PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
2676015-11	1989	Treatment of BMCs with high-dose interleukin-2 (IL-2) for 1 week followed by PMA plus ionomycin resulted in a lymphocyte population in which 50% and 3% of cells expressed GM-CSF and IL-3 mRNA, respectively.	bmcs	13-17	interleukin 2	Homo sapiens	33-46
2676015-5	1989	On stimulation of BMCs with phorbol myristate acetate (PMA) and phytohemagglutinin or PMA and the calcium ionophore ionomycin, approximately 5% expressed GM-CSF mRNA and approximately 1% IL-3 mRNA.	bmcs	18-22	colony stimulating factor 2	Homo sapiens	154-160
2676015-11	1989	Treatment of BMCs with high-dose interleukin-2 (IL-2) for 1 week followed by PMA plus ionomycin resulted in a lymphocyte population in which 50% and 3% of cells expressed GM-CSF and IL-3 mRNA, respectively.	bmcs	13-17	interleukin 2	Homo sapiens	48-52
2676015-5	1989	On stimulation of BMCs with phorbol myristate acetate (PMA) and phytohemagglutinin or PMA and the calcium ionophore ionomycin, approximately 5% expressed GM-CSF mRNA and approximately 1% IL-3 mRNA.	bmcs	18-22	interleukin 3	Homo sapiens	187-191
2676015-11	1989	Treatment of BMCs with high-dose interleukin-2 (IL-2) for 1 week followed by PMA plus ionomycin resulted in a lymphocyte population in which 50% and 3% of cells expressed GM-CSF and IL-3 mRNA, respectively.	bmcs	13-17	colony stimulating factor 2	Homo sapiens	171-177
2676015-11	1989	Treatment of BMCs with high-dose interleukin-2 (IL-2) for 1 week followed by PMA plus ionomycin resulted in a lymphocyte population in which 50% and 3% of cells expressed GM-CSF and IL-3 mRNA, respectively.	bmcs	13-17	interleukin 3	Homo sapiens	182-186
29908885-4	2018	In the present study, we found that the expression of miR-188-5p was decreased in cultured hypoxic MSCs and BMCs within laser-induced CNV in mice.	bmcs	108-112	microRNA 188	Mus musculus	54-61
31472168-11	2020	The promoter region of NKX2-5 was more highly methylated in BMCs and HDFs compared to CPCs, and to a lesser extent in BMC-iPSCs compared to CPC-iPSCs.	bmcs	60-64	NK2 homeobox 5	Homo sapiens	23-29
2518374-3	1989	In the two patients in whom TNF was induced in the ascites, TNF production by BMCs and ALCs was noted during priming.	bmcs	78-82	tumor necrosis factor	Homo sapiens	28-31
2518374-3	1989	In the two patients in whom TNF was induced in the ascites, TNF production by BMCs and ALCs was noted during priming.	bmcs	78-82	tumor necrosis factor	Homo sapiens	60-63
29908885-6	2018	Accordingly, increased expression of MMP-2/13 was found in hypoxic MSCs and BMCs in CNV lesions.	bmcs	76-80	matrix metallopeptidase 2	Mus musculus	37-42
29908885-8	2018	Intravitreal injections of a miR-188-5p agomir attenuated the severity of CNV and inhibited the migration of BMCs into CNV lesions in mice.	bmcs	109-113	microRNA 188	Mus musculus	29-36
29908885-9	2018	Our study suggests that miR-188-5p regulates the contribution of BMCs to CNV development by targeting MMP-2/13-mediated extracellular matrix degeneration, and miR-188-5p serves as a therapeutic target to treat CNV-related diseases.	bmcs	65-69	microRNA 188	Mus musculus	24-31
29908885-9	2018	Our study suggests that miR-188-5p regulates the contribution of BMCs to CNV development by targeting MMP-2/13-mediated extracellular matrix degeneration, and miR-188-5p serves as a therapeutic target to treat CNV-related diseases.	bmcs	65-69	matrix metallopeptidase 2	Mus musculus	102-107
29264652-10	2018	Furthermore, BMCs administration increased expression of CD163-positive cells in perivascular areas and maintained the increased mRNA expression of IL-10.	bmcs	13-17	CD163 molecule	Rattus norvegicus	57-62
30261919-8	2018	RESULTS: We showed that Sdf-1 treatment increased the number of CXCR4+BMCs able to bind the myofiber and occupy the satellite cell niche.	bmcs	70-74	C-X-C motif chemokine ligand 12	Homo sapiens	24-29
30261919-8	2018	RESULTS: We showed that Sdf-1 treatment increased the number of CXCR4+BMCs able to bind the myofiber and occupy the satellite cell niche.	bmcs	70-74	C-X-C motif chemokine receptor 4	Homo sapiens	64-69
30261919-9	2018	Moreover, interaction with myofibers induced the expression of myogenic regulatory factors (MRFs) in CXCR4+BMCs.	bmcs	107-111	C-X-C motif chemokine receptor 4	Homo sapiens	101-106
30261919-10	2018	CXCR4+BMCs, pretreated by the coculture with myofibers and Sdf-1, participated in myotube formation in vitro and also myofiber reconstruction in vivo.	bmcs	6-10	C-X-C motif chemokine receptor 4	Homo sapiens	0-5
30261919-10	2018	CXCR4+BMCs, pretreated by the coculture with myofibers and Sdf-1, participated in myotube formation in vitro and also myofiber reconstruction in vivo.	bmcs	6-10	C-X-C motif chemokine ligand 12	Homo sapiens	59-64
30261919-11	2018	We also showed that Sdf-1 overexpression in vivo (in injured and regenerating muscles) supported the participation of CXCR4+BMCs in new myofiber formation.	bmcs	124-128	C-X-C motif chemokine ligand 12	Homo sapiens	20-25
30261919-13	2018	CXCR4+BMCs, pretreated using such a method of culture, were able to participate in skeletal muscle regeneration.	bmcs	6-10	C-X-C motif chemokine receptor 4	Homo sapiens	0-5
