Contractile phenotype of ASMC in transwell culture was assessed by immunoblotting of alpha-smooth muscle actin (alpha-SMA) and myosin light chain kinase (MLCK).	asmc	25-29	myosin light chain kinase	Homo sapiens	127-152
25255717-8	2014	Contractile phenotype of ASMC in transwell culture was assessed by immunoblotting of alpha-smooth muscle actin (alpha-SMA) and myosin light chain kinase (MLCK).	asmc	25-29	myosin light chain kinase	Homo sapiens	154-158
25255717-9	2014	RESULTS: Fibrocytes did not affect ASMC proliferation and expression of TGF-beta1, eotaxin, alpha-SMA and MLCK; however, ASMC production of IL-8 and IL-6 was increased in the co-culture and transwell culture by FC.	asmc	121-125	C-X-C motif chemokine ligand 8	Homo sapiens	140-144
25255717-9	2014	RESULTS: Fibrocytes did not affect ASMC proliferation and expression of TGF-beta1, eotaxin, alpha-SMA and MLCK; however, ASMC production of IL-8 and IL-6 was increased in the co-culture and transwell culture by FC.	asmc	121-125	interleukin 6	Homo sapiens	149-153
25255717-10	2014	ASMC treated with FCCM were immunopositive for IL-8/IL-6 and produced more IL-8/IL-6.	asmc	0-4	C-X-C motif chemokine ligand 8	Homo sapiens	47-51
25255717-10	2014	ASMC treated with FCCM were immunopositive for IL-8/IL-6 and produced more IL-8/IL-6.	asmc	0-4	interleukin 6	Homo sapiens	52-56
25255717-10	2014	ASMC treated with FCCM were immunopositive for IL-8/IL-6 and produced more IL-8/IL-6.	asmc	0-4	C-X-C motif chemokine ligand 8	Homo sapiens	75-79
25255717-10	2014	ASMC treated with FCCM were immunopositive for IL-8/IL-6 and produced more IL-8/IL-6.	asmc	0-4	interleukin 6	Homo sapiens	80-84
25255717-11	2014	Furthermore, siRNA silencing of NF-kappaB-p65 or ERK1/2 in transwell cultures of asthmatic ASMC with normal subject FC decreased IL-8 and IL-6 production.	asmc	91-95	RELA proto-oncogene, NF-kB subunit	Homo sapiens	42-45
25255717-11	2014	Furthermore, siRNA silencing of NF-kappaB-p65 or ERK1/2 in transwell cultures of asthmatic ASMC with normal subject FC decreased IL-8 and IL-6 production.	asmc	91-95	mitogen-activated protein kinase 3	Homo sapiens	49-55
25255717-11	2014	Furthermore, siRNA silencing of NF-kappaB-p65 or ERK1/2 in transwell cultures of asthmatic ASMC with normal subject FC decreased IL-8 and IL-6 production.	asmc	91-95	C-X-C motif chemokine ligand 8	Homo sapiens	129-133
25255717-11	2014	Furthermore, siRNA silencing of NF-kappaB-p65 or ERK1/2 in transwell cultures of asthmatic ASMC with normal subject FC decreased IL-8 and IL-6 production.	asmc	91-95	interleukin 6	Homo sapiens	138-142
25255717-12	2014	CONCLUSIONS AND CLINICAL RELEVANCE: Fibrocytes promoted IL-8 and IL-6 production by ASMC, demonstrating a proinflammatory role for FC and a possible mechanism of the inflammatory phenotype in asthma.	asmc	84-88	C-X-C motif chemokine ligand 8	Homo sapiens	56-60
25255717-12	2014	CONCLUSIONS AND CLINICAL RELEVANCE: Fibrocytes promoted IL-8 and IL-6 production by ASMC, demonstrating a proinflammatory role for FC and a possible mechanism of the inflammatory phenotype in asthma.	asmc	84-88	interleukin 6	Homo sapiens	65-69
24377382-7	2013	Mitogens as, epidermal growth factor (EGF), Tumor necrosis factor-alpha (TNF-alpha) and fetal bovine serum (FBS) increased ASMC proliferation (p < 0.05, n = 5).	asmc	123-127	epidermal growth factor like 1	Rattus norvegicus	13-36
24981451-3	2014	In this study, we present a detailed examination of the inhibitory effect of CXCL1 on human primary ASMC migration and the role of the decoy receptor, Duffy AgR for chemokines (DARC), in this inhibition.	asmc	100-104	C-X-C motif chemokine ligand 1	Homo sapiens	77-82
24981451-7	2014	In conclusion, we demonstrated DARC"s ability to facilitate CXCL1 inhibition of ASMC migration through modulation of the ERK-1/2 MAPK-signaling pathway.	asmc	80-84	atypical chemokine receptor 1 (Duffy blood group)	Homo sapiens	31-35
24981451-7	2014	In conclusion, we demonstrated DARC"s ability to facilitate CXCL1 inhibition of ASMC migration through modulation of the ERK-1/2 MAPK-signaling pathway.	asmc	80-84	C-X-C motif chemokine ligand 1	Homo sapiens	60-65
24981451-7	2014	In conclusion, we demonstrated DARC"s ability to facilitate CXCL1 inhibition of ASMC migration through modulation of the ERK-1/2 MAPK-signaling pathway.	asmc	80-84	mitogen-activated protein kinase 3	Homo sapiens	121-128
24981451-7	2014	In conclusion, we demonstrated DARC"s ability to facilitate CXCL1 inhibition of ASMC migration through modulation of the ERK-1/2 MAPK-signaling pathway.	asmc	80-84	mitogen-activated protein kinase 3	Homo sapiens	129-133
24392954-7	2014	We show that ASMC proliferation in response to TRPV4 activity is associated with calcineurin-dependent nuclear translocation of the NFATc3 isoform tagged with green florescent protein.	asmc	13-17	transient receptor potential cation channel subfamily V member 4	Homo sapiens	47-52
24392954-7	2014	We show that ASMC proliferation in response to TRPV4 activity is associated with calcineurin-dependent nuclear translocation of the NFATc3 isoform tagged with green florescent protein.	asmc	13-17	nuclear factor of activated T cells 3	Homo sapiens	132-138
24392954-8	2014	Our findings suggest that Ca(2+) microdomains created by TRPV4 Ca(2+) sparklets activate calcineurin to stimulate nuclear translocation of NFAT and ASMC proliferation.	asmc	148-152	transient receptor potential cation channel subfamily V member 4	Homo sapiens	57-62
24377382-7	2013	Mitogens as, epidermal growth factor (EGF), Tumor necrosis factor-alpha (TNF-alpha) and fetal bovine serum (FBS) increased ASMC proliferation (p < 0.05, n = 5).	asmc	123-127	epidermal growth factor like 1	Rattus norvegicus	38-41
24377382-7	2013	Mitogens as, epidermal growth factor (EGF), Tumor necrosis factor-alpha (TNF-alpha) and fetal bovine serum (FBS) increased ASMC proliferation (p < 0.05, n = 5).	asmc	123-127	tumor necrosis factor	Rattus norvegicus	44-71
24377382-7	2013	Mitogens as, epidermal growth factor (EGF), Tumor necrosis factor-alpha (TNF-alpha) and fetal bovine serum (FBS) increased ASMC proliferation (p < 0.05, n = 5).	asmc	123-127	tumor necrosis factor	Rattus norvegicus	73-82
24010863-7	2013	RESULTS: Compared with the control group, the asthma group showed an increased expression of TRPV1 and [Ca2+](i) in rat ASMC.	asmc	120-124	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	93-98
23534390-4	2014	Furthermore, we found that the 12-LOX inhibitors cinnamyl-3,4-dihydroxy-alpha-cyanocinnamate (CDC) and Baicalein prevented platelet activation in a co-cultures of platelets and ASMC.	asmc	177-181	arachidonate 15-lipoxygenase	Homo sapiens	31-37
23534390-7	2014	Importantly, platelet-induced ASMC proliferation and ROS production generated during the platelet/ASMC interaction was significantly inhibited in the presence of 12-LOX inhibitors.	asmc	30-34	arachidonate 15-lipoxygenase	Homo sapiens	162-168
23534390-7	2014	Importantly, platelet-induced ASMC proliferation and ROS production generated during the platelet/ASMC interaction was significantly inhibited in the presence of 12-LOX inhibitors.	asmc	98-102	arachidonate 15-lipoxygenase	Homo sapiens	162-168
23534390-8	2014	In conclusion, our findings reveal that 12-LOX is crucial for the observed enhancement of ASMC proliferation in co-cultures of platelets and ASMC.	asmc	90-94	arachidonate 15-lipoxygenase	Homo sapiens	40-46
23534390-8	2014	In conclusion, our findings reveal that 12-LOX is crucial for the observed enhancement of ASMC proliferation in co-cultures of platelets and ASMC.	asmc	141-145	arachidonate 15-lipoxygenase	Homo sapiens	40-46
23534390-9	2014	The present result suggests that 12-LOX activity is important in the initial step of platelet/ASMC interaction and platelet activation.	asmc	94-98	arachidonate 15-lipoxygenase	Homo sapiens	33-39
24010863-8	2013	The expression of PCNA and absorbance of MTT assay in asthma rat ASMC was also significantly increased.	asmc	65-69	proliferating cell nuclear antigen	Rattus norvegicus	18-22
24010863-9	2013	SMI could significantly decrease the expression of TRPV1 channel and [Ca2+](i) in the asthmatic rat ASMC.	asmc	100-104	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	51-56
24010863-10	2013	Furthermore, the expression of PCNA and absorbance of MTT assay in asthmatic rat ASMC was significantly reduced after SMI treatment.	asmc	81-85	proliferating cell nuclear antigen	Rattus norvegicus	31-35
24010863-11	2013	CONCLUSIONS: SMI may prevent asthma-induced ASMC over-proliferation probably by inhibiting the expression of TRPV1 channel, which regulates the intracellular calcium concentration.	asmc	44-48	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	109-114
23919305-3	2013	This study explores the expression of TRPV1 channel and its effect on the proliferation and apoptosis in rat ASMC, in order to find a new target to treat airway remodeling in asthma.	asmc	109-113	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	38-43
23919305-10	2013	RESULTS: (1) The expression of PCNA was significantly increased in intact asthmatic rat ASMC.	asmc	88-92	proliferating cell nuclear antigen	Rattus norvegicus	31-35
23919305-11	2013	(2) The expression of TRPV1 channel was significantly increased in asthmatic rat ASMC.	asmc	81-85	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	22-27
23919305-13	2013	After treatment with TRPV1 agonist capsaicin (CAP), [Ca(2+)]i was further increased, whereas [Ca(2+)]i was decreased after administration of TRPV1 antagonist capsazepine (CPZ) in ASMC of the asthmatic group.	asmc	179-183	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	141-146
23919305-17	2013	CONCLUSION: TRPV1 channel was involved in the regulation of proliferation and apoptosis in asthmatic ASMC.	asmc	101-105	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	12-17
23564506-7	2013	BAPTA-AM abolished early CXCL10/CXCL11 mRNA production, whereas thapsigargin reduced it in asthmatic cells and inhibited CXCL10/CXCL11 release by both ASMC types.	asmc	151-155	C-X-C motif chemokine ligand 10	Homo sapiens	121-127
23904157-5	2013	We established the ability of CXCL2 and CXCL3, but not CXCL1, to induce ASMC migration at the tested concentrations using normal ASMCs.	asmc	72-76	C-X-C motif chemokine ligand 2	Homo sapiens	30-35
23904157-5	2013	We established the ability of CXCL2 and CXCL3, but not CXCL1, to induce ASMC migration at the tested concentrations using normal ASMCs.	asmc	72-76	C-X-C motif chemokine ligand 3	Homo sapiens	40-45
23904157-6	2013	We found CXCL2-induced ASMC migration to be dependent on p38 MAPK and CXCR2, whereas CXCL3-induced migration was dependent on p38 and ERK1/2 MAPK pathways via CXCR1 and CXCR2.	asmc	23-27	C-X-C motif chemokine ligand 2	Homo sapiens	9-14
23904157-6	2013	We found CXCL2-induced ASMC migration to be dependent on p38 MAPK and CXCR2, whereas CXCL3-induced migration was dependent on p38 and ERK1/2 MAPK pathways via CXCR1 and CXCR2.	asmc	23-27	mitogen-activated protein kinase 1	Homo sapiens	57-60
23904157-6	2013	We found CXCL2-induced ASMC migration to be dependent on p38 MAPK and CXCR2, whereas CXCL3-induced migration was dependent on p38 and ERK1/2 MAPK pathways via CXCR1 and CXCR2.	asmc	23-27	mitogen-activated protein kinase 3	Homo sapiens	61-65
23904157-6	2013	We found CXCL2-induced ASMC migration to be dependent on p38 MAPK and CXCR2, whereas CXCL3-induced migration was dependent on p38 and ERK1/2 MAPK pathways via CXCR1 and CXCR2.	asmc	23-27	C-X-C motif chemokine receptor 2	Homo sapiens	70-75
23904157-7	2013	While investigating the effect of CXCL2 and CXCL3 on asthmatic ASMC migration, we found that they induced greater migration of asthmatic ASMCs compared with normal ones.	asmc	63-67	C-X-C motif chemokine ligand 2	Homo sapiens	34-39
23904157-7	2013	While investigating the effect of CXCL2 and CXCL3 on asthmatic ASMC migration, we found that they induced greater migration of asthmatic ASMCs compared with normal ones.	asmc	63-67	C-X-C motif chemokine ligand 3	Homo sapiens	44-49
23904157-8	2013	Interestingly, unlike normal ASMCs, CXCL2- and CXCL3-induced asthmatic ASMC migration was mainly mediated by the PI3K pathway through CXCR1.	asmc	29-33	C-X-C motif chemokine ligand 3	Homo sapiens	47-52
23904157-9	2013	In conclusion, our results establish a new role of CXCR1 in ASMC migration and demonstrate the diverse mechanisms by which CXCL2 and CXCL3 mediate normal and asthmatic ASMC migration, suggesting that they may play a role in the pathogenesis of airway remodeling in asthma.	asmc	60-64	C-X-C motif chemokine receptor 1	Homo sapiens	51-56