29264652-8	2018	Intratracheal administration of autologous BMCs prevented pulmonary vessel wall thickening and perivascular infiltration, and increased CD163-positive M2-like macrophages in perivascular areas.	bmcs	43-47	CD163 molecule	Rattus norvegicus	136-141
29264652-10	2018	Furthermore, BMCs administration increased expression of CD163-positive cells in perivascular areas and maintained the increased mRNA expression of IL-10.	bmcs	13-17	interleukin 10	Rattus norvegicus	148-153
26277401-6	2015	Accordingly, BPA-treatment of BMCs from non lupus-prone C57BL/6 and the lupus-prone (NZBxNZW)F1 mice activated the type I IFN-signaling, induced the expression of p202, and activated an inflammasome activity.	bmcs	30-34	interferon activated gene 202B	Mus musculus	163-167
26880135-6	2016	Cytokines such as vascular endothelial growth factor, granulocyte colony-stimulating factor and erythropoietin are involved in the mobilization of BMCs.	bmcs	147-151	vascular endothelial growth factor A	Homo sapiens	18-52
26880135-6	2016	Cytokines such as vascular endothelial growth factor, granulocyte colony-stimulating factor and erythropoietin are involved in the mobilization of BMCs.	bmcs	147-151	erythropoietin	Homo sapiens	96-110
26880135-7	2016	Studies have also demonstrated a key role of cytokines such as stromal cell-derived factor-1, tumor necrosis factor-alpha, as well as vascular endothelial growth factor, in regulating the migration of BMCs.	bmcs	201-205	C-X-C motif chemokine ligand 12	Homo sapiens	63-121
26880135-7	2016	Studies have also demonstrated a key role of cytokines such as stromal cell-derived factor-1, tumor necrosis factor-alpha, as well as vascular endothelial growth factor, in regulating the migration of BMCs.	bmcs	201-205	vascular endothelial growth factor A	Homo sapiens	134-168
26841878-13	2016	This study suggested that macrophages promoted the vasculogenesis of retinal NV, particularly the contribution of BMCs in the mouse OIR model, which might be triggered by VEGF and SDF-1 production.	bmcs	114-118	vascular endothelial growth factor A	Mus musculus	171-175
26841878-13	2016	This study suggested that macrophages promoted the vasculogenesis of retinal NV, particularly the contribution of BMCs in the mouse OIR model, which might be triggered by VEGF and SDF-1 production.	bmcs	114-118	chemokine (C-X-C motif) ligand 12	Mus musculus	180-185
27162722-12	2016	CONCLUSION: Hyperglycemia promots the vasculogenesis of CNV, especially the contribution of BMCs, which might be triggered by VEGF and SDF-1 production.	bmcs	92-96	vascular endothelial growth factor A	Mus musculus	126-130
27162722-12	2016	CONCLUSION: Hyperglycemia promots the vasculogenesis of CNV, especially the contribution of BMCs, which might be triggered by VEGF and SDF-1 production.	bmcs	92-96	chemokine (C-X-C motif) ligand 12	Mus musculus	135-140
26025301-10	2015	RESULTS: Our findings showed that the expression of the most common reference genes, beta-actin, and Glyceraldehydes-3-phosphate dehydrogenase (GAPDH), are significantly decreased at 24 hours after culturing BMCs, even without any treatment.	bmcs	208-212	beta actin	Bos taurus	85-142
26232617-3	2015	We observed that miR-34c was significantly induced by high glucose treatment and blunted tube formation of BMCs.	bmcs	107-111	microRNA 34c	Mus musculus	17-24
26232617-5	2015	SCF knockdown by siRNA induced Kruppel-like factor 4 (KLF4) and resulted in the blockade of angiogenesis of BMCs.	bmcs	108-112	kit ligand	Mus musculus	0-3
26232617-11	2015	Our results show that the angiogenic activity of BMCs is finely regulated by the miR-34c-SCF-KLF4 axis, which is a potent translational target for optimizing the therapeutic activity of autologous BMCs for cardiac repair.	bmcs	49-53	microRNA 34c	Mus musculus	81-88
26232617-11	2015	Our results show that the angiogenic activity of BMCs is finely regulated by the miR-34c-SCF-KLF4 axis, which is a potent translational target for optimizing the therapeutic activity of autologous BMCs for cardiac repair.	bmcs	49-53	kit ligand	Mus musculus	89-92
26232617-11	2015	Our results show that the angiogenic activity of BMCs is finely regulated by the miR-34c-SCF-KLF4 axis, which is a potent translational target for optimizing the therapeutic activity of autologous BMCs for cardiac repair.	bmcs	49-53	Kruppel-like factor 4 (gut)	Mus musculus	93-97
26232617-11	2015	Our results show that the angiogenic activity of BMCs is finely regulated by the miR-34c-SCF-KLF4 axis, which is a potent translational target for optimizing the therapeutic activity of autologous BMCs for cardiac repair.	bmcs	197-201	microRNA 34c	Mus musculus	81-88
26232617-11	2015	Our results show that the angiogenic activity of BMCs is finely regulated by the miR-34c-SCF-KLF4 axis, which is a potent translational target for optimizing the therapeutic activity of autologous BMCs for cardiac repair.	bmcs	197-201	kit ligand	Mus musculus	89-92
26232617-11	2015	Our results show that the angiogenic activity of BMCs is finely regulated by the miR-34c-SCF-KLF4 axis, which is a potent translational target for optimizing the therapeutic activity of autologous BMCs for cardiac repair.	bmcs	197-201	Kruppel-like factor 4 (gut)	Mus musculus	93-97
26025301-12	2015	Only the expression of C-terminal binding protein 1 (CTBP1) and RAD50 among all tested genes were consistent after treatment of cultured BMCs with C. albicans whole yeast extract and Hen Egg White Lysozyme (HEWL), respectively.	bmcs	137-141	C-terminal binding protein 1	Bos taurus	53-58