23784541-4	2013	Comparison of the current in ASMC with current mediated by NaV1.5 alpha-subunits expressed in human embryonic kidney cells revealed similar voltage dependences of activation (V1/2 = -42 mV for NaV1.5) and sensitivities to TTX (IC50 = 1.1 and 1.2 muM for ASMC and NaV1.5, respectively).	asmc	29-33	sodium voltage-gated channel alpha subunit 5	Homo sapiens	193-199
23784541-10	2013	We conclude that freshly dispersed rabbit ASMC express a fast voltage-gated Na(+) current that is mediated mainly by the NaV1.5 subtype.	asmc	42-46	sodium voltage-gated channel alpha subunit 5	Homo sapiens	121-127
23564506-7	2013	BAPTA-AM abolished early CXCL10/CXCL11 mRNA production, whereas thapsigargin reduced it in asthmatic cells and inhibited CXCL10/CXCL11 release by both ASMC types.	asmc	151-155	C-X-C motif chemokine ligand 11	Homo sapiens	128-134
23452113-8	2013	The proliferation of ASMC stimulated with 2.5% FBS was promoted by TGF-beta1, and partly inhibited by non-specific Ca(2+) channel blocker SKF-96365 (10 muM) and Ni(2+) (100 muM).	asmc	21-25	transforming growth factor, beta 1	Rattus norvegicus	67-76
23452113-10	2013	CONCLUSION: TGF-beta1 promotes ASMC proliferation partly through increasing the expression and activity of SOC channels.	asmc	31-35	transforming growth factor, beta 1	Rattus norvegicus	12-21
23328183-14	2012	CONCLUSION: Leptin can significantly inhibit ASMC apoptosis partially via the PI3K/Akt signaling pathway.	asmc	45-49	leptin	Rattus norvegicus	12-18
23042471-11	2013	CONCLUSION: Ahnak protein plays an important scaffolding function connecting Erk and Rac activation in PDGF-dependent migration of ASMC.	asmc	131-135	AHNAK nucleoprotein (desmoyokin)	Mus musculus	12-17
23042471-11	2013	CONCLUSION: Ahnak protein plays an important scaffolding function connecting Erk and Rac activation in PDGF-dependent migration of ASMC.	asmc	131-135	mitogen-activated protein kinase 1	Mus musculus	77-80
23042471-11	2013	CONCLUSION: Ahnak protein plays an important scaffolding function connecting Erk and Rac activation in PDGF-dependent migration of ASMC.	asmc	131-135	thymoma viral proto-oncogene 1	Mus musculus	85-88
23457497-7	2013	Using inhibitors of cyclooxygenase and prostaglandin receptor antagonists, we found that beta2 adrenoceptor desensitization was mediated through ASMC derived COX-2 induced prostaglandins.	asmc	145-149	adrenoceptor beta 2	Homo sapiens	89-107
23457497-7	2013	Using inhibitors of cyclooxygenase and prostaglandin receptor antagonists, we found that beta2 adrenoceptor desensitization was mediated through ASMC derived COX-2 induced prostaglandins.	asmc	145-149	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	158-163
23457497-9	2013	The combination of TLR agonists poly I:C and imiquimod induced PGE2 and beta2 adrenoceptor desensitization on ASMC as did the RNA extracted from RV-induced conditioned medium.	asmc	110-114	adrenoceptor beta 2	Homo sapiens	72-90
23354389-7	2013	CONCLUSIONS: Some HDL subclasses enriched in a novel isoform of apoC-I induce extensive ASMC apoptosis in vitro.	asmc	88-92	apolipoprotein C1	Homo sapiens	64-70
23328183-14	2012	CONCLUSION: Leptin can significantly inhibit ASMC apoptosis partially via the PI3K/Akt signaling pathway.	asmc	45-49	AKT serine/threonine kinase 1	Rattus norvegicus	83-86
23014880-7	2012	Here, we show that STIM1 and Orai1 protein levels are greatly upregulated in ASMC isolated from ovalbumin-challenged asthmatic mice, compared to control mice.	asmc	77-81	stromal interaction molecule 1	Mus musculus	19-24
23014880-7	2012	Here, we show that STIM1 and Orai1 protein levels are greatly upregulated in ASMC isolated from ovalbumin-challenged asthmatic mice, compared to control mice.	asmc	77-81	ORAI calcium release-activated calcium modulator 1	Mus musculus	29-34
23014880-12	2012	We show that either STIM1 or Orai1 knockdown significantly inhibited ASMC proliferation and chemotactic migration in response to PDGF.	asmc	69-73	stromal interaction molecule 1	Mus musculus	20-25
23014880-12	2012	We show that either STIM1 or Orai1 knockdown significantly inhibited ASMC proliferation and chemotactic migration in response to PDGF.	asmc	69-73	ORAI calcium release-activated calcium modulator 1	Mus musculus	29-34
23014880-13	2012	These results implicate STIM1 and Orai1 in PDGF-induced ASMC proliferation and migration and suggest the potential use of STIM1 and Orai1 as targets for ASMC remodeling during asthma.	asmc	56-60	stromal interaction molecule 1	Mus musculus	24-29
23014880-13	2012	These results implicate STIM1 and Orai1 in PDGF-induced ASMC proliferation and migration and suggest the potential use of STIM1 and Orai1 as targets for ASMC remodeling during asthma.	asmc	56-60	ORAI calcium release-activated calcium modulator 1	Mus musculus	34-39
23014880-13	2012	These results implicate STIM1 and Orai1 in PDGF-induced ASMC proliferation and migration and suggest the potential use of STIM1 and Orai1 as targets for ASMC remodeling during asthma.	asmc	153-157	stromal interaction molecule 1	Mus musculus	122-127
23014880-13	2012	These results implicate STIM1 and Orai1 in PDGF-induced ASMC proliferation and migration and suggest the potential use of STIM1 and Orai1 as targets for ASMC remodeling during asthma.	asmc	153-157	ORAI calcium release-activated calcium modulator 1	Mus musculus	132-137
22698519-5	2012	METHODS: The effect of IL-17-induced supernatants on human ASMC migration was investigated.	asmc	59-63	interleukin 17A	Homo sapiens	23-28
22698519-8	2012	RESULTS: IL-17-induced supernatants promoted ASMC migration.	asmc	45-49	interleukin 17A	Homo sapiens	9-14
22698519-11	2012	CONCLUSION: These findings suggest that IL-17-induced GROs can be an important mediator of ASMC migration and therefore might contribute to the pathogenesis of airway remodeling in asthmatic patients.	asmc	91-95	interleukin 17A	Homo sapiens	40-45
22616553-4	2012	ASMC was derived from rat airway tissue and cultured in vitro, then incubated with 10 ng/mL of TNF-alpha.	asmc	0-4	tumor necrosis factor	Rattus norvegicus	95-104
22616553-7	2012	Stimulation with TNF-alpha increased IL-8 and eotaxin secretion, with increased IL-8 secretion by allergen-exposed compared with naive control ASMC, post-TNF-alpha stimulation (P = 0.001).	asmc	143-147	tumor necrosis factor	Rattus norvegicus	17-26
22616553-8	2012	Baseline phosphorylation of ERK1/2 (p-ERK1/2) and NF-kappaB p65 was higher in allergen-exposed than in control ASMC.	asmc	111-115	mitogen activated protein kinase 3	Rattus norvegicus	28-34
22616553-8	2012	Baseline phosphorylation of ERK1/2 (p-ERK1/2) and NF-kappaB p65 was higher in allergen-exposed than in control ASMC.	asmc	111-115	mitogen activated protein kinase 3	Rattus norvegicus	38-44
22616553-8	2012	Baseline phosphorylation of ERK1/2 (p-ERK1/2) and NF-kappaB p65 was higher in allergen-exposed than in control ASMC.	asmc	111-115	synaptotagmin 1	Rattus norvegicus	60-63
22616553-9	2012	TNF-alpha increased p-ERK1/2 and NF-kappaB p65 levels, with higher levels in allergen-exposed ASMC, post-TNF-alpha stimulation (P < 0.001).	asmc	94-98	tumor necrosis factor	Rattus norvegicus	0-9
24049651-4	2012	Regarding rabbit tracheal ASMC proliferation, TNF- alpha , IL-1 beta , TGF, and PDGF increased methyl-[(3)H]thymidine incorporation in a PI3K- and MAPK-dependent manner.	asmc	26-30	interleukin-1 beta	Oryctolagus cuniculus	59-68
22268118-5	2012	ASMC stimulation with IL-1beta, TNF-alpha, and IFNgamma (cytomix) induced the highest level of syndecan-4 shedding.	asmc	0-4	interleukin 1 beta	Homo sapiens	22-30
22268118-5	2012	ASMC stimulation with IL-1beta, TNF-alpha, and IFNgamma (cytomix) induced the highest level of syndecan-4 shedding.	asmc	0-4	tumor necrosis factor	Homo sapiens	32-41
22268118-5	2012	ASMC stimulation with IL-1beta, TNF-alpha, and IFNgamma (cytomix) induced the highest level of syndecan-4 shedding.	asmc	0-4	interferon gamma	Homo sapiens	47-55
22268118-5	2012	ASMC stimulation with IL-1beta, TNF-alpha, and IFNgamma (cytomix) induced the highest level of syndecan-4 shedding.	asmc	0-4	syndecan 4	Homo sapiens	95-105
22268118-10	2012	In conclusion, ASMC produce and shed syndecan-4 and although this is increased by the Th1 cytokines, the MAPK ERK only regulates shedding.	asmc	15-19	syndecan 4	Homo sapiens	37-47
22268118-10	2012	In conclusion, ASMC produce and shed syndecan-4 and although this is increased by the Th1 cytokines, the MAPK ERK only regulates shedding.	asmc	15-19	negative elongation factor complex member C/D	Homo sapiens	86-89
22268118-11	2012	ASMC syndecan-4 production during Th1 inflammatory conditions may regulate chemokine activity and mast cell recruitment to the ASM in asthma.	asmc	0-4	syndecan 4	Homo sapiens	5-15
22268118-11	2012	ASMC syndecan-4 production during Th1 inflammatory conditions may regulate chemokine activity and mast cell recruitment to the ASM in asthma.	asmc	0-4	negative elongation factor complex member C/D	Homo sapiens	34-37
22227408-3	2012	The aim of the present study was to investigate the role of HA, the HA-binding surface receptor CD44 and focal adhesion kinase (FAK) in platelet-induced ASMC proliferation.	asmc	153-157	CD44 molecule (Indian blood group)	Homo sapiens	96-100
22227408-3	2012	The aim of the present study was to investigate the role of HA, the HA-binding surface receptor CD44 and focal adhesion kinase (FAK) in platelet-induced ASMC proliferation.	asmc	153-157	protein tyrosine kinase 2	Homo sapiens	105-126
22227408-3	2012	The aim of the present study was to investigate the role of HA, the HA-binding surface receptor CD44 and focal adhesion kinase (FAK) in platelet-induced ASMC proliferation.	asmc	153-157	protein tyrosine kinase 2	Homo sapiens	128-131
22227408-4	2012	Proliferation of ASMC was measured using the MTS-assay, and we found that the CD44 blocking antibody and the HA synthase inhibitor 4-Methylumbelliferone (4-MU) significantly inhibited platelet-induced ASMC proliferation.	asmc	17-21	CD44 molecule (Indian blood group)	Homo sapiens	78-82
22227408-4	2012	Proliferation of ASMC was measured using the MTS-assay, and we found that the CD44 blocking antibody and the HA synthase inhibitor 4-Methylumbelliferone (4-MU) significantly inhibited platelet-induced ASMC proliferation.	asmc	201-205	CD44 molecule (Indian blood group)	Homo sapiens	78-82
22227408-7	2012	We observed that ASMC produced HA and that a CD44 blocking antibody and 4-MU significantly inhibited platelet binding to the area surrounding the ASMC.	asmc	146-150	CD44 molecule (Indian blood group)	Homo sapiens	45-49
22227408-8	2012	Furthermore, the FAK-inhibitor PF 573228 inhibited platelet-induced ASMC proliferation.	asmc	68-72	protein tyrosine kinase 2	Homo sapiens	17-20
22227408-9	2012	Co-culture of ASMC and platelets also resulted in increased phosphorylation of FAK as detected by Western blot analysis.	asmc	14-18	protein tyrosine kinase 2	Homo sapiens	79-82
22227408-12	2012	Specifically, we propose that HA produced by ASMC is recognised by platelet CD44.	asmc	45-49	CD44 molecule (Indian blood group)	Homo sapiens	76-80
22003087-8	2012	TGF-beta(1) upregulated deposition of perlecan by ASMC from COPD subjects only.	asmc	50-54	transforming growth factor beta 1	Homo sapiens	0-11
22159081-10	2012	GRK2 and arrestin expression are essential for agonist-stimulated ASMC migration, which, as a key process in vascular remodeling, highlights the potential roles of GRK2 and arrestin proteins in the progression of vascular disease.	asmc	66-70	G protein-coupled receptor kinase 2	Rattus norvegicus	0-4
22159081-10	2012	GRK2 and arrestin expression are essential for agonist-stimulated ASMC migration, which, as a key process in vascular remodeling, highlights the potential roles of GRK2 and arrestin proteins in the progression of vascular disease.	asmc	66-70	G protein-coupled receptor kinase 2	Rattus norvegicus	164-168
22159994-8	2012	ASMC proliferation under hypoxia did not decrease during incubation with VEGFR-2-neutralizing antibody but did decrease upon PDGFR antagonist incubation.	asmc	0-4	platelet derived growth factor receptor beta	Homo sapiens	125-130
22003087-9	2012	TGF-beta(1) upregulated release of IL-6 into the supernatant of ASMC from all subjects.	asmc	64-68	transforming growth factor beta 1	Homo sapiens	0-11
22003087-9	2012	TGF-beta(1) upregulated release of IL-6 into the supernatant of ASMC from all subjects.	asmc	64-68	interleukin 6	Homo sapiens	35-39
22003087-10	2012	Inhibitors of SMAD and JNK signaling molecules decreased TGF-beta(1)-induced perlecan deposition by COPD ASMC.	asmc	105-109	transforming growth factor beta 1	Homo sapiens	57-68