26025301-12	2015	Only the expression of C-terminal binding protein 1 (CTBP1) and RAD50 among all tested genes were consistent after treatment of cultured BMCs with C. albicans whole yeast extract and Hen Egg White Lysozyme (HEWL), respectively.	bmcs	137-141	RAD50 double strand break repair protein	Bos taurus	64-69
25047264-8	2014	mRNA levels of SDF-1 was increased whereas its major inhibitor dipeptidylpeptidase IV (DPP IV) is decreased in PA, suggesting that the SDF-1 axis plays a role in the migration of BMCs into PA.	bmcs	179-183	C-X-C motif chemokine ligand 12	Homo sapiens	15-20
25833353-4	2015	Using a mouse model of ischemic AKI, we provide evidence that incorporation of BMCs in vascular components (such as endothelial and smooth muscle cells) becomes evident within four days after renal ischemia and reperfusion, associated with an increase in stromal cell-derived factor-1 (SDF1) in endothelium and that in CXCR4/SDF1-receptor in BMCs.	bmcs	79-83	chemokine (C-X-C motif) ligand 12	Mus musculus	255-284
25833353-4	2015	Using a mouse model of ischemic AKI, we provide evidence that incorporation of BMCs in vascular components (such as endothelial and smooth muscle cells) becomes evident within four days after renal ischemia and reperfusion, associated with an increase in stromal cell-derived factor-1 (SDF1) in endothelium and that in CXCR4/SDF1-receptor in BMCs.	bmcs	79-83	chemokine (C-X-C motif) ligand 12	Mus musculus	286-290
25833353-4	2015	Using a mouse model of ischemic AKI, we provide evidence that incorporation of BMCs in vascular components (such as endothelial and smooth muscle cells) becomes evident within four days after renal ischemia and reperfusion, associated with an increase in stromal cell-derived factor-1 (SDF1) in endothelium and that in CXCR4/SDF1-receptor in BMCs.	bmcs	79-83	chemokine (C-X-C motif) receptor 4	Mus musculus	319-324
25833353-4	2015	Using a mouse model of ischemic AKI, we provide evidence that incorporation of BMCs in vascular components (such as endothelial and smooth muscle cells) becomes evident within four days after renal ischemia and reperfusion, associated with an increase in stromal cell-derived factor-1 (SDF1) in endothelium and that in CXCR4/SDF1-receptor in BMCs.	bmcs	79-83	chemokine (C-X-C motif) receptor 4	Mus musculus	325-338
25833353-5	2015	Notably, anti-CXCR4 antibody decreased the numbers of infiltrated BMCs and BMC-derived endothelium-like cells, but not of BMC-derived smooth muscle cell-like cells.	bmcs	66-70	chemokine (C-X-C motif) receptor 4	Mus musculus	14-19
25833353-6	2015	These results suggest that reconstitution of renal endothelium post-ischemia partially depends on a paracrine loop of SDF1-CXCR4 between resident endothelium and BMCs.	bmcs	162-166	chemokine (C-X-C motif) ligand 12	Mus musculus	118-122
25833353-6	2015	These results suggest that reconstitution of renal endothelium post-ischemia partially depends on a paracrine loop of SDF1-CXCR4 between resident endothelium and BMCs.	bmcs	162-166	chemokine (C-X-C motif) receptor 4	Mus musculus	123-128
25754690-1	2015	Granulocyte-colony stimulating factor (G-CSF) has been shown to promote mobilization of bone marrow-derived stem cells (BMCs) into the bloodstream associated with improved survival and cardiac function after myocardial infarction.	bmcs	120-124	colony stimulating factor 3 (granulocyte)	Mus musculus	0-37
25754690-1	2015	Granulocyte-colony stimulating factor (G-CSF) has been shown to promote mobilization of bone marrow-derived stem cells (BMCs) into the bloodstream associated with improved survival and cardiac function after myocardial infarction.	bmcs	120-124	colony stimulating factor 3 (granulocyte)	Mus musculus	39-44
25047264-8	2014	mRNA levels of SDF-1 was increased whereas its major inhibitor dipeptidylpeptidase IV (DPP IV) is decreased in PA, suggesting that the SDF-1 axis plays a role in the migration of BMCs into PA.	bmcs	179-183	dipeptidyl peptidase 4	Homo sapiens	87-93
25047264-8	2014	mRNA levels of SDF-1 was increased whereas its major inhibitor dipeptidylpeptidase IV (DPP IV) is decreased in PA, suggesting that the SDF-1 axis plays a role in the migration of BMCs into PA.	bmcs	179-183	C-X-C motif chemokine ligand 12	Homo sapiens	135-140
22806973-5	2012	Expression levels of cell surface co-stimulatory molecules, CD80, CD86, CD54, and CD40, were significantly higher for F4/80(+)BMCs than F4/80(+)PECs.	bmcs	126-130	CD80 molecule	Homo sapiens	60-64
25364726-4	2014	We found that SDF-1 expression was increased around the defects at as early as 1 week after injury and that BMCs were mobilized to the defects, while GFP+/CD45+ were rarely observed.	bmcs	108-112	chemokine (C-X-C motif) ligand 12	Mus musculus	14-19
24697123-13	2014	Jurkat cells containing the cDNAs of TCRalpha and TCRbeta chains cloned from the dominant CD8+ cell clone had cytolytic activity against donor"s BMCs, patient"s leukemic cells, and BMCs from an unrelated subject accounting for 43%, 15%, and 0.42%, respectively.	bmcs	145-149	T cell receptor alpha constant	Homo sapiens	37-45
24697123-13	2014	Jurkat cells containing the cDNAs of TCRalpha and TCRbeta chains cloned from the dominant CD8+ cell clone had cytolytic activity against donor"s BMCs, patient"s leukemic cells, and BMCs from an unrelated subject accounting for 43%, 15%, and 0.42%, respectively.	bmcs	145-149	T cell receptor beta constant 1	Homo sapiens	50-57
24697123-13	2014	Jurkat cells containing the cDNAs of TCRalpha and TCRbeta chains cloned from the dominant CD8+ cell clone had cytolytic activity against donor"s BMCs, patient"s leukemic cells, and BMCs from an unrelated subject accounting for 43%, 15%, and 0.42%, respectively.	bmcs	145-149	CD8a molecule	Homo sapiens	90-93
26202037-2	2013	Administration of granulocyte colony-stimulating factor (G-CSF) induces the circulation of BMCs in the peripheral blood.	bmcs	91-95	colony stimulating factor 3	Homo sapiens	18-55
26202037-2	2013	Administration of granulocyte colony-stimulating factor (G-CSF) induces the circulation of BMCs in the peripheral blood.	bmcs	91-95	colony stimulating factor 3	Homo sapiens	57-62
23620693-8	2012	These results suggest that G-CSF mobilizes BMCs to the peripheral circulation but does not increase recruitment to the infarcted myocardium despite preservation of the stromal-derived factor-1 alpha/CXCR4 axis.	bmcs	43-47	colony stimulating factor 3	Rattus norvegicus	27-32
24697123-13	2014	Jurkat cells containing the cDNAs of TCRalpha and TCRbeta chains cloned from the dominant CD8+ cell clone had cytolytic activity against donor"s BMCs, patient"s leukemic cells, and BMCs from an unrelated subject accounting for 43%, 15%, and 0.42%, respectively.	bmcs	181-185	T cell receptor alpha constant	Homo sapiens	37-45
24697123-13	2014	Jurkat cells containing the cDNAs of TCRalpha and TCRbeta chains cloned from the dominant CD8+ cell clone had cytolytic activity against donor"s BMCs, patient"s leukemic cells, and BMCs from an unrelated subject accounting for 43%, 15%, and 0.42%, respectively.	bmcs	181-185	T cell receptor beta constant 1	Homo sapiens	50-57
24697123-13	2014	Jurkat cells containing the cDNAs of TCRalpha and TCRbeta chains cloned from the dominant CD8+ cell clone had cytolytic activity against donor"s BMCs, patient"s leukemic cells, and BMCs from an unrelated subject accounting for 43%, 15%, and 0.42%, respectively.	bmcs	181-185	CD8a molecule	Homo sapiens	90-93
23657866-3	2014	The BMCs seeded onto the PVF sponges with water-holding capability showed more significant increases in DNA content, alkaline phosphatase (ALP) activity, osteocalcin content, and calcium deposition than those without water-holding capability.	bmcs	4-8	bone gamma-carboxyglutamate protein	Rattus norvegicus	154-165
24065117-10	2013	Mobilization of BMCs by G-CSF boosted migration along the VCAM-1/VLA-4 axis and reduced apoptosis of cardiomyocytes.	bmcs	16-20	peripheral blood stem cell response to granulocyte colony stimulating factor 1	Mus musculus	24-29
24065117-10	2013	Mobilization of BMCs by G-CSF boosted migration along the VCAM-1/VLA-4 axis and reduced apoptosis of cardiomyocytes.	bmcs	16-20	vascular cell adhesion molecule 1	Mus musculus	58-64
24065117-13	2013	This is the first study showing that in virus-induced DCM VCAM-1/VLA-4 interaction is crucial for recruitment of circulating BMCs leading to beneficial anti-apoptotic effects resulting in improved cardiac function after G-CSF-induced mobilization.	bmcs	125-129	vascular cell adhesion molecule 1	Mus musculus	58-64
24065117-13	2013	This is the first study showing that in virus-induced DCM VCAM-1/VLA-4 interaction is crucial for recruitment of circulating BMCs leading to beneficial anti-apoptotic effects resulting in improved cardiac function after G-CSF-induced mobilization.	bmcs	125-129	peripheral blood stem cell response to granulocyte colony stimulating factor 1	Mus musculus	220-225
22938055-7	2013	TNF-alpha release was observed in an in vitro (BMCs) and in vivo (mice) CoQ10 deficiency model.	bmcs	47-51	tumor necrosis factor	Mus musculus	0-9
22806973-5	2012	Expression levels of cell surface co-stimulatory molecules, CD80, CD86, CD54, and CD40, were significantly higher for F4/80(+)BMCs than F4/80(+)PECs.	bmcs	126-130	CD86 molecule	Homo sapiens	66-70
22806973-5	2012	Expression levels of cell surface co-stimulatory molecules, CD80, CD86, CD54, and CD40, were significantly higher for F4/80(+)BMCs than F4/80(+)PECs.	bmcs	126-130	intercellular adhesion molecule 1	Homo sapiens	72-76
22806973-5	2012	Expression levels of cell surface co-stimulatory molecules, CD80, CD86, CD54, and CD40, were significantly higher for F4/80(+)BMCs than F4/80(+)PECs.	bmcs	126-130	CD40 molecule	Homo sapiens	82-86
22619278-11	2012	CONCLUSIONS: Genetic modification of BMCs with Pim-1 may serve as a therapeutic approach to promote recovery of myocardial structure.	bmcs	37-41	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	47-52
22651868-6	2012	RESULTS: We identified several miRs that are up-regulated in BMCs from patients with myocardial infarction compared with BMCs from healthy controls, including the pro-apoptotic and antiproliferative miR-34a and the hypoxia-controlled miR-210.	bmcs	61-65	microRNA 34a	Homo sapiens	199-206
22651868-6	2012	RESULTS: We identified several miRs that are up-regulated in BMCs from patients with myocardial infarction compared with BMCs from healthy controls, including the pro-apoptotic and antiproliferative miR-34a and the hypoxia-controlled miR-210.	bmcs	61-65	microRNA 210	Homo sapiens	234-241