22003087-10	2012	Inhibitors of SMAD and JNK signaling molecules decreased TGF-beta(1)-induced perlecan deposition by COPD ASMC.	asmc	105-109	COPD	Homo sapiens	100-104
22003087-11	2012	Attachment of COPD ASMC was upregulated by collagen I and perlecan domains IV and V, while perlecan domain II upregulated attachment only of asthmatic ASMC.	asmc	19-23	COPD	Homo sapiens	14-18
22003087-11	2012	Attachment of COPD ASMC was upregulated by collagen I and perlecan domains IV and V, while perlecan domain II upregulated attachment only of asthmatic ASMC.	asmc	151-155	COPD	Homo sapiens	14-18
22003087-13	2012	TGF-beta(1)-induced perlecan deposition may enhance attachment of migrating ASMC in vivo and thus may be a mechanism for ASMC layer hypertrophy in COPD.	asmc	76-80	transforming growth factor beta 1	Homo sapiens	0-11
22003087-13	2012	TGF-beta(1)-induced perlecan deposition may enhance attachment of migrating ASMC in vivo and thus may be a mechanism for ASMC layer hypertrophy in COPD.	asmc	121-125	transforming growth factor beta 1	Homo sapiens	0-11
22003087-13	2012	TGF-beta(1)-induced perlecan deposition may enhance attachment of migrating ASMC in vivo and thus may be a mechanism for ASMC layer hypertrophy in COPD.	asmc	121-125	COPD	Homo sapiens	147-151
22085644-4	2012	These results suggest that Ankrd1 and desmin may play important roles on ASMC homeostasis.	asmc	73-77	ankyrin repeat domain 1	Homo sapiens	27-33
22092970-4	2012	OBJECTIVE: To determine the production and the regulation of CCL15 by ASMC and to investigate its production in asthmatic airways.	asmc	70-74	C-C motif chemokine ligand 15	Homo sapiens	61-66
22092970-9	2012	RESULTS: CCL15 is constitutively expressed in human ASMC and is strongly up-regulated by TNF-alpha.	asmc	52-56	C-C motif chemokine ligand 15	Homo sapiens	9-14
22092970-14	2012	CONCLUSION AND CLINICAL RELEVANCE: Our results show that ASMC are a potent source of CCL15 in the airways and may directly participate in the recruitment of inflammatory cells to asthmatic airways.	asmc	57-61	C-C motif chemokine ligand 15	Homo sapiens	85-90
22092970-15	2012	Targeting the production of CCL15 by ASMC might reduce the inflammatory response within the airways of asthmatic patients.	asmc	37-41	C-C motif chemokine ligand 15	Homo sapiens	28-33
22085644-4	2012	These results suggest that Ankrd1 and desmin may play important roles on ASMC homeostasis.	asmc	73-77	desmin	Homo sapiens	38-44
22085644-10	2012	Overall, our data provide a new link between desmin and Ankrd1 regulation, which may be important for ASMC homeostasis.	asmc	102-106	desmin	Homo sapiens	45-51
22085644-10	2012	Overall, our data provide a new link between desmin and Ankrd1 regulation, which may be important for ASMC homeostasis.	asmc	102-106	ankyrin repeat domain 1	Homo sapiens	56-62
21903578-8	2011	These results suggest that desmin may play an important role in ASMC homeostasis.	asmc	64-68	desmin	Homo sapiens	27-33
21903578-14	2011	Overall, our data demonstrate a novel role for desmin as an anti-hypertrophic protein necessary for ASMC homeostasis and identifies desmin as a novel regulator of microRNA.	asmc	100-104	desmin	Homo sapiens	47-53
21777465-11	2011	Flow cytometric analysis (FCM) revealed that most asthmatic rat ASMC stayed at G1 phase after combined treatment with WIN62577 and IL-13 in vitro.	asmc	64-68	interleukin 13	Rattus norvegicus	131-136
21799075-9	2011	Nrf2 activation attenuated TGF-beta-mediated reduction in HO-1,ASMC proliferation, and IL-6 release.	asmc	63-67	NFE2 like bZIP transcription factor 2	Homo sapiens	0-4
21799075-9	2011	Nrf2 activation attenuated TGF-beta-mediated reduction in HO-1,ASMC proliferation, and IL-6 release.	asmc	63-67	transforming growth factor beta 1	Homo sapiens	27-35
21817107-8	2011	CONCLUSION: The results suggest that miR-21 is able to regulate ASMC function by targeting tropomyosin 1.	asmc	64-68	microRNA 21	Homo sapiens	37-43
21777465-13	2011	Therefore, we conclude that NK-1R is related to asthma mechanisms and a NK-1R antagonist downregulates calcium concentration in asthmatic ASMC by increasing Serca2 mRNA and decreasing Ip3r mRNA expression.	asmc	138-142	tachykinin receptor 1	Rattus norvegicus	72-77
21777465-14	2011	The NK-1R antagonist WIN62577 inhibited ASMC IL-13-induced proliferation and ASMC migration in vitro and therefore may be a new therapeutic option in asthma.	asmc	40-44	tachykinin receptor 1	Rattus norvegicus	4-9
21777465-14	2011	The NK-1R antagonist WIN62577 inhibited ASMC IL-13-induced proliferation and ASMC migration in vitro and therefore may be a new therapeutic option in asthma.	asmc	40-44	interleukin 13	Rattus norvegicus	45-50
21777465-14	2011	The NK-1R antagonist WIN62577 inhibited ASMC IL-13-induced proliferation and ASMC migration in vitro and therefore may be a new therapeutic option in asthma.	asmc	77-81	tachykinin receptor 1	Rattus norvegicus	4-9
21777465-14	2011	The NK-1R antagonist WIN62577 inhibited ASMC IL-13-induced proliferation and ASMC migration in vitro and therefore may be a new therapeutic option in asthma.	asmc	77-81	interleukin 13	Rattus norvegicus	45-50
21330611-7	2011	In this study, we investigated whether STIM1/Orai1-mediated SOCE is involved in rat ASMC proliferation.	asmc	84-88	stromal interaction molecule 1	Rattus norvegicus	39-44
21460123-6	2011	We found that IL-13 inhibits human ASMC proliferation (expression of Ki67 and bromodeoxyuridine incorporation) in response to serum, increasing the number of cells in G0/G1 phase and decreasing the number of cells in G2/M phases of the cell cycle.	asmc	35-39	interleukin 13	Homo sapiens	14-19
21460123-8	2011	In parallel, IL-13 increased calcium signaling and the stiffening of human ASMC in response to 1 muM histamine, whereas the stiffening response to 30 mM KCl was unchanged.	asmc	75-79	interleukin 13	Homo sapiens	13-18
21460123-8	2011	In parallel, IL-13 increased calcium signaling and the stiffening of human ASMC in response to 1 muM histamine, whereas the stiffening response to 30 mM KCl was unchanged.	asmc	75-79	latexin	Homo sapiens	97-100
21460123-10	2011	We conclude that IL-13 inhibits proliferation via the IL-13Ralpha2 receptor and induces hypercontractility of human ASMC without change of the phenotypic markers of contractility.	asmc	116-120	interleukin 13	Homo sapiens	17-22
21306579-6	2011	Both CSE and acrolein (30 microM) induced VEGF mRNA expression in ASMC cultures, suggesting an effect at transcriptional level.	asmc	66-70	vascular endothelial growth factor A	Homo sapiens	42-46
21330611-7	2011	In this study, we investigated whether STIM1/Orai1-mediated SOCE is involved in rat ASMC proliferation.	asmc	84-88	ORAI calcium release-activated calcium modulator 1	Rattus norvegicus	45-50
21330611-8	2011	We found that SOCE was upregulated during ASMC proliferation accompanied by a mild increase of STIM1 and a significant increase of Orai1 mRNA expression, whereas the proliferation of ASMCs was partially inhibited by the SOC channel blockers SKF-96365, NiCl(2), and BTP-2.	asmc	42-46	stromal interaction molecule 1	Homo sapiens	95-100
21330611-8	2011	We found that SOCE was upregulated during ASMC proliferation accompanied by a mild increase of STIM1 and a significant increase of Orai1 mRNA expression, whereas the proliferation of ASMCs was partially inhibited by the SOC channel blockers SKF-96365, NiCl(2), and BTP-2.	asmc	42-46	ORAI calcium release-activated calcium modulator 1	Homo sapiens	131-136
21330611-9	2011	Suppressing the mRNA expression of STIM1 or Orai1 with specific short hairpin RNA resulted in the attenuation of SOCE and ASMC proliferation.	asmc	122-126	stromal interaction molecule 1	Homo sapiens	35-40
21330611-9	2011	Suppressing the mRNA expression of STIM1 or Orai1 with specific short hairpin RNA resulted in the attenuation of SOCE and ASMC proliferation.	asmc	122-126	ORAI calcium release-activated calcium modulator 1	Homo sapiens	44-49
21330611-11	2011	These results suggested that STIM1/Orai1-mediated SOCE is involved in ASMC proliferation.	asmc	70-74	stromal interaction molecule 1	Homo sapiens	29-34
21330611-11	2011	These results suggested that STIM1/Orai1-mediated SOCE is involved in ASMC proliferation.	asmc	70-74	ORAI calcium release-activated calcium modulator 1	Homo sapiens	35-40
21194398-8	2011	In the present work we established that platelet membrane-induced ASMC proliferation was reduced in the presence of the NADPH oxidase inhibitor DPI and the 5-LOX inhibitor AA-861.	asmc	66-70	arachidonate 5-lipoxygenase	Homo sapiens	156-161
21239533-9	2011	T-bet expression also reduces chemotactic migration of ASMC in response to serum and PDGF, which contributes to airway hyperplasia.	asmc	55-59	T-box transcription factor 21	Homo sapiens	0-5
21368236-5	2011	The objective of the current study is to test the hypothesis that chemokines (eotaxin, RANTES, IL-8, and MIP-1alpha) can directly influence ASMC mass by increasing the rate of proliferation or enhancing the survival of these cells.	asmc	140-144	C-C motif chemokine ligand 11	Homo sapiens	78-85
21368236-5	2011	The objective of the current study is to test the hypothesis that chemokines (eotaxin, RANTES, IL-8, and MIP-1alpha) can directly influence ASMC mass by increasing the rate of proliferation or enhancing the survival of these cells.	asmc	140-144	C-C motif chemokine ligand 5	Homo sapiens	87-93
21368236-5	2011	The objective of the current study is to test the hypothesis that chemokines (eotaxin, RANTES, IL-8, and MIP-1alpha) can directly influence ASMC mass by increasing the rate of proliferation or enhancing the survival of these cells.	asmc	140-144	C-X-C motif chemokine ligand 8	Homo sapiens	95-99
21368236-5	2011	The objective of the current study is to test the hypothesis that chemokines (eotaxin, RANTES, IL-8, and MIP-1alpha) can directly influence ASMC mass by increasing the rate of proliferation or enhancing the survival of these cells.	asmc	140-144	C-C motif chemokine ligand 3	Homo sapiens	105-115
21368236-10	2011	In a concentration-dependent manner, chemokines including eotaxin, RANTES, IL-8, and MIP-1alpha increased ASMC"s [(3)H]thymidine incorporation and DNA synthesis.	asmc	106-110	C-C motif chemokine ligand 11	Homo sapiens	58-65
21368236-10	2011	In a concentration-dependent manner, chemokines including eotaxin, RANTES, IL-8, and MIP-1alpha increased ASMC"s [(3)H]thymidine incorporation and DNA synthesis.	asmc	106-110	C-C motif chemokine ligand 5	Homo sapiens	67-73
21368236-10	2011	In a concentration-dependent manner, chemokines including eotaxin, RANTES, IL-8, and MIP-1alpha increased ASMC"s [(3)H]thymidine incorporation and DNA synthesis.	asmc	106-110	C-X-C motif chemokine ligand 8	Homo sapiens	75-79
21368236-10	2011	In a concentration-dependent manner, chemokines including eotaxin, RANTES, IL-8, and MIP-1alpha increased ASMC"s [(3)H]thymidine incorporation and DNA synthesis.	asmc	106-110	C-C motif chemokine ligand 3	Homo sapiens	85-95
21131394-3	2011	An important effect of TGF-beta on ASMC inflammatory responses is the induction of IL-6 release.	asmc	35-39	transforming growth factor beta 1	Homo sapiens	23-31
21131394-3	2011	An important effect of TGF-beta on ASMC inflammatory responses is the induction of IL-6 release.	asmc	35-39	interleukin 6	Homo sapiens	83-87
21211367-2	2010	METHODS: integrin beta1 gene was silenced by using RNAi technology in the fifth generation ASMC of normal and asthmatic mice.	asmc	91-95	integrin beta 1 (fibronectin receptor beta)	Mus musculus	9-23
21211367-15	2010	CONCLUSION: gene silencing targeting integrin beta1 inhibited proliferation and secretion, but promoted apoptosis of ASMC from asthmatic mice.	asmc	117-121	integrin beta 1 (fibronectin receptor beta)	Mus musculus	37-51
20961405-3	2010	Earlier we reported that Dimethylfumarate (DMF) inhibits platelet-derived growth factor (PDGF)-BB induced mitogen and stress activated kinase (MSK)-1 and CREB activity as well as IL-6 secretion by ASMC.	asmc	197-201	interleukin 6	Homo sapiens	179-183
20619097-6	2010	ASMC were treated with ERK activator epidermal growth factor (EGF) and inhibitor PD98059.	asmc	0-4	Eph receptor B1	Rattus norvegicus	23-26
20649593-6	2010	CONCLUSIONS AND IMPLICATIONS: Combining analysis of P2Y receptor expression with functional analyses using selective agonists and antagonists, we isolated the Ca(2+) signals evoked in ASMC by activation of P2Y1, P2Y2, P2Y4 and P2Y6 receptors.	asmc	184-188	purinergic receptor P2Y1	Rattus norvegicus	206-210
20649593-6	2010	CONCLUSIONS AND IMPLICATIONS: Combining analysis of P2Y receptor expression with functional analyses using selective agonists and antagonists, we isolated the Ca(2+) signals evoked in ASMC by activation of P2Y1, P2Y2, P2Y4 and P2Y6 receptors.	asmc	184-188	purinergic receptor P2Y2	Rattus norvegicus	212-216
20649593-6	2010	CONCLUSIONS AND IMPLICATIONS: Combining analysis of P2Y receptor expression with functional analyses using selective agonists and antagonists, we isolated the Ca(2+) signals evoked in ASMC by activation of P2Y1, P2Y2, P2Y4 and P2Y6 receptors.	asmc	184-188	pyrimidinergic receptor P2Y4	Rattus norvegicus	218-222
20649593-6	2010	CONCLUSIONS AND IMPLICATIONS: Combining analysis of P2Y receptor expression with functional analyses using selective agonists and antagonists, we isolated the Ca(2+) signals evoked in ASMC by activation of P2Y1, P2Y2, P2Y4 and P2Y6 receptors.	asmc	184-188	pyrimidinergic receptor P2Y6	Rattus norvegicus	227-231
20619097-6	2010	ASMC were treated with ERK activator epidermal growth factor (EGF) and inhibitor PD98059.	asmc	0-4	epidermal growth factor like 1	Rattus norvegicus	37-60
20619097-6	2010	ASMC were treated with ERK activator epidermal growth factor (EGF) and inhibitor PD98059.	asmc	0-4	epidermal growth factor like 1	Rattus norvegicus	62-65
20619097-8	2010	After treatment with PD98059, the apoptotic index, the percentage of the early apoptotic cells, the expression of bax and the expression of caspase-3 protein in ASMC from chronic asthmatic group were significantly increased, and the expression of bcl-2 in ASMC from chronic asthmatic group were significantly decreased.	asmc	161-165	caspase 3	Rattus norvegicus	140-149
20619097-13	2010	The bcl-2 family and caspase-3 may participate in the regulation mechanism of cell apoptosis by ERK signaling pathway in ASMC from chronic asthmatic group.	asmc	121-125	BCL2, apoptosis regulator	Rattus norvegicus	4-9
20619097-13	2010	The bcl-2 family and caspase-3 may participate in the regulation mechanism of cell apoptosis by ERK signaling pathway in ASMC from chronic asthmatic group.	asmc	121-125	caspase 3	Rattus norvegicus	21-30
20619097-13	2010	The bcl-2 family and caspase-3 may participate in the regulation mechanism of cell apoptosis by ERK signaling pathway in ASMC from chronic asthmatic group.	asmc	121-125	Eph receptor B1	Rattus norvegicus	96-99
19465513-3	2009	In this study, we determined the effect of DMF on platelet-derived growth factor (PDGF)-BB- and TNFalpha-induced asthma-relevant cytokines and NF-kappaB activation by primary human asthmatic and nonasthmatic airway smooth muscle cells (ASMC).	asmc	236-240	tumor necrosis factor	Homo sapiens	96-104
19712046-5	2010	The expression of elastin and elastin-associated proteins was increased in V3 and control ASMC monolayer cultures when ascorbic acid, which promotes collagen synthesis and inhibits elastogenesis, was removed from the medium.	asmc	90-94	elastin	Rattus norvegicus	18-25
19712046-5	2010	The expression of elastin and elastin-associated proteins was increased in V3 and control ASMC monolayer cultures when ascorbic acid, which promotes collagen synthesis and inhibits elastogenesis, was removed from the medium.	asmc	90-94	elastin	Rattus norvegicus	30-37
19801525-6	2009	IL-33 expression by ASMC was determined by PCR, ELISA, and Western blotting.	asmc	20-24	interleukin 33	Homo sapiens	0-5
19801525-9	2009	IL-33 and TNF-alpha transcript levels correlate in the lung tissues, and TNF-alpha up-regulates IL-33 expression by cultured ASMC in a time- and dose-dependent manner.	asmc	125-129	tumor necrosis factor	Homo sapiens	73-82
19801525-9	2009	IL-33 and TNF-alpha transcript levels correlate in the lung tissues, and TNF-alpha up-regulates IL-33 expression by cultured ASMC in a time- and dose-dependent manner.	asmc	125-129	interleukin 33	Homo sapiens	96-101
19801525-13	2009	ASMC are a source of the IL-33 cytokine.	asmc	0-4	interleukin 33	Homo sapiens	25-30
19465513-7	2009	TNFalpha-induced eotaxin, RANTES, and IL-6 as well as PDGF-BB-induced IL-6 expression was inhibited by DMF and by dexamethasone from asthmatic and nonasthmatic ASMC, but the combination of both drugs showed no glucocorticoid sparing effect in either of the two groups.	asmc	160-164	tumor necrosis factor	Homo sapiens	0-8
19465513-7	2009	TNFalpha-induced eotaxin, RANTES, and IL-6 as well as PDGF-BB-induced IL-6 expression was inhibited by DMF and by dexamethasone from asthmatic and nonasthmatic ASMC, but the combination of both drugs showed no glucocorticoid sparing effect in either of the two groups.	asmc	160-164	interleukin 6	Homo sapiens	70-74
18948257-8	2008	We conclude the following: 1) maintaining normal HA levels in cell cultures requires normal cell cholesterol homeostasis; 2) HA degradation may contribute to but is not the predominant mechanism to increase high molecular mass HA accumulation in low density lipoprotein receptor-deficient WHHL ASMC cultures; and 3) elevated accumulation of HA depends on cellular or membrane cholesterol content and, potentially, intact cholesterol-rich microdomains.	asmc	294-298	low-density lipoprotein receptor	Oryctolagus cuniculus	246-278
18583257-5	2008	Rho-kinase inhibitor Y-27632 showed a dose-dependent inhibitory effect on ET-1-induced ASMC migration, and in cells exposed to 10 nmol/L ET-1, Y-27632 at 10 micromol/L significantly blocked ASMC migration (P<0.01).	asmc	87-91	endothelin 1	Homo sapiens	74-78
18501114-5	2008	The effect of the construct recombinant plasmid pcDNA3.1-antisense cyclinD1 (pcDNA3.1-ascyclinD1) on the proliferation of ASMC was found to be induced by PMA.	asmc	122-126	cyclin D1	Rattus norvegicus	67-75
18501114-6	2008	RESULTS: The data showed phorbol ester-dependent PKCalpha promoted the proliferation of ASMC.	asmc	88-92	protein kinase C, alpha	Rattus norvegicus	49-57
18501114-10	2008	CONCLUSION: The proliferation of ASMC by PKC might by regulated by the cyclinD1 expression in asthmatic rats.	asmc	33-37	protein kinase C, gamma	Rattus norvegicus	41-44
18501114-10	2008	CONCLUSION: The proliferation of ASMC by PKC might by regulated by the cyclinD1 expression in asthmatic rats.	asmc	33-37	cyclin D1	Rattus norvegicus	71-79
19080409-14	2008	The AI of ASMC was negatively correlated with Wam/Pbm (r = -0.860, P < 0.01) and the relative content of Bcl-2 protein (r = -0.783, P < 0.01), but was positively correlated with the relative content of Bax protein (r = 0.873, P < 0.01).	asmc	10-14	BCL2, apoptosis regulator	Rattus norvegicus	108-113
19080409-14	2008	The AI of ASMC was negatively correlated with Wam/Pbm (r = -0.860, P < 0.01) and the relative content of Bcl-2 protein (r = -0.783, P < 0.01), but was positively correlated with the relative content of Bax protein (r = 0.873, P < 0.01).	asmc	10-14	BCL2 associated X, apoptosis regulator	Rattus norvegicus	208-211
19080409-16	2008	Dexamethasone induces ASMC apoptosis possibly by the increase of Bax expression and the decrease of Bcl-2 expression in airway smooth muscles.	asmc	22-26	BCL2 associated X, apoptosis regulator	Rattus norvegicus	65-68
19080409-16	2008	Dexamethasone induces ASMC apoptosis possibly by the increase of Bax expression and the decrease of Bcl-2 expression in airway smooth muscles.	asmc	22-26	BCL2, apoptosis regulator	Rattus norvegicus	100-105
18583257-5	2008	Rho-kinase inhibitor Y-27632 showed a dose-dependent inhibitory effect on ET-1-induced ASMC migration, and in cells exposed to 10 nmol/L ET-1, Y-27632 at 10 micromol/L significantly blocked ASMC migration (P<0.01).	asmc	190-194	endothelin 1	Homo sapiens	74-78
18583257-5	2008	Rho-kinase inhibitor Y-27632 showed a dose-dependent inhibitory effect on ET-1-induced ASMC migration, and in cells exposed to 10 nmol/L ET-1, Y-27632 at 10 micromol/L significantly blocked ASMC migration (P<0.01).	asmc	190-194	endothelin 1	Homo sapiens	137-141
17575078-5	2007	ddADAM-15 also inhibited platelet-derived growth factor (PDGF)-induced ASMC migration, and this was reversed by an anti-beta(1)-integrin antibody.	asmc	71-75	integrin subunit beta 1	Homo sapiens	120-136
18630259-8	2008	There was significant change of CyclinD1 expression between vector and sense CyclinD1 transfected cells, and the expression level of CyclinD1 in ASMC transfected with antisense CyclinD1 was lower than that in vector transfected cells (P <0.01); (3) In the asthmatic groups, compared with the vecter group, the percentage of S + G2M phase, absorbance A value of MTT and the expression rate of PCNA protein in ASMC transfected with pcDNA3.	asmc	145-149	cyclin D1	Rattus norvegicus	77-85
18630259-8	2008	There was significant change of CyclinD1 expression between vector and sense CyclinD1 transfected cells, and the expression level of CyclinD1 in ASMC transfected with antisense CyclinD1 was lower than that in vector transfected cells (P <0.01); (3) In the asthmatic groups, compared with the vecter group, the percentage of S + G2M phase, absorbance A value of MTT and the expression rate of PCNA protein in ASMC transfected with pcDNA3.	asmc	145-149	cyclin D1	Rattus norvegicus	77-85
18630259-8	2008	There was significant change of CyclinD1 expression between vector and sense CyclinD1 transfected cells, and the expression level of CyclinD1 in ASMC transfected with antisense CyclinD1 was lower than that in vector transfected cells (P <0.01); (3) In the asthmatic groups, compared with the vecter group, the percentage of S + G2M phase, absorbance A value of MTT and the expression rate of PCNA protein in ASMC transfected with pcDNA3.	asmc	145-149	cyclin D1	Rattus norvegicus	77-85
18630259-8	2008	There was significant change of CyclinD1 expression between vector and sense CyclinD1 transfected cells, and the expression level of CyclinD1 in ASMC transfected with antisense CyclinD1 was lower than that in vector transfected cells (P <0.01); (3) In the asthmatic groups, compared with the vecter group, the percentage of S + G2M phase, absorbance A value of MTT and the expression rate of PCNA protein in ASMC transfected with pcDNA3.	asmc	145-149	proliferating cell nuclear antigen	Rattus norvegicus	395-399
18630259-13	2008	Sense CyclinD1 eukaryotic expression vectors could have a positive effect on the proliferation of ASMC, however the antisence one have a negative effect, which implicated that CyclinD1 might contribute to the process of airway smooth muscle cell proliferation.	asmc	98-102	cyclin D1	Rattus norvegicus	6-14
18630259-13	2008	Sense CyclinD1 eukaryotic expression vectors could have a positive effect on the proliferation of ASMC, however the antisence one have a negative effect, which implicated that CyclinD1 might contribute to the process of airway smooth muscle cell proliferation.	asmc	98-102	cyclin D1	Rattus norvegicus	176-184
18380907-9	2008	CONCLUSION: Gram-positive or gram-negative bacteria activate human ASMC to release CXCL-8.	asmc	67-71	C-X-C motif chemokine ligand 8	Homo sapiens	83-89
18380907-12	2008	Our findings that ASMC can respond directly to gram-negative and gram-positive bacteria by releasing the neutrophil selective chemokine, CXCL-8, is consistent with what we know about the role of neutrophil recruitment in bacterial infections in the lung.	asmc	18-22	C-X-C motif chemokine ligand 8	Homo sapiens	137-143
18178867-5	2008	We first demonstrated that CCR1 mRNA is increased in the airways of asthmatic vs control subjects and showed for the first time that ASMC express CCR1 mRNA and protein, both in vitro and in vivo.	asmc	133-137	C-C motif chemokine receptor 1	Homo sapiens	27-31
18178867-5	2008	We first demonstrated that CCR1 mRNA is increased in the airways of asthmatic vs control subjects and showed for the first time that ASMC express CCR1 mRNA and protein, both in vitro and in vivo.	asmc	133-137	C-C motif chemokine receptor 1	Homo sapiens	146-150
18178867-6	2008	Calcium mobilization by CCR1 ligands confirmed its functionality on ASMC.	asmc	68-72	C-C motif chemokine receptor 1	Homo sapiens	24-28
18178867-7	2008	Stimulation of ASMC with TNF-alpha and, to a lesser extent, IFN-gamma resulted in an up-regulation of CCR1 expression, which was totally suppressed by both dexamethasone or mithramycin.	asmc	15-19	tumor necrosis factor	Homo sapiens	25-34
18178867-7	2008	Stimulation of ASMC with TNF-alpha and, to a lesser extent, IFN-gamma resulted in an up-regulation of CCR1 expression, which was totally suppressed by both dexamethasone or mithramycin.	asmc	15-19	interferon gamma	Homo sapiens	60-69
18178867-7	2008	Stimulation of ASMC with TNF-alpha and, to a lesser extent, IFN-gamma resulted in an up-regulation of CCR1 expression, which was totally suppressed by both dexamethasone or mithramycin.	asmc	15-19	C-C motif chemokine receptor 1	Homo sapiens	102-106