22651868-6	2012	RESULTS: We identified several miRs that are up-regulated in BMCs from patients with myocardial infarction compared with BMCs from healthy controls, including the pro-apoptotic and antiproliferative miR-34a and the hypoxia-controlled miR-210.	bmcs	121-125	microRNA 34a	Homo sapiens	199-206
22651868-7	2012	Inhibition of miR-34 by LNA-34a significantly reduced miR-34a expression and blocked hydrogen peroxide-induced cell death of BMC in vitro, whereas overexpression of miR-34a reduced the survival of BMCs in vitro.	bmcs	197-201	microRNA 34a	Homo sapiens	165-172
22651868-9	2012	CONCLUSIONS: These results demonstrate that cardiovascular disease modulates the miR expression of BMCs in humans.	bmcs	99-103	membrane associated ring-CH-type finger 8	Homo sapiens	81-84
22651868-10	2012	Reducing the expression of the pro-apoptotic miR-34a improves the survival of BMCs in vitro and enhances the therapeutic benefit of cell therapy in mice after AMI.	bmcs	78-82	microRNA 34a	Mus musculus	45-52
21362129-10	2012	EPO-treated animals revealed an enhanced mobilization of BMCs into peripheral blood.	bmcs	57-61	erythropoietin	Mus musculus	0-3
22403243-3	2012	METHODS AND RESULTS: We demonstrated that intramyocardial delivery of BMCs in infarcted mice regulates the expression of cardiac miRNAs and significantly downregulates the proapoptotic miR-34a.	bmcs	70-74	microRNA 34a	Mus musculus	185-192
21362129-15	2012	Our study shows that EPO treatment after MI enhances the migration capacity of BMCs into ischaemic tissue, which may attribute to an improved perfusion and reduced size of infarction, respectively.	bmcs	79-83	erythropoietin	Mus musculus	21-24
22532869-9	2012	RESULTS: We found decreased CoQ(10), catalase and ATP levels in BMCs from FM patients as compared to normal control (P < 0.05 and P < 0.001, respectively) We also found increased level of LPO in BMCs from FM patients as compared to normal control (P < 0.001).	bmcs	64-68	catalase	Homo sapiens	37-45
21855069-8	2011	CONCLUSION: Evolution of atherosclerosis in ApoE(-/-) mice is paralleled by progressive loss of mobility of BMCs with reductions of CXCR4 expression, and reduced levels of SDF-1 in both serum and bone marrow.	bmcs	108-112	apolipoprotein E	Mus musculus	44-48
21851170-9	2011	RESULTS: BMCs trafficked around laser lesion adjacent to RPE layer 4 h after laser photocoagulation, where SDF-1 expression was relatively higher.	bmcs	9-13	chemokine (C-X-C motif) ligand 12	Mus musculus	107-112
21143386-4	2011	Indeed we found that both the basal and calcium-induced surface expression of CXCR4 on BMCs was significantly reduced in 25-month-old mice compared with 2-month-old mice.	bmcs	87-91	chemokine (C-X-C motif) receptor 4	Mus musculus	78-83
21851170-10	2011	With increasing expression of SDF-1, more BMCs were infiltrated into laser lesion to participate in CNV, and both reached peak at 3 d (p < 0.05).	bmcs	42-46	chemokine (C-X-C motif) ligand 12	Mus musculus	30-35
21851170-11	2011	About 81% BMCs involved in CNV were CXCR4+.	bmcs	10-14	chemokine (C-X-C motif) receptor 4	Mus musculus	36-41
21851170-13	2011	The constituent ratio of CD34+ and CD31+ BMCs increased with SDF-1 expression.	bmcs	41-45	platelet/endothelial cell adhesion molecule 1	Mus musculus	35-39
21851170-13	2011	The constituent ratio of CD34+ and CD31+ BMCs increased with SDF-1 expression.	bmcs	41-45	chemokine (C-X-C motif) ligand 12	Mus musculus	61-66
21851170-15	2011	CONCLUSIONS: These findings suggested that hypoxia-induced SDF-1 expression in RPE might be a critical initiator for recruitment of BMCs in CNV.	bmcs	132-136	chemokine (C-X-C motif) ligand 12	Mus musculus	59-64
21851170-16	2011	SDF-1 might be another important factor in BMCs" differentiation into endothelial cells to participate in the CNV.	bmcs	43-47	chemokine (C-X-C motif) ligand 12	Mus musculus	0-5
18583711-4	2008	Here we show that hindlimb ischemia of mice significantly increases Nox2 expression and ROS production in BM-mononuclear cells (BMCs), which is associated with an increase in circulating EPC-like cells.	bmcs	128-132	cytochrome b-245, beta polypeptide	Mus musculus	68-72
21266779-5	2011	We then identified granulin (GRN) as the most upregulated gene in instigating Sca1+ cKit- BMCs relative to counterpart control cells.	bmcs	90-94	granulin precursor	Homo sapiens	19-27
21266779-5	2011	We then identified granulin (GRN) as the most upregulated gene in instigating Sca1+ cKit- BMCs relative to counterpart control cells.	bmcs	90-94	granulin precursor	Homo sapiens	29-32
21266779-6	2011	The GRN+ BMCs that were recruited to the responding tumors induced resident tissue fibroblasts to express genes that promoted malignant tumor progression; indeed, treatment with recombinant GRN alone was sufficient to promote desmoplastic responding tumor growth.	bmcs	9-13	granulin precursor	Homo sapiens	190-193
21876756-8	2011	Along with altered BMCs functions, phosphorylation and activation of AMPK and endothelial nitric oxide synthase, the target of activated AMPK, were both increased which could be blocked by EP4 blocking peptide and simulated by the agonist of EP4 but not EP1, EP2 or EP3.	bmcs	19-23	prostaglandin E receptor 4 (subtype EP4)	Mus musculus	189-192