18178867-8	2008	Taken together, our data suggest that CCR1 might be involved in the pathogenesis of asthma, through the activation of ASMC by its ligands.	asmc	118-122	C-C motif chemokine receptor 1	Homo sapiens	38-42
17575078-6	2007	PDGF induced the activation of phosphoinositol-3-kinase (PI3K) and p38 mitogen-activated protein kinase (MAPK), and selective inhibitors of these kinases inhibited PDGF-induced ASMC migration.	asmc	177-181	mitogen-activated protein kinase 14	Homo sapiens	67-103
17579786-2	2007	ASMC proliferation was examined by flow cytometry analysis, methyl thiazolyl tetrazolium (MTT) colorimetric assay, [(3)H]-thymidine (TdR) incorporation and proliferating cell nuclear antigen (PCNA) immunocytochemical staining.	asmc	0-4	proliferating cell nuclear antigen	Rattus norvegicus	192-196
17932440-6	2007	3-(4,5- dimethylthiazole-2-yl)-2,5-diphenyltetrazolium-bromide (MTT) assay was to investigate the effects of PAF on ASMC proliferation and to confirm its optimum concentration for action.	asmc	116-120	PCNA clamp associated factor	Rattus norvegicus	109-112
17932440-9	2007	RESULTS: PAF stimulated ASMC proliferation with its peak at 100 nM.	asmc	24-28	PCNA clamp associated factor	Rattus norvegicus	9-12
17932440-12	2007	INTERPRETATION & CONCLUSION: The present findings demonstrated that PAF could promote ASMC proliferation, suggesting its potential involvement in airway remodeling.	asmc	90-94	PCNA clamp associated factor	Rattus norvegicus	72-75
17579786-10	2007	The ERK signaling pathway might play an important role in regulating ASMC proliferation, leading to asthmatic airway remodeling.	asmc	69-73	Eph receptor B1	Rattus norvegicus	4-7
17106207-6	2007	The effects of IL-4 and IL-13 on bronchial reactivity were paralleled by the effects on ASMC proliferation.	asmc	88-92	interleukin 4	Homo sapiens	15-19
17226775-10	2007	These data demonstrate that IL-1beta selectively downregulates versican synthesis by ASMC, while positively regulating the synthesis of other proteoglycans.	asmc	85-89	interleukin 1 beta	Homo sapiens	28-36
17226775-10	2007	These data demonstrate that IL-1beta selectively downregulates versican synthesis by ASMC, while positively regulating the synthesis of other proteoglycans.	asmc	85-89	versican	Homo sapiens	63-71
17513787-7	2007	The inhibitory effect of dexamethasone on GRO-alpha release was partially reversed in ASMC treated with MKP-1 siRNA compared with those treated with scrambled siRNA.	asmc	86-90	C-X-C motif chemokine ligand 1	Homo sapiens	42-51
17513787-7	2007	The inhibitory effect of dexamethasone on GRO-alpha release was partially reversed in ASMC treated with MKP-1 siRNA compared with those treated with scrambled siRNA.	asmc	86-90	dual specificity phosphatase 1	Homo sapiens	104-109
17513787-9	2007	Nuclear translocation of the glucocorticoid receptor was increased in ASMC exposed to dexamethasone and IL-1beta.	asmc	70-74	nuclear receptor subfamily 3 group C member 1	Homo sapiens	29-52
17513787-9	2007	Nuclear translocation of the glucocorticoid receptor was increased in ASMC exposed to dexamethasone and IL-1beta.	asmc	70-74	interleukin 1 beta	Homo sapiens	104-112
17226774-9	2007	This study illustrates that decorin derived from ASMC selectively accumulates in fibrin and modifies fibrin architecture and mechanical properties.	asmc	49-53	decorin	Homo sapiens	28-35
17106207-7	2007	Fifty nanograms per milliliter of IL-4 and IL-13 increased the Ca(2+) response of human ASMC to ACH.	asmc	88-92	interleukin 4	Homo sapiens	34-38
17106207-7	2007	Fifty nanograms per milliliter of IL-4 and IL-13 increased the Ca(2+) response of human ASMC to ACH.	asmc	88-92	interleukin 13	Homo sapiens	43-48
17106207-10	2007	Blocking IL-13Ralpha2, the loss of the effect of IL-4 and IL-13 at 100 ng/ml on human ASMC proliferation and the ACH-induced Ca(2+) response were no longer present.	asmc	86-90	interleukin 4	Homo sapiens	49-53
17106207-11	2007	CONCLUSIONS: IL-4 and IL-13 induce bronchial hyperreactivity by changing the Ca(2+) homeostasis of ASMC.	asmc	99-103	interleukin 4	Homo sapiens	13-17
17106207-11	2007	CONCLUSIONS: IL-4 and IL-13 induce bronchial hyperreactivity by changing the Ca(2+) homeostasis of ASMC.	asmc	99-103	interleukin 13	Homo sapiens	22-27
16721826-9	2006	The p38 inhibitor, PD169316, partially inhibited etoposide-induced ASMC apoptosis, but induced apoptosis in VSMCs.	asmc	67-71	mitogen-activated protein kinase 1	Homo sapiens	4-7
17065572-2	2006	It has been reported that platelet-derived growth factor (PDGF) can stimulate the proliferation of ASMC through phosphatidylinositol 3-kinase (PI3 K) signaling pathway, which can activate Akt protein.	asmc	99-103	phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit gamma	Rattus norvegicus	112-141
17065572-2	2006	It has been reported that platelet-derived growth factor (PDGF) can stimulate the proliferation of ASMC through phosphatidylinositol 3-kinase (PI3 K) signaling pathway, which can activate Akt protein.	asmc	99-103	AKT serine/threonine kinase 1	Rattus norvegicus	188-191
17065572-4	2006	This investigation demonstrated that pentoxifylline (PTX) inhibited the PDGF-stimulated proliferation of ASMC by suppressing activation of the Akt/NF-kappaB pathway.	asmc	105-109	AKT serine/threonine kinase 1	Rattus norvegicus	143-146
17065572-9	2006	These data reveal that the down-regulation of the Akt/NF-kappaB signaling pathway by PTX inhibited the proliferation of ASMC.	asmc	120-124	AKT serine/threonine kinase 1	Rattus norvegicus	50-53
16822944-4	2006	The aim of this study was to determine whether human ASMC (HASMC) express functional IL-8 receptors (CXCR1 and CXCR2) linked to cell contraction and migration.	asmc	53-57	C-X-C motif chemokine ligand 8	Homo sapiens	85-89
16822944-4	2006	The aim of this study was to determine whether human ASMC (HASMC) express functional IL-8 receptors (CXCR1 and CXCR2) linked to cell contraction and migration.	asmc	53-57	C-X-C motif chemokine receptor 1	Homo sapiens	101-106
16822944-4	2006	The aim of this study was to determine whether human ASMC (HASMC) express functional IL-8 receptors (CXCR1 and CXCR2) linked to cell contraction and migration.	asmc	53-57	C-X-C motif chemokine receptor 2	Homo sapiens	111-116
16935934-4	2006	The TLR3 agonist poly(I:C) activated epithelial cells, primary endothelial cells, and two types of primary human smooth muscle cells (airway [ASMC] and vascular) directly, while the TLR7/8 agonist R848 required the presence of leukocytes to activate ASMC.	asmc	250-254	toll like receptor 3	Homo sapiens	4-8
16935934-5	2006	In keeping with these data, ASMC expressed TLR3 but not TLR7 or TLR8.	asmc	28-32	toll like receptor 3	Homo sapiens	43-47
16935934-6	2006	Activation of ASMC by poly(I:C) induced a specific cytokine repertoire characterized by induction of CXCL10 generation and the potential to recruit mast cells.	asmc	14-18	C-X-C motif chemokine ligand 10	Homo sapiens	101-107
16390551-2	2006	TGF-beta1 has been found to increase ASMC proliferation.	asmc	37-41	transforming growth factor beta 1	Bos taurus	0-9
16617094-2	2006	We investigated the production of the CXC chemokine growth-related oncogene protein-alpha (GRO-alpha) from ASMC induced by cytokines and the role of MAPK and NF-kappaB pathways.	asmc	107-111	C-X-C motif chemokine ligand 1	Homo sapiens	91-100
16617094-3	2006	ASMC were cultured from human airways, grown to confluence, and exposed to cytokines IL-1beta and TNF-alpha after growth arrest.	asmc	0-4	interleukin 1 beta	Homo sapiens	85-93
16617094-3	2006	ASMC were cultured from human airways, grown to confluence, and exposed to cytokines IL-1beta and TNF-alpha after growth arrest.	asmc	0-4	tumor necrosis factor	Homo sapiens	98-107
16617094-7	2006	Supernatants from IL-1beta-stimulated ASMC were chemotactic for neutrophils; this effect was inhibited by anti-GRO-alpha blocking antibody.	asmc	38-42	interleukin 1 beta	Homo sapiens	18-26
16617094-7	2006	Supernatants from IL-1beta-stimulated ASMC were chemotactic for neutrophils; this effect was inhibited by anti-GRO-alpha blocking antibody.	asmc	38-42	C-X-C motif chemokine ligand 1	Homo sapiens	111-120
16617094-12	2006	IL-1beta- and TNF-alpha-stimulated expression of GRO-alpha from ASMC is regulated by independent pathways involving NF-kappaB activation and ERK and JNK pathways.	asmc	64-68	interleukin 1 beta	Homo sapiens	0-8
16617094-12	2006	IL-1beta- and TNF-alpha-stimulated expression of GRO-alpha from ASMC is regulated by independent pathways involving NF-kappaB activation and ERK and JNK pathways.	asmc	64-68	tumor necrosis factor	Homo sapiens	14-23
16617094-12	2006	IL-1beta- and TNF-alpha-stimulated expression of GRO-alpha from ASMC is regulated by independent pathways involving NF-kappaB activation and ERK and JNK pathways.	asmc	64-68	C-X-C motif chemokine ligand 1	Homo sapiens	49-58
16617094-12	2006	IL-1beta- and TNF-alpha-stimulated expression of GRO-alpha from ASMC is regulated by independent pathways involving NF-kappaB activation and ERK and JNK pathways.	asmc	64-68	nuclear factor kappa B subunit 1	Homo sapiens	116-125
16617094-12	2006	IL-1beta- and TNF-alpha-stimulated expression of GRO-alpha from ASMC is regulated by independent pathways involving NF-kappaB activation and ERK and JNK pathways.	asmc	64-68	mitogen-activated protein kinase 1	Homo sapiens	141-144
16617094-12	2006	IL-1beta- and TNF-alpha-stimulated expression of GRO-alpha from ASMC is regulated by independent pathways involving NF-kappaB activation and ERK and JNK pathways.	asmc	64-68	mitogen-activated protein kinase 8	Homo sapiens	149-152
16617094-13	2006	GRO-alpha released from ASMC participates in neutrophil chemotaxis.	asmc	24-28	C-X-C motif chemokine ligand 1	Homo sapiens	0-9
16935934-4	2006	The TLR3 agonist poly(I:C) activated epithelial cells, primary endothelial cells, and two types of primary human smooth muscle cells (airway [ASMC] and vascular) directly, while the TLR7/8 agonist R848 required the presence of leukocytes to activate ASMC.	asmc	142-146	toll like receptor 3	Homo sapiens	4-8
16489116-3	2006	The aim of this study was to evaluate 1) the secretion of leukemia inhibitory factor (LIF) (an IL-6 family neurotrophic cytokine) by ASMC; 2) intracellular calcium concentration ([Ca(2+)](i)) signaling; and 3) the effect of LIF on mast cell chemotaxis and rat airway contractility.	asmc	133-137	LIF, interleukin 6 family cytokine	Rattus norvegicus	58-90
16489116-3	2006	The aim of this study was to evaluate 1) the secretion of leukemia inhibitory factor (LIF) (an IL-6 family neurotrophic cytokine) by ASMC; 2) intracellular calcium concentration ([Ca(2+)](i)) signaling; and 3) the effect of LIF on mast cell chemotaxis and rat airway contractility.	asmc	133-137	LIF, interleukin 6 family cytokine	Rattus norvegicus	86-89
16489116-6	2006	TNF-alpha-stimulated immature ASMC produce more LIF mRNA and protein than adult ASMC, although this cytokine induces a moderate increase in DNA synthesis (+20%) in adult ASMC only.	asmc	30-34	tumor necrosis factor	Homo sapiens	0-9
16489116-6	2006	TNF-alpha-stimulated immature ASMC produce more LIF mRNA and protein than adult ASMC, although this cytokine induces a moderate increase in DNA synthesis (+20%) in adult ASMC only.	asmc	30-34	LIF interleukin 6 family cytokine	Homo sapiens	48-51
16489116-8	2006	In immature ASMC, ACh-induced [Ca(2+)](i) response was enhanced twofold after incubation with LIF, whereas TNF-alpha increased the [Ca(2+)](i) to U-46619 threefold.	asmc	12-16	acyl-CoA thioesterase 12	Rattus norvegicus	18-21
16489116-8	2006	In immature ASMC, ACh-induced [Ca(2+)](i) response was enhanced twofold after incubation with LIF, whereas TNF-alpha increased the [Ca(2+)](i) to U-46619 threefold.	asmc	12-16	LIF interleukin 6 family cytokine	Homo sapiens	94-97
16489116-9	2006	In TNF-alpha-exposed adult ASMC, [Ca(2+)](i) responses to ACh were of greater magnitude (sixfold increase) than in immature ASMC.	asmc	27-31	tumor necrosis factor	Homo sapiens	3-12
16489116-9	2006	In TNF-alpha-exposed adult ASMC, [Ca(2+)](i) responses to ACh were of greater magnitude (sixfold increase) than in immature ASMC.	asmc	27-31	acyl-CoA thioesterase 12	Rattus norvegicus	58-61
16489116-9	2006	In TNF-alpha-exposed adult ASMC, [Ca(2+)](i) responses to ACh were of greater magnitude (sixfold increase) than in immature ASMC.	asmc	124-128	tumor necrosis factor	Homo sapiens	3-12
16617351-4	2006	pcDNA3.1/rCklf1 was also transfected into ASMC and the proliferation of transfected cells was detected by MTT assays.	asmc	42-46	chemokine-like factor	Rattus norvegicus	9-15
16617351-7	2006	CONCLUSION: rCklf1 has mitogenic and GiPCR-dependent chemotactic effects on rat ASMC,indicating that rCklf1 may be involved in the pathological process of atherosclerosis.	asmc	80-84	chemokine-like factor	Rattus norvegicus	12-18
16617351-7	2006	CONCLUSION: rCklf1 has mitogenic and GiPCR-dependent chemotactic effects on rat ASMC,indicating that rCklf1 may be involved in the pathological process of atherosclerosis.	asmc	80-84	chemokine-like factor	Rattus norvegicus	101-107
16390551-4	2006	In the present study, we determined the role of phosphorylated MAPKs in TGF-beta1 induced ASMC proliferation.	asmc	90-94	transforming growth factor beta 1	Bos taurus	72-81
16390551-9	2006	TGF-beta1 also enhanced serum-induced ASMC proliferation.	asmc	38-42	transforming growth factor beta 1	Bos taurus	0-9
16390551-14	2006	These findings suggest that TGF-beta1 which is expressed in airways of asthmatics may contribute to irreversible airway remodeling by enhancing ASMC proliferation.	asmc	144-148	transforming growth factor beta 1	Bos taurus	28-37
16081847-3	2005	The aims of this study were to examine the expression of CCR3 on ASMC, to compare this expression between asthmatic and nonasthmatic subjects, and to determine the implications of CCR3 expression in the migration of ASMC.	asmc	65-69	C-C motif chemokine receptor 3	Homo sapiens	57-61
16308545-5	2006	OBJECTIVES: We wanted to know whether the production of eotaxin, an important proinflammatory cytokine, through a cell-to-cell contact mechanism of human ASMC activation by MC was mediated by p38 MAPK.	asmc	154-158	C-C motif chemokine ligand 11	Homo sapiens	56-63
16308545-5	2006	OBJECTIVES: We wanted to know whether the production of eotaxin, an important proinflammatory cytokine, through a cell-to-cell contact mechanism of human ASMC activation by MC was mediated by p38 MAPK.	asmc	154-158	mitogen-activated protein kinase 14	Homo sapiens	192-195
16308545-7	2006	RESULTS: When cultured together, human ASMC and HMC-1 contact induced eotaxin secretion.	asmc	39-43	C-C motif chemokine ligand 11	Homo sapiens	70-77
16308545-10	2006	HMC-1-derived cellular membranes caused an increase in eotaxin production in human ASMC.	asmc	83-87	C-C motif chemokine ligand 11	Homo sapiens	55-62
16378110-4	2005	In primary cultures of rat airway smooth muscle cells (ASMC), activities of calcineurin, PKC, MAPK, and cross-talk induced by urotensin II (UII ), a recently identified strong mitogen, were measured.	asmc	55-59	urotensin 2	Rattus norvegicus	140-143
16378110-7	2005	(2) UII 10(-7) mol/L stimulated ASMC PKC and MAPK activities by 44% and 24% (P<0.01), respectively, after incubating for 20 min.	asmc	32-36	urotensin 2	Rattus norvegicus	4-7
16081847-3	2005	The aims of this study were to examine the expression of CCR3 on ASMC, to compare this expression between asthmatic and nonasthmatic subjects, and to determine the implications of CCR3 expression in the migration of ASMC.	asmc	216-220	C-C motif chemokine receptor 3	Homo sapiens	180-184
16081847-5	2005	Interestingly, TNF-alpha increases ASMC surface expression of CCR3 from 33 to 74%.	asmc	35-39	tumor necrosis factor	Homo sapiens	15-24
16081847-5	2005	Interestingly, TNF-alpha increases ASMC surface expression of CCR3 from 33 to 74%.	asmc	35-39	C-C motif chemokine receptor 3	Homo sapiens	62-66
16081847-7	2005	Functionality of the receptor was demonstrated by calcium assay; the addition of CCR3 ligand eotaxin to ASMC resulted in an increase in intracellular calcium production.	asmc	104-108	C-C motif chemokine receptor 3	Homo sapiens	81-85
16081847-7	2005	Functionality of the receptor was demonstrated by calcium assay; the addition of CCR3 ligand eotaxin to ASMC resulted in an increase in intracellular calcium production.	asmc	104-108	C-C motif chemokine ligand 11	Homo sapiens	93-100
16081847-8	2005	Interestingly, ASMC was seen to demonstrate a positive chemotactic response to eotaxin.	asmc	15-19	C-C motif chemokine ligand 11	Homo sapiens	79-86
16081847-9	2005	Indeed, ASMC significantly migrated toward 100 ng/ml eotaxin (2.2-fold increase, compared with control).	asmc	8-12	C-C motif chemokine ligand 11	Homo sapiens	53-60
16081847-10	2005	In conclusion, the expression of CCR3 by ASMC is increased in asthmatics, and our data show that a CCR3 ligand such as eotaxin induces migration of ASMC in vitro.	asmc	41-45	C-C motif chemokine receptor 3	Homo sapiens	33-37
15890643-1	2005	We recently demonstrated that the chemokine CXCL16 is expressed in aortic smooth muscle cells (ASMC) and induces ASMC adhesion and proliferation (Chandrasekar, B., Bysani, S., and Mummidi, S. (2004) J. Biol.	asmc	95-99	C-X-C motif chemokine ligand 16	Rattus norvegicus	44-50
15890643-1	2005	We recently demonstrated that the chemokine CXCL16 is expressed in aortic smooth muscle cells (ASMC) and induces ASMC adhesion and proliferation (Chandrasekar, B., Bysani, S., and Mummidi, S. (2004) J. Biol.	asmc	113-117	C-X-C motif chemokine ligand 16	Rattus norvegicus	44-50
15890643-11	2005	Importantly, IL-18 stimulated ASMC proliferation in a CXCL16-dependent manner.	asmc	30-34	interleukin 18	Rattus norvegicus	13-18
15890643-11	2005	Importantly, IL-18 stimulated ASMC proliferation in a CXCL16-dependent manner.	asmc	30-34	C-X-C motif chemokine ligand 16	Rattus norvegicus	54-60
15890643-12	2005	These data provide for the first time a mechanism of IL-18-mediated CXCL16 gene transcription and CXCL16-dependent ASMC proliferation and suggest a role for IL-18-CXCL16 cross-talk in atherogenesis and restenosis following angioplasty.	asmc	115-119	C-X-C motif chemokine ligand 16	Rattus norvegicus	98-104
15890643-12	2005	These data provide for the first time a mechanism of IL-18-mediated CXCL16 gene transcription and CXCL16-dependent ASMC proliferation and suggest a role for IL-18-CXCL16 cross-talk in atherogenesis and restenosis following angioplasty.	asmc	115-119	C-X-C motif chemokine ligand 16	Rattus norvegicus	98-104
16081847-10	2005	In conclusion, the expression of CCR3 by ASMC is increased in asthmatics, and our data show that a CCR3 ligand such as eotaxin induces migration of ASMC in vitro.	asmc	41-45	C-C motif chemokine receptor 3	Homo sapiens	99-103
16081847-10	2005	In conclusion, the expression of CCR3 by ASMC is increased in asthmatics, and our data show that a CCR3 ligand such as eotaxin induces migration of ASMC in vitro.	asmc	41-45	C-C motif chemokine ligand 11	Homo sapiens	119-126
16081847-10	2005	In conclusion, the expression of CCR3 by ASMC is increased in asthmatics, and our data show that a CCR3 ligand such as eotaxin induces migration of ASMC in vitro.	asmc	148-152	C-C motif chemokine receptor 3	Homo sapiens	33-37
16081847-10	2005	In conclusion, the expression of CCR3 by ASMC is increased in asthmatics, and our data show that a CCR3 ligand such as eotaxin induces migration of ASMC in vitro.	asmc	148-152	C-C motif chemokine receptor 3	Homo sapiens	99-103
16081847-10	2005	In conclusion, the expression of CCR3 by ASMC is increased in asthmatics, and our data show that a CCR3 ligand such as eotaxin induces migration of ASMC in vitro.	asmc	148-152	C-C motif chemokine ligand 11	Homo sapiens	119-126
15907205-3	2005	It has been previously shown that the expression of CD23 on ASMC in rabbits can be induced by the IgE component of the atopic serum.	asmc	60-64	Fc epsilon receptor II	Homo sapiens	52-56
15863496-4	2005	Here we show that a recently identified carbon monoxide-releasing molecule, [Ru(CO)3Cl2]2 (or CORM-2) 1) inhibits NAD(P)H oxidase cytochrome b558 activity, 2) increases oxidant production by the mitochondria, and 3) inhibits ASMC proliferation and phosphorylation of the ERK1/2 mitogen-activated protein kinase and expression of cyclin D1, two critical pathways involved in muscle proliferation.	asmc	225-229	mitochondrially encoded cytochrome b	Homo sapiens	130-142
15863496-4	2005	Here we show that a recently identified carbon monoxide-releasing molecule, [Ru(CO)3Cl2]2 (or CORM-2) 1) inhibits NAD(P)H oxidase cytochrome b558 activity, 2) increases oxidant production by the mitochondria, and 3) inhibits ASMC proliferation and phosphorylation of the ERK1/2 mitogen-activated protein kinase and expression of cyclin D1, two critical pathways involved in muscle proliferation.	asmc	225-229	mitogen-activated protein kinase 3	Homo sapiens	271-277
15863496-4	2005	Here we show that a recently identified carbon monoxide-releasing molecule, [Ru(CO)3Cl2]2 (or CORM-2) 1) inhibits NAD(P)H oxidase cytochrome b558 activity, 2) increases oxidant production by the mitochondria, and 3) inhibits ASMC proliferation and phosphorylation of the ERK1/2 mitogen-activated protein kinase and expression of cyclin D1, two critical pathways involved in muscle proliferation.	asmc	225-229	cyclin D1	Homo sapiens	329-338
15907205-15	2005	Upregulation of CD23 in huASMC by IL-4 and GM-CSF can contribute to changes in huASMC and may provide an avenue for new therapeutic options in asthma targeting ASMC.	asmc	26-30	Fc epsilon receptor II	Homo sapiens	16-20
15907205-15	2005	Upregulation of CD23 in huASMC by IL-4 and GM-CSF can contribute to changes in huASMC and may provide an avenue for new therapeutic options in asthma targeting ASMC.	asmc	26-30	interleukin 4	Homo sapiens	34-38
15907205-15	2005	Upregulation of CD23 in huASMC by IL-4 and GM-CSF can contribute to changes in huASMC and may provide an avenue for new therapeutic options in asthma targeting ASMC.	asmc	26-30	colony stimulating factor 2	Homo sapiens	43-49
15377500-6	2005	T helper lymphocyte 2-derived cytokines, IL-4 and IL-13, attenuated TGF-beta 1-stimulated mRNA and protein expression of CTGF and inhibited TGF-beta 1-stimulated ERK1/2 and Smad2/3 activation in ASMC.	asmc	195-199	interleukin 4	Homo sapiens	41-45
15653931-3	2005	When co-incubated with neutrophils (0.1-1 x 10(6) cells/ml), attachment of human ASMC was reduced to 12.3 +/- 4.3% compared with untreated controls after 72 h. HASMC showed nuclear condensation and fragmentation (41.6 +/- 8.1% compared with baseline of 3.1 +/- 0.4%), and the biochemical markers of apoptosis, annexin V binding (9.7 +/- 0.7%; baseline 1.1 +/- 0.3%) and cleaved caspase-3 expression, were observed.	asmc	81-85	annexin A5	Homo sapiens	310-319
15653931-3	2005	When co-incubated with neutrophils (0.1-1 x 10(6) cells/ml), attachment of human ASMC was reduced to 12.3 +/- 4.3% compared with untreated controls after 72 h. HASMC showed nuclear condensation and fragmentation (41.6 +/- 8.1% compared with baseline of 3.1 +/- 0.4%), and the biochemical markers of apoptosis, annexin V binding (9.7 +/- 0.7%; baseline 1.1 +/- 0.3%) and cleaved caspase-3 expression, were observed.	asmc	81-85	caspase 3	Homo sapiens	378-387
15257984-3	2005	The mechanism by which overexpression of CGRP inhibits proliferation in pulmonary artery smooth muscle cells (PASMC) and ASMC following in vitro transfection by the gene coding for prepro-CGRP was investigated.	asmc	111-115	calcitonin related polypeptide alpha	Homo sapiens	41-45
15257984-6	2005	In this study, CGRP was shown to inhibit ASMC and PASMC proliferation.	asmc	41-45	calcitonin related polypeptide alpha	Homo sapiens	15-19
15257984-10	2005	ASMC treated with CGRP and then PKAi or PKGi recovered only when exposed to the PKAi and not PKGi.	asmc	0-4	calcitonin related polypeptide alpha	Homo sapiens	18-22
15257984-12	2005	It is concluded that p53 plays a role in CGRP-induced inhibition of cell proliferation and cAMP/PKA appears to mediate this effect in ASMC and PASMC, whereas cGMP appears to be involved in PASMC proliferation.	asmc	134-138	tumor protein p53	Homo sapiens	21-24
15257984-12	2005	It is concluded that p53 plays a role in CGRP-induced inhibition of cell proliferation and cAMP/PKA appears to mediate this effect in ASMC and PASMC, whereas cGMP appears to be involved in PASMC proliferation.	asmc	134-138	calcitonin related polypeptide alpha	Homo sapiens	41-45
15499046-8	2005	ACAT inhibition by Fujirebio compound F1394 suppressed CCC-induced foam cell formation in rat and human ASMC, but, notably, did not induce significant cytotoxicity.	asmc	104-108	sterol O-acyltransferase 1	Homo sapiens	0-4
15377500-6	2005	T helper lymphocyte 2-derived cytokines, IL-4 and IL-13, attenuated TGF-beta 1-stimulated mRNA and protein expression of CTGF and inhibited TGF-beta 1-stimulated ERK1/2 and Smad2/3 activation in ASMC.	asmc	195-199	interleukin 13	Homo sapiens	50-55
15377500-6	2005	T helper lymphocyte 2-derived cytokines, IL-4 and IL-13, attenuated TGF-beta 1-stimulated mRNA and protein expression of CTGF and inhibited TGF-beta 1-stimulated ERK1/2 and Smad2/3 activation in ASMC.	asmc	195-199	transforming growth factor beta 1	Homo sapiens	68-78