21876756-10	2011	Therefore, by promoting the differentiation and migration of BMCs, PGE2 reinforced their neovascularization by binding to the receptor of EP4 in an AMPK-dependent manner.	bmcs	61-65	prostaglandin E receptor 4 (subtype EP4)	Mus musculus	138-141
20207820-9	2010	Both G-CSF and PTH treatment resulted in an augmented mobilization of BMCs in the peripheral blood.	bmcs	70-74	colony stimulating factor 3 (granulocyte)	Mus musculus	5-10
20207820-9	2010	Both G-CSF and PTH treatment resulted in an augmented mobilization of BMCs in the peripheral blood.	bmcs	70-74	parathyroid hormone	Mus musculus	15-18
20207820-10	2010	Contrary to G-CSF and controls, PTH and the combination showed significant migration of BMCs in ischemic myocardium associated with a significant reduction of perfusion defects from day 6 to day 30.	bmcs	88-92	parathyroid hormone	Mus musculus	32-35
20015609-6	2010	This recruitment was enhanced by topical injections of vascular endothelial growth factor (VEGF)-A, and a VEGF-dependent increase in the recruitment of BMCs was inhibited by a COX-2 inhibitor, celecoxib.	bmcs	152-156	vascular endothelial growth factor A	Mus musculus	91-95
20015609-6	2010	This recruitment was enhanced by topical injections of vascular endothelial growth factor (VEGF)-A, and a VEGF-dependent increase in the recruitment of BMCs was inhibited by a COX-2 inhibitor, celecoxib.	bmcs	152-156	vascular endothelial growth factor A	Mus musculus	106-110
20015609-6	2010	This recruitment was enhanced by topical injections of vascular endothelial growth factor (VEGF)-A, and a VEGF-dependent increase in the recruitment of BMCs was inhibited by a COX-2 inhibitor, celecoxib.	bmcs	152-156	prostaglandin-endoperoxide synthase 2	Mus musculus	176-181
20015609-7	2010	FACS analysis of the granulation tissues after treatment with collagenase revealed that the Mac-1-positive macrophage fraction was enhanced by topical injections of VEGF-A, and that this increased recruitment of Mac-1-positive BMCs was inhibited by celecoxib.	bmcs	227-231	integrin alpha M	Mus musculus	92-97
20015609-7	2010	FACS analysis of the granulation tissues after treatment with collagenase revealed that the Mac-1-positive macrophage fraction was enhanced by topical injections of VEGF-A, and that this increased recruitment of Mac-1-positive BMCs was inhibited by celecoxib.	bmcs	227-231	vascular endothelial growth factor A	Mus musculus	165-171
20015609-7	2010	FACS analysis of the granulation tissues after treatment with collagenase revealed that the Mac-1-positive macrophage fraction was enhanced by topical injections of VEGF-A, and that this increased recruitment of Mac-1-positive BMCs was inhibited by celecoxib.	bmcs	227-231	integrin alpha M	Mus musculus	212-217
20015609-8	2010	Selective knockdown of EP3 performed by BM transplantation with BMCs isolated from EP3 knockout (EP3) mice reduced sponge-induced angiogenesis, as estimated by mean vascular number and CD31 expression in the granulation tissues.	bmcs	64-68	prostaglandin E receptor 3 (subtype EP3)	Mus musculus	23-26
20015609-8	2010	Selective knockdown of EP3 performed by BM transplantation with BMCs isolated from EP3 knockout (EP3) mice reduced sponge-induced angiogenesis, as estimated by mean vascular number and CD31 expression in the granulation tissues.	bmcs	64-68	prostaglandin E receptor 3 (subtype EP3)	Mus musculus	83-86
20015609-8	2010	Selective knockdown of EP3 performed by BM transplantation with BMCs isolated from EP3 knockout (EP3) mice reduced sponge-induced angiogenesis, as estimated by mean vascular number and CD31 expression in the granulation tissues.	bmcs	64-68	prostaglandin E receptor 3 (subtype EP3)	Mus musculus	83-86
20015609-8	2010	Selective knockdown of EP3 performed by BM transplantation with BMCs isolated from EP3 knockout (EP3) mice reduced sponge-induced angiogenesis, as estimated by mean vascular number and CD31 expression in the granulation tissues.	bmcs	64-68	platelet/endothelial cell adhesion molecule 1	Mus musculus	185-189
20015609-9	2010	This reduction in angiogenesis in EP3(-/-) BM chimeric mice was accompanied by reductions in the recruitment of BMCs, especially of Mac-1-positive cells and Gr-1-positive cells.	bmcs	112-116	prostaglandin E receptor 3 (subtype EP3)	Mus musculus	34-37
19920031-8	2010	FACS analysis of BMC-injected hearts at day 7 revealed that GFP(+) BMCs expressed hematopoietic (CD45, Mac-1, Gr-1), minimal progenitor (Sca-1, c-kit), and no endothelial (CD133, Flk-1) or cardiac (Trop-T) cell markers.	bmcs	67-71	acyl-CoA synthetase long-chain family member 1	Mus musculus	0-4
19920031-8	2010	FACS analysis of BMC-injected hearts at day 7 revealed that GFP(+) BMCs expressed hematopoietic (CD45, Mac-1, Gr-1), minimal progenitor (Sca-1, c-kit), and no endothelial (CD133, Flk-1) or cardiac (Trop-T) cell markers.	bmcs	67-71	protein tyrosine phosphatase, receptor type, C	Mus musculus	97-101
19920031-8	2010	FACS analysis of BMC-injected hearts at day 7 revealed that GFP(+) BMCs expressed hematopoietic (CD45, Mac-1, Gr-1), minimal progenitor (Sca-1, c-kit), and no endothelial (CD133, Flk-1) or cardiac (Trop-T) cell markers.	bmcs	67-71	integrin alpha M	Mus musculus	103-108