15377500-6	2005	T helper lymphocyte 2-derived cytokines, IL-4 and IL-13, attenuated TGF-beta 1-stimulated mRNA and protein expression of CTGF and inhibited TGF-beta 1-stimulated ERK1/2 and Smad2/3 activation in ASMC.	asmc	195-199	cellular communication network factor 2	Homo sapiens	121-125
15377500-6	2005	T helper lymphocyte 2-derived cytokines, IL-4 and IL-13, attenuated TGF-beta 1-stimulated mRNA and protein expression of CTGF and inhibited TGF-beta 1-stimulated ERK1/2 and Smad2/3 activation in ASMC.	asmc	195-199	transforming growth factor beta 1	Homo sapiens	140-150
15321787-3	2004	We investigated FKN expression by human ASMC in response to the proinflammatory cytokines IL-1beta, TNF-alpha, and IFN-gamma, the T helper 2-type cytokines IL-4, IL-10, and IL-13, and the fibrogenic cytokine transforming growth factor (TGF)-beta.	asmc	40-44	C-X3-C motif chemokine ligand 1	Homo sapiens	16-19
15321787-3	2004	We investigated FKN expression by human ASMC in response to the proinflammatory cytokines IL-1beta, TNF-alpha, and IFN-gamma, the T helper 2-type cytokines IL-4, IL-10, and IL-13, and the fibrogenic cytokine transforming growth factor (TGF)-beta.	asmc	40-44	interleukin 1 beta	Homo sapiens	90-98
15321787-3	2004	We investigated FKN expression by human ASMC in response to the proinflammatory cytokines IL-1beta, TNF-alpha, and IFN-gamma, the T helper 2-type cytokines IL-4, IL-10, and IL-13, and the fibrogenic cytokine transforming growth factor (TGF)-beta.	asmc	40-44	tumor necrosis factor	Homo sapiens	100-109
15321787-3	2004	We investigated FKN expression by human ASMC in response to the proinflammatory cytokines IL-1beta, TNF-alpha, and IFN-gamma, the T helper 2-type cytokines IL-4, IL-10, and IL-13, and the fibrogenic cytokine transforming growth factor (TGF)-beta.	asmc	40-44	interferon gamma	Homo sapiens	115-124
11934835-8	2002	In addition to UTP, UDP also induced ASMC migration even when UTP regeneration was inhibited, suggesting the involvement of UDP receptor P2Y(6).	asmc	37-41	pyrimidinergic receptor P2Y6	Rattus norvegicus	137-143
14733770-2	2004	Our previous study showed that UII is a potent mitogen of airway smooth muscle cells (ASMC) inducing ASMC proliferation in a dose-dependent manner.	asmc	86-90	urotensin 2	Homo sapiens	31-34
14733770-2	2004	Our previous study showed that UII is a potent mitogen of airway smooth muscle cells (ASMC) inducing ASMC proliferation in a dose-dependent manner.	asmc	101-105	urotensin 2	Homo sapiens	31-34
14733770-4	2004	This study was conducted to investigate the signal transduction pathway in the proliferation of ASMC induced by UII.	asmc	96-100	urotensin 2	Homo sapiens	112-115
14733770-9	2004	RESULTS: UII 10(-7) mol/L stimulated ASMC PKC and MAPK activities by 44% and 24% (P < 0.01), respectively, after incubating for 20 minutes.	asmc	37-41	urotensin 2	Homo sapiens	9-12
14733770-9	2004	RESULTS: UII 10(-7) mol/L stimulated ASMC PKC and MAPK activities by 44% and 24% (P < 0.01), respectively, after incubating for 20 minutes.	asmc	37-41	proline rich transmembrane protein 2	Homo sapiens	42-45
12915398-3	2003	ERalpha, ERbeta, and PR levels were higher in the aorta and ASMC of atherosclerosis-susceptible B6 mice.	asmc	60-64	estrogen receptor 1 (alpha)	Mus musculus	0-7
12915398-3	2003	ERalpha, ERbeta, and PR levels were higher in the aorta and ASMC of atherosclerosis-susceptible B6 mice.	asmc	60-64	estrogen receptor 2 (beta)	Mus musculus	9-15
12915398-3	2003	ERalpha, ERbeta, and PR levels were higher in the aorta and ASMC of atherosclerosis-susceptible B6 mice.	asmc	60-64	progesterone receptor	Mus musculus	21-23
12915398-4	2003	In transfection studies using an estrogen response element-driven reporter plasmid, E2 elicited a >2-fold increase in luciferase activity in ASMC of B6 (B6-ASMC), which demonstrated the transcriptional activity of ER in atherosclerosis-susceptible cells.	asmc	144-148	estrogen receptor 1 (alpha)	Mus musculus	217-219
12915398-4	2003	In transfection studies using an estrogen response element-driven reporter plasmid, E2 elicited a >2-fold increase in luciferase activity in ASMC of B6 (B6-ASMC), which demonstrated the transcriptional activity of ER in atherosclerosis-susceptible cells.	asmc	159-163	estrogen receptor 1 (alpha)	Mus musculus	217-219
12789234-13	2003	CONCLUSIONS: T(H)2 cytokines and TGF-beta stimulate ASMC release of VEGF.	asmc	52-56	vascular endothelial growth factor A	Homo sapiens	68-72
15321787-11	2004	In summary, FKN production by human ASMC in vitro is regulated by inflammatory and anti-inflammatory factors.	asmc	36-40	C-X3-C motif chemokine ligand 1	Homo sapiens	12-15
15479432-4	2004	ASMC were induced to synthesize GM-CSF by stimulation with IL-1beta and TNF-alpha followed by 10% human serum.	asmc	0-4	colony stimulating factor 2	Homo sapiens	32-38
15479432-4	2004	ASMC were induced to synthesize GM-CSF by stimulation with IL-1beta and TNF-alpha followed by 10% human serum.	asmc	0-4	interleukin 1 beta	Homo sapiens	59-67
15479432-4	2004	ASMC were induced to synthesize GM-CSF by stimulation with IL-1beta and TNF-alpha followed by 10% human serum.	asmc	0-4	tumor necrosis factor	Homo sapiens	72-81
15479432-7	2004	Simultaneous analysis of intracellular GM-CSF and CFSE revealed that GM-CSF producing cells were present in both the divided and undivided ASMC populations.	asmc	139-143	colony stimulating factor 2	Homo sapiens	69-75
14670935-7	2004	CONCLUSIONS: ApoC-I and apoC-I-enriched HDL activate the N-SMase-ceramide signaling pathway, leading to apoptosis in human ASMC, which is an effect that may promote plaque rupture in vivo.	asmc	123-127	apolipoprotein C1	Homo sapiens	13-19
14670935-7	2004	CONCLUSIONS: ApoC-I and apoC-I-enriched HDL activate the N-SMase-ceramide signaling pathway, leading to apoptosis in human ASMC, which is an effect that may promote plaque rupture in vivo.	asmc	123-127	apolipoprotein C1	Homo sapiens	24-30
14670935-7	2004	CONCLUSIONS: ApoC-I and apoC-I-enriched HDL activate the N-SMase-ceramide signaling pathway, leading to apoptosis in human ASMC, which is an effect that may promote plaque rupture in vivo.	asmc	123-127	sphingomyelin phosphodiesterase 2	Homo sapiens	57-64
12789234-3	2003	ASMC were incubated for 24 hours with various concentrations of T(H)2 cytokines (IL-4, IL-5, IL-10, and IL-13); transforming growth factor (TGF)-beta1, TGF-beta2, or TGF-beta3; and IL-1beta or TNF-alpha with or without IFN-gamma.	asmc	0-4	interleukin 4	Homo sapiens	81-85
12789234-3	2003	ASMC were incubated for 24 hours with various concentrations of T(H)2 cytokines (IL-4, IL-5, IL-10, and IL-13); transforming growth factor (TGF)-beta1, TGF-beta2, or TGF-beta3; and IL-1beta or TNF-alpha with or without IFN-gamma.	asmc	0-4	interleukin 5	Homo sapiens	87-91
12789234-3	2003	ASMC were incubated for 24 hours with various concentrations of T(H)2 cytokines (IL-4, IL-5, IL-10, and IL-13); transforming growth factor (TGF)-beta1, TGF-beta2, or TGF-beta3; and IL-1beta or TNF-alpha with or without IFN-gamma.	asmc	0-4	interleukin 13	Homo sapiens	104-109
12789234-3	2003	ASMC were incubated for 24 hours with various concentrations of T(H)2 cytokines (IL-4, IL-5, IL-10, and IL-13); transforming growth factor (TGF)-beta1, TGF-beta2, or TGF-beta3; and IL-1beta or TNF-alpha with or without IFN-gamma.	asmc	0-4	transforming growth factor beta 2	Homo sapiens	152-161
12789234-6	2003	RESULTS: IL-4, IL-5, and IL-13 alone but not IL-10 enhanced VEGF production by ASMC in a concentration-dependent manner.	asmc	79-83	interleukin 4	Homo sapiens	9-13
12789234-6	2003	RESULTS: IL-4, IL-5, and IL-13 alone but not IL-10 enhanced VEGF production by ASMC in a concentration-dependent manner.	asmc	79-83	interleukin 5	Homo sapiens	15-19
12789234-6	2003	RESULTS: IL-4, IL-5, and IL-13 alone but not IL-10 enhanced VEGF production by ASMC in a concentration-dependent manner.	asmc	79-83	interleukin 13	Homo sapiens	25-30
12789234-6	2003	RESULTS: IL-4, IL-5, and IL-13 alone but not IL-10 enhanced VEGF production by ASMC in a concentration-dependent manner.	asmc	79-83	vascular endothelial growth factor A	Homo sapiens	60-64
12789234-7	2003	IFN-gamma alone inhibited spontaneous VEGF release by ASMC and concentration-dependently attenuated IL-4-augmented, IL-5-augmented, or IL-13-augmented production of VEGF (P <.01).	asmc	54-58	interferon gamma	Homo sapiens	0-9
12789234-7	2003	IFN-gamma alone inhibited spontaneous VEGF release by ASMC and concentration-dependently attenuated IL-4-augmented, IL-5-augmented, or IL-13-augmented production of VEGF (P <.01).	asmc	54-58	vascular endothelial growth factor A	Homo sapiens	38-42
12789234-13	2003	CONCLUSIONS: T(H)2 cytokines and TGF-beta stimulate ASMC release of VEGF.	asmc	52-56	transforming growth factor beta 1	Homo sapiens	33-41
12471017-3	2003	The findings in this study demonstrate that GM-CSF induces confluent, prolonged, serum-deprived cultures of ASMC to increase expression of collagen I and fibronectin.	asmc	108-112	colony stimulating factor 2	Homo sapiens	44-50
12471017-3	2003	The findings in this study demonstrate that GM-CSF induces confluent, prolonged, serum-deprived cultures of ASMC to increase expression of collagen I and fibronectin.	asmc	108-112	fibronectin 1	Homo sapiens	139-165
12471017-4	2003	GM-CSF also induced ASMC to increase the expression of transforming growth factor (TGF)-beta receptors type I, II, and III (TbetaR-I, TbetaR-II, TbetaR-III), but had no detectable effect on the release of TGF-beta1 by the same ASMC.	asmc	20-24	colony stimulating factor 2	Homo sapiens	0-6
12471017-4	2003	GM-CSF also induced ASMC to increase the expression of transforming growth factor (TGF)-beta receptors type I, II, and III (TbetaR-I, TbetaR-II, TbetaR-III), but had no detectable effect on the release of TGF-beta1 by the same ASMC.	asmc	20-24	transforming growth factor beta receptor 1	Homo sapiens	55-122
12471017-4	2003	GM-CSF also induced ASMC to increase the expression of transforming growth factor (TGF)-beta receptors type I, II, and III (TbetaR-I, TbetaR-II, TbetaR-III), but had no detectable effect on the release of TGF-beta1 by the same ASMC.	asmc	20-24	transforming growth factor beta receptor 1	Homo sapiens	124-132
12471017-4	2003	GM-CSF also induced ASMC to increase the expression of transforming growth factor (TGF)-beta receptors type I, II, and III (TbetaR-I, TbetaR-II, TbetaR-III), but had no detectable effect on the release of TGF-beta1 by the same ASMC.	asmc	20-24	transforming growth factor beta receptor 2	Homo sapiens	134-143
12471017-4	2003	GM-CSF also induced ASMC to increase the expression of transforming growth factor (TGF)-beta receptors type I, II, and III (TbetaR-I, TbetaR-II, TbetaR-III), but had no detectable effect on the release of TGF-beta1 by the same ASMC.	asmc	20-24	transforming growth factor beta 1	Homo sapiens	205-214
12471017-4	2003	GM-CSF also induced ASMC to increase the expression of transforming growth factor (TGF)-beta receptors type I, II, and III (TbetaR-I, TbetaR-II, TbetaR-III), but had no detectable effect on the release of TGF-beta1 by the same ASMC.	asmc	227-231	colony stimulating factor 2	Homo sapiens	0-6
12471017-8	2003	In conclusion, GM-CSF increases the responsiveness of ASMC to TGF-beta1-mediated connective tissue expression by induction of TbetaRs, which is inhibited by corticosteroids.	asmc	54-58	colony stimulating factor 2	Homo sapiens	15-21
12471017-8	2003	In conclusion, GM-CSF increases the responsiveness of ASMC to TGF-beta1-mediated connective tissue expression by induction of TbetaRs, which is inhibited by corticosteroids.	asmc	54-58	transforming growth factor beta 1	Homo sapiens	62-71
11934835-10	2002	Taken together, these results suggest a prominent role for the UTP receptor, P2Y(2), and for the UDP receptor, P2Y(6), in UTP-induced rat ASMC migration.	asmc	138-142	pyrimidinergic receptor P2Y6	Rattus norvegicus	111-117
11290525-4	2001	In this study, we demonstrate that bovine ASMC-derived TGF-beta associates with the TGF-beta latency binding protein-1 (LTBP-1) expressed by the same cells.	asmc	42-46	latent transforming growth factor beta binding protein 1	Bos taurus	120-126
11132773-2	2000	Interleukin-1beta (IL-1beta) and tumour necrosis factor-alpha (TNF-alpha) induce ASMC to release inflammatory mediators in vitro.	asmc	81-85	interleukin 1 beta	Homo sapiens	0-17
11372388-4	2000	RESULTS: (1) LTC4 induced ET-1 mRNA expression in 16-HBE and ASMC was significantly inhibited by zafirlukast (10(-8) mol/L) 0.23 +/- 0.10 vs. 0.10 +/- 0.03 (16-HBE), t = 3.698, P = 0.034; 0.13 +/- 0.04 vs. 0.04 +/- 0.02 ASMC, t = 4.629, P = 0.019.	asmc	220-224	endothelin 1	Homo sapiens	26-30
11372388-6	2000	(3) There was a significant negative linear correlation between ET-1 levels and zafirlukast concentrations in LTC4-treated 16-HBE and ASMC (16-HBE: r = -0.9177, P = 0.0289; ASMC: r = -0.9451, P = 0.0153).	asmc	134-138	endothelin 1	Homo sapiens	64-68
11372388-6	2000	(3) There was a significant negative linear correlation between ET-1 levels and zafirlukast concentrations in LTC4-treated 16-HBE and ASMC (16-HBE: r = -0.9177, P = 0.0289; ASMC: r = -0.9451, P = 0.0153).	asmc	173-177	endothelin 1	Homo sapiens	64-68
11372388-7	2000	CONCLUSIONS: These data suggest that zafirlukast inhibit LTC4-induced ET-1 over-expression 16-HBE and ASMC, which may be one of the anti-inflammatory mechanism of LTs receptor antagonists.	asmc	102-106	endothelin 1	Homo sapiens	70-74
10629262-2	2000	High insulin and glucose levels, which are present in patients with type II diabetes, have an additive effect in infragenicular ASMC proliferation in vitro.	asmc	128-132	insulin	Homo sapiens	5-12
10629262-10	2000	The data suggest that thiamine inhibits human infragenicular ASMC proliferation induced by high glucose and insulin.	asmc	61-65	insulin	Homo sapiens	108-115
10728372-12	2000	In contrast to A10 and their controls not exposed to continuous heparin, heparin-selected PAC-1 and ASMC showed a diminished ability to induce c-fos in response to serum.	asmc	100-104	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	143-148
11132773-2	2000	Interleukin-1beta (IL-1beta) and tumour necrosis factor-alpha (TNF-alpha) induce ASMC to release inflammatory mediators in vitro.	asmc	81-85	interleukin 1 beta	Homo sapiens	19-27
11132773-2	2000	Interleukin-1beta (IL-1beta) and tumour necrosis factor-alpha (TNF-alpha) induce ASMC to release inflammatory mediators in vitro.	asmc	81-85	tumor necrosis factor	Homo sapiens	63-72
11132773-4	2000	We determined whether; (1) allergic asthmatic serum (AAS) modulates ASMC mediator release in response to IL-1beta and TNF-alpha, and (2) IL-1beta/TNF-alpha prime ASMC to release mediators in response to AAS.	asmc	68-72	interleukin 1 beta	Homo sapiens	105-113
11132773-4	2000	We determined whether; (1) allergic asthmatic serum (AAS) modulates ASMC mediator release in response to IL-1beta and TNF-alpha, and (2) IL-1beta/TNF-alpha prime ASMC to release mediators in response to AAS.	asmc	68-72	tumor necrosis factor	Homo sapiens	118-127
11132773-4	2000	We determined whether; (1) allergic asthmatic serum (AAS) modulates ASMC mediator release in response to IL-1beta and TNF-alpha, and (2) IL-1beta/TNF-alpha prime ASMC to release mediators in response to AAS.	asmc	162-166	interleukin 1 beta	Homo sapiens	137-145
11132773-4	2000	We determined whether; (1) allergic asthmatic serum (AAS) modulates ASMC mediator release in response to IL-1beta and TNF-alpha, and (2) IL-1beta/TNF-alpha prime ASMC to release mediators in response to AAS.	asmc	162-166	tumor necrosis factor	Homo sapiens	146-155
11132773-6	2000	IL-1beta and TNF-alpha induced GM-CSF release in ASMC pre-incubated with AAS was not greater than that in ASMC pre-incubated with NAS or Monomed.	asmc	49-53	interleukin 1 beta	Homo sapiens	0-8
11132773-6	2000	IL-1beta and TNF-alpha induced GM-CSF release in ASMC pre-incubated with AAS was not greater than that in ASMC pre-incubated with NAS or Monomed.	asmc	49-53	tumor necrosis factor	Homo sapiens	13-22
11132773-6	2000	IL-1beta and TNF-alpha induced GM-CSF release in ASMC pre-incubated with AAS was not greater than that in ASMC pre-incubated with NAS or Monomed.	asmc	49-53	colony stimulating factor 2	Homo sapiens	31-37
11132773-7	2000	IL-1beta and TNF-alpha, however, primed ASMC to release GM-CSF in response to human serum.	asmc	40-44	interleukin 1 beta	Homo sapiens	0-8
11132773-7	2000	IL-1beta and TNF-alpha, however, primed ASMC to release GM-CSF in response to human serum.	asmc	40-44	tumor necrosis factor	Homo sapiens	13-22
11132773-7	2000	IL-1beta and TNF-alpha, however, primed ASMC to release GM-CSF in response to human serum.	asmc	40-44	colony stimulating factor 2	Homo sapiens	56-62
9374724-4	1997	We demonstrate that the NO donor spermine NONOate (SNN) increases steady-state levels of HO-1 mRNA in aortic vascular smooth muscle cells (aSMC) in both a time- and dose-dependent manner.	asmc	139-143	heme oxygenase 1	Homo sapiens	89-93
10498047-3	1999	Dexamethasone (25-250 nM) significantly inhibited DNA synthesis and cell division induced by beta-hexosaminidase A (Hex A, 50 nM) in bovine ASMC.	asmc	140-144	beta-hexosaminidase subunit alpha	Bos taurus	93-114
10498047-3	1999	Dexamethasone (25-250 nM) significantly inhibited DNA synthesis and cell division induced by beta-hexosaminidase A (Hex A, 50 nM) in bovine ASMC.	asmc	140-144	beta-hexosaminidase subunit alpha	Bos taurus	116-121
9831891-17	1998	Heparin inhibited serum and TGF-beta1-induced DNA synthesis in confluent ASMC (55%), consistent with our previous observation of inhibition of division in sparsely populated ASMC (Kilfeather et al., 1995a).	asmc	73-77	transforming growth factor beta 1	Bos taurus	28-37
10374636-2	1998	METHODS: To measure the effects of angiotensin II (Ang), captopril (Cap), saralasin (Sar) on proliferation, Ang and angiotensin converting enzyme (ACE) levels in cultured ASMC from WKY and SHR rats.	asmc	171-175	angiotensinogen	Rattus norvegicus	35-49
10374636-2	1998	METHODS: To measure the effects of angiotensin II (Ang), captopril (Cap), saralasin (Sar) on proliferation, Ang and angiotensin converting enzyme (ACE) levels in cultured ASMC from WKY and SHR rats.	asmc	171-175	angiotensin I converting enzyme	Rattus norvegicus	147-150
10374636-3	1998	RESULTS: Ang was a bifunctional growth factor, which induced SHR ASMC hyperplasia in 2% FCS-RPMI 1640 medium, but not in serum free (SF)-medium.	asmc	65-69	angiotensinogen	Rattus norvegicus	9-12
10958382-5	2000	Pre-treatment of ASMC for 24h with TNF-alpha, 10 nM, significantly increased eosinophil adhesion to 149 and 157% of control after 2 and 20 h. These results provide evidence that eosinophil interactions with ASMC involve VCAM-1 and ICAM-1 and are modulated by TNF-alpha.	asmc	17-21	tumor necrosis factor	Homo sapiens	35-44
10958382-5	2000	Pre-treatment of ASMC for 24h with TNF-alpha, 10 nM, significantly increased eosinophil adhesion to 149 and 157% of control after 2 and 20 h. These results provide evidence that eosinophil interactions with ASMC involve VCAM-1 and ICAM-1 and are modulated by TNF-alpha.	asmc	17-21	vascular cell adhesion molecule 1	Homo sapiens	220-226
10958382-5	2000	Pre-treatment of ASMC for 24h with TNF-alpha, 10 nM, significantly increased eosinophil adhesion to 149 and 157% of control after 2 and 20 h. These results provide evidence that eosinophil interactions with ASMC involve VCAM-1 and ICAM-1 and are modulated by TNF-alpha.	asmc	17-21	intercellular adhesion molecule 1	Homo sapiens	231-237
10958382-5	2000	Pre-treatment of ASMC for 24h with TNF-alpha, 10 nM, significantly increased eosinophil adhesion to 149 and 157% of control after 2 and 20 h. These results provide evidence that eosinophil interactions with ASMC involve VCAM-1 and ICAM-1 and are modulated by TNF-alpha.	asmc	17-21	tumor necrosis factor	Homo sapiens	259-268
10958382-5	2000	Pre-treatment of ASMC for 24h with TNF-alpha, 10 nM, significantly increased eosinophil adhesion to 149 and 157% of control after 2 and 20 h. These results provide evidence that eosinophil interactions with ASMC involve VCAM-1 and ICAM-1 and are modulated by TNF-alpha.	asmc	207-211	tumor necrosis factor	Homo sapiens	35-44
10958382-5	2000	Pre-treatment of ASMC for 24h with TNF-alpha, 10 nM, significantly increased eosinophil adhesion to 149 and 157% of control after 2 and 20 h. These results provide evidence that eosinophil interactions with ASMC involve VCAM-1 and ICAM-1 and are modulated by TNF-alpha.	asmc	207-211	vascular cell adhesion molecule 1	Homo sapiens	220-226
10958382-5	2000	Pre-treatment of ASMC for 24h with TNF-alpha, 10 nM, significantly increased eosinophil adhesion to 149 and 157% of control after 2 and 20 h. These results provide evidence that eosinophil interactions with ASMC involve VCAM-1 and ICAM-1 and are modulated by TNF-alpha.	asmc	207-211	intercellular adhesion molecule 1	Homo sapiens	231-237
10958382-5	2000	Pre-treatment of ASMC for 24h with TNF-alpha, 10 nM, significantly increased eosinophil adhesion to 149 and 157% of control after 2 and 20 h. These results provide evidence that eosinophil interactions with ASMC involve VCAM-1 and ICAM-1 and are modulated by TNF-alpha.	asmc	207-211	tumor necrosis factor	Homo sapiens	259-268
10385599-4	1999	These data suggest that Hex A activates p44/42(MAPK) in a p21Ras- and PKC-dependent manner and that this activation mediates Hex A- induced mitogenesis in bovine ASMC.	asmc	162-166	beta-hexosaminidase subunit alpha	Bos taurus	24-29
10385599-4	1999	These data suggest that Hex A activates p44/42(MAPK) in a p21Ras- and PKC-dependent manner and that this activation mediates Hex A- induced mitogenesis in bovine ASMC.	asmc	162-166	interferon induced protein 44	Homo sapiens	40-43
10385599-4	1999	These data suggest that Hex A activates p44/42(MAPK) in a p21Ras- and PKC-dependent manner and that this activation mediates Hex A- induced mitogenesis in bovine ASMC.	asmc	162-166	KRAS proto-oncogene, GTPase	Bos taurus	58-73
10385599-4	1999	These data suggest that Hex A activates p44/42(MAPK) in a p21Ras- and PKC-dependent manner and that this activation mediates Hex A- induced mitogenesis in bovine ASMC.	asmc	162-166	beta-hexosaminidase subunit alpha	Bos taurus	125-130
11715477-7	1999	The mRNA expression of PDGF-A chain and bFGF stimulated by fetal calf serum (FCS) with thrombin were both downregulated in pig ASMC with expressed ATR gene.	asmc	127-131	coagulation factor II, thrombin	Sus scrofa	87-95
11775854-2	1999	METHODS: ASMC transfected with the antisense oligonucleodides of ECE vectored with lipofectin were established.	asmc	9-13	endothelin converting enzyme 1	Homo sapiens	65-68
11775854-4	1999	RESULTS: ET-1 levels (10.1 +/- 0.3) ng/L and ECE expression (ECE/beta-actin: 0.228 +/- 0.015) in cultured ASMC incubated with 1,000 U/ml TNF-alpha were significantly higher than those in controls without TNF-alpha incubation (7.3 +/- 0.8) ng/L, (0.132 +/- 0.032, all P < 0.01).	asmc	106-110	endothelin converting enzyme 1	Homo sapiens	45-48
11775854-4	1999	RESULTS: ET-1 levels (10.1 +/- 0.3) ng/L and ECE expression (ECE/beta-actin: 0.228 +/- 0.015) in cultured ASMC incubated with 1,000 U/ml TNF-alpha were significantly higher than those in controls without TNF-alpha incubation (7.3 +/- 0.8) ng/L, (0.132 +/- 0.032, all P < 0.01).	asmc	106-110	endothelin converting enzyme 1	Homo sapiens	61-64
11775854-7	1999	CONCLUSIONS: Abnormal expression of ECE mRNA may be a keypoint responsible for TNF-alpha induced ET-1 release in human ASMC; TNF-alpha induced ET-1 release and ECE mRNA expression from human ASMC are inhibited by antisense oligonucleotide of ECE.	asmc	119-123	endothelin converting enzyme 1	Homo sapiens	36-39
11775854-7	1999	CONCLUSIONS: Abnormal expression of ECE mRNA may be a keypoint responsible for TNF-alpha induced ET-1 release in human ASMC; TNF-alpha induced ET-1 release and ECE mRNA expression from human ASMC are inhibited by antisense oligonucleotide of ECE.	asmc	119-123	tumor necrosis factor	Homo sapiens	79-88
11775854-7	1999	CONCLUSIONS: Abnormal expression of ECE mRNA may be a keypoint responsible for TNF-alpha induced ET-1 release in human ASMC; TNF-alpha induced ET-1 release and ECE mRNA expression from human ASMC are inhibited by antisense oligonucleotide of ECE.	asmc	119-123	tumor necrosis factor	Homo sapiens	125-134
9920505-9	1999	These data indicated that ERK1 and PI 3-kinase play a major role in C5b-9 induced ASMC proliferation.	asmc	82-86	mitogen-activated protein kinase 3	Homo sapiens	26-30
10088982-5	1999	Analyses of SMA (i.e., serum independent of PDGF) revealed an increase in mitogenic effect for cultured human aSMC when hostility was treated as a dichotomous modifier.	asmc	110-114	survival of motor neuron 1, telomeric	Homo sapiens	12-15
9596960-7	1997	Moreover, 5% CSE evoked time-dependent release of endogenous ET-1 from ASMC.	asmc	71-75	endothelin 1	Homo sapiens	61-65
9596960-8	1997	CONCLUSION: These data demonstrate that 5% CSE mediates ASMC proliferation via release and autocrine mitogenic action ET-1.	asmc	56-60	endothelin 1	Homo sapiens	118-122