19920031-8	2010	FACS analysis of BMC-injected hearts at day 7 revealed that GFP(+) BMCs expressed hematopoietic (CD45, Mac-1, Gr-1), minimal progenitor (Sca-1, c-kit), and no endothelial (CD133, Flk-1) or cardiac (Trop-T) cell markers.	bmcs	67-71	lymphocyte antigen 6 complex, locus G	Mus musculus	110-114
19920031-8	2010	FACS analysis of BMC-injected hearts at day 7 revealed that GFP(+) BMCs expressed hematopoietic (CD45, Mac-1, Gr-1), minimal progenitor (Sca-1, c-kit), and no endothelial (CD133, Flk-1) or cardiac (Trop-T) cell markers.	bmcs	67-71	ataxin 1	Mus musculus	137-142
19920031-8	2010	FACS analysis of BMC-injected hearts at day 7 revealed that GFP(+) BMCs expressed hematopoietic (CD45, Mac-1, Gr-1), minimal progenitor (Sca-1, c-kit), and no endothelial (CD133, Flk-1) or cardiac (Trop-T) cell markers.	bmcs	67-71	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	144-149
19920031-8	2010	FACS analysis of BMC-injected hearts at day 7 revealed that GFP(+) BMCs expressed hematopoietic (CD45, Mac-1, Gr-1), minimal progenitor (Sca-1, c-kit), and no endothelial (CD133, Flk-1) or cardiac (Trop-T) cell markers.	bmcs	67-71	prominin 1	Mus musculus	172-177
19920031-8	2010	FACS analysis of BMC-injected hearts at day 7 revealed that GFP(+) BMCs expressed hematopoietic (CD45, Mac-1, Gr-1), minimal progenitor (Sca-1, c-kit), and no endothelial (CD133, Flk-1) or cardiac (Trop-T) cell markers.	bmcs	67-71	kinase insert domain protein receptor	Mus musculus	179-184
19696399-5	2009	CXCR4(+) BMCs showed a significantly higher invasion capacity under basal conditions and after SDF-1 stimulation.	bmcs	9-13	chemokine (C-X-C motif) receptor 4	Mus musculus	0-5
19696399-5	2009	CXCR4(+) BMCs showed a significantly higher invasion capacity under basal conditions and after SDF-1 stimulation.	bmcs	9-13	chemokine (C-X-C motif) ligand 12	Mus musculus	95-100
19696399-11	2009	CONCLUSIONS: CXCR4(+) BMCs exhibit an increased therapeutic potential for blood flow recovery after acute ischemia.	bmcs	22-26	chemokine (C-X-C motif) receptor 4	Mus musculus	13-18
21245057-2	2011	Moreover, PTH treatment after myocardial infarction (MI) improved survival and myocardial function associated with enhanced homing of bone marrow-derived stem cells (BMCs).	bmcs	166-170	parathyroid hormone	Mus musculus	10-13
21245057-8	2011	PTH-treated animals revealed an enhanced homing of CXCR4(+) BMCs associated with an increased protein level of the corresponding homing factor SDF-1 in the ischaemic heart.	bmcs	60-64	parathyroid hormone	Mus musculus	0-3
21245057-8	2011	PTH-treated animals revealed an enhanced homing of CXCR4(+) BMCs associated with an increased protein level of the corresponding homing factor SDF-1 in the ischaemic heart.	bmcs	60-64	chemokine (C-X-C motif) receptor 4	Mus musculus	51-56
21327765-5	2011	RANKL expression in +AL BMCs was 57% of that in controls (P = 0.001), and OPG expression in +AL BMCs was greater than in controls (153%, P = 0.01).	bmcs	24-28	TNF superfamily member 11	Homo sapiens	0-5
21327765-6	2011	The mean RANKL/OPG ratio in BMCs was 0.65 +- 0.35 for +AL specimens and 1.28 +- 0.53 for controls (P = 0.031).	bmcs	28-32	TNF superfamily member 11	Homo sapiens	9-14
21327765-6	2011	The mean RANKL/OPG ratio in BMCs was 0.65 +- 0.35 for +AL specimens and 1.28 +- 0.53 for controls (P = 0.031).	bmcs	28-32	basic transcription factor 3 pseudogene 11	Homo sapiens	15-18
21738617-6	2011	Exposure of BMCs to CSE induced IL-8 and TGF-beta1 production, which was dependent on NF-kappaB and ERK1/2, but not on AKT.	bmcs	12-16	C-X-C motif chemokine ligand 8	Homo sapiens	32-36
21738617-6	2011	Exposure of BMCs to CSE induced IL-8 and TGF-beta1 production, which was dependent on NF-kappaB and ERK1/2, but not on AKT.	bmcs	12-16	transforming growth factor beta 1	Homo sapiens	41-50
21738617-6	2011	Exposure of BMCs to CSE induced IL-8 and TGF-beta1 production, which was dependent on NF-kappaB and ERK1/2, but not on AKT.	bmcs	12-16	mitogen-activated protein kinase 3	Homo sapiens	100-106
20207947-7	2010	Seeded BMCs secreted significant amounts of monocyte chemoattractant protein-1 and increased early monocyte recruitment.	bmcs	7-11	chemokine (C-C motif) ligand 2	Mus musculus	44-78
18827024-14	2009	This may be explained by mobilization of BMCs, which are homing via the CXCR-4/SDF-1 axis.	bmcs	41-45	chemokine (C-X-C motif) receptor 4	Mus musculus	72-78
18827024-14	2009	This may be explained by mobilization of BMCs, which are homing via the CXCR-4/SDF-1 axis.	bmcs	41-45	chemokine (C-X-C motif) ligand 12	Mus musculus	79-84
18566117-2	2008	We have previously clarified that adenovirus-mediated forced expression of SF-1 can transform long-term cultured mouse bone marrow mesenchymal cells (BMCs) into ACTH-responsive steroidogenic cells.	bmcs	150-154	splicing factor 1	Mus musculus	75-79
18566117-6	2008	In response to increased SF-1 expression and/or treatment with retinoic acid, AMCs were much more prone to produce adrenal steroid, corticosterone rather than gonadal steroid, testosterone, whereas the contrary was evident in BMCs.	bmcs	226-230	splicing factor 1	Mus musculus	25-29
18504066-10	2008	RESULTS: Stimulation with PTH showed a significant increase of all characterized subpopulations of bone marrow-derived progenitor cells (BMCs) in peripheral blood (1.5- to 9.8-fold) similar to G-CSF.	bmcs	137-141	parathyroid hormone	Mus musculus	26-29
18504066-17	2008	The novel function of PTH on mobilization and regeneration of BMCs may pave the way for new therapeutic options in bone marrow and stem cell transplantation as well as in the field of ischemic disorders.	bmcs	62-66	parathyroid hormone	Mus musculus	22-25
18583711-7	2008	Intravenous infusion of WT- and Nox2-deficient BMCs into WT mice reveals that neovascularization and homing capacity are impaired in Nox2-deficient BMCs in vivo.	bmcs	47-51	cytochrome b-245, beta polypeptide	Mus musculus	32-36
18583711-7	2008	Intravenous infusion of WT- and Nox2-deficient BMCs into WT mice reveals that neovascularization and homing capacity are impaired in Nox2-deficient BMCs in vivo.	bmcs	47-51	cytochrome b-245, beta polypeptide	Mus musculus	133-137
18583711-7	2008	Intravenous infusion of WT- and Nox2-deficient BMCs into WT mice reveals that neovascularization and homing capacity are impaired in Nox2-deficient BMCs in vivo.	bmcs	148-152	cytochrome b-245, beta polypeptide	Mus musculus	32-36
18583711-7	2008	Intravenous infusion of WT- and Nox2-deficient BMCs into WT mice reveals that neovascularization and homing capacity are impaired in Nox2-deficient BMCs in vivo.	bmcs	148-152	cytochrome b-245, beta polypeptide	Mus musculus	133-137
18346841-1	2008	OBJECTIVE: Besides its classical function in the field of autologous and allogenic stem cell transplantation, granulocyte colony-stimulating factor (G-CSF) was shown to have protective effects after myocardial infarction (MI) by mobilization of bone marrow-derived progenitor cells (BMCs) and in addition by activation of multiple signaling pathways.	bmcs	283-287	colony stimulating factor 3 (granulocyte)	Mus musculus	110-147
18346841-1	2008	OBJECTIVE: Besides its classical function in the field of autologous and allogenic stem cell transplantation, granulocyte colony-stimulating factor (G-CSF) was shown to have protective effects after myocardial infarction (MI) by mobilization of bone marrow-derived progenitor cells (BMCs) and in addition by activation of multiple signaling pathways.	bmcs	283-287	colony stimulating factor 3 (granulocyte)	Mus musculus	149-154
18346841-2	2008	In the present study, we focused on the impact of G-CSF on migration of BMCs and the impact on resident cardiac cells after MI.	bmcs	72-76	colony stimulating factor 3 (granulocyte)	Mus musculus	50-55
18346841-12	2008	CONCLUSION: Our study shows that G-CSF treatment after MI reduces migration capacity of BMCs into ischemic tissue, but increases the number of resident cardiac cells.	bmcs	88-92	colony stimulating factor 3 (granulocyte)	Mus musculus	33-38
18583711-5	2008	Mice lacking Nox2 show reduction of ischemia-induced flow recovery, ROS levels in BMCs, as well as EPC mobilization from BM.	bmcs	82-86	cytochrome b-245, beta polypeptide	Mus musculus	13-17
17898268-8	2007	BMCs in both the corneal stroma and the subconjunctiva expressed scavenger receptor CD163.	bmcs	0-4	CD163 molecule	Homo sapiens	84-89
17658619-8	2007	For example, IL-18 was up-regulated in BMCs but not MSCs of mastitic quarters, while IL-17 was more highly expressed in MSCs compared to BMCs.	bmcs	39-43	interleukin 18	Bos taurus	13-18
17911347-11	2007	Serum levels of G-CSF, EPO, and SCF known to mobilize BMCs were even decreased or remained unchanged, suggesting a direct effect of PTH on stem cell mobilization.	bmcs	54-58	KIT ligand	Homo sapiens	32-35
17911347-12	2007	Our data suggest a new function of PTH mobilizing BMCs into peripheral blood.	bmcs	50-54	parathyroid hormone	Homo sapiens	35-38
17898268-9	2007	Macrophage mannose receptor CD206 was expressed by BMCs in the substantia propria of the conjunctiva, but not by BMCs in the corneal stroma or epithelium.	bmcs	51-55	mannose receptor C-type 1	Homo sapiens	28-33
17898268-10	2007	CONCLUSIONS: These findings demonstrated that the main population of BMCs in the substantia propria of normal human conjunctiva is CD68(+)CD14(+)HLA-DR(+) cells.	bmcs	69-73	CD68 molecule	Homo sapiens	131-135
17898268-10	2007	CONCLUSIONS: These findings demonstrated that the main population of BMCs in the substantia propria of normal human conjunctiva is CD68(+)CD14(+)HLA-DR(+) cells.	bmcs	69-73	CD14 molecule	Homo sapiens	138-142
11803205-3	2002	Mesangial deposits of IgA and C3 and glomerular sclerosis in HIGA recipients of BMCs from B6 mice (B6-->HIGA) were decreased as compared with those in HIGA recipients of BMCs from HIGA mice (HIGA-->HIGA).	bmcs	80-84	immunoglobulin heavy constant alpha	Mus musculus	22-25
17724223-4	2007	Using an animal model of sodium iodate (NaIO(3))-induced RPE degeneration, BMCs were mobilized into the peripheral circulation by granulocyte-colony stimulating factor, flt3 ligand, or both.	bmcs	75-79	colony stimulating factor 3 (granulocyte)	Mus musculus	130-180
17724223-7	2007	In vivo, BMCs were identified in the subretinal space as Sca-1(+) or c-kit(+) cells.	bmcs	9-13	lymphocyte antigen 6 complex, locus A	Mus musculus	57-65
15358665-3	2004	BMCs showed tropism for and ability to graft into the damaged mouse cardiac tissue and, after 1 week, acquired a cardiomyocyte phenotype and expressed cardiac proteins, including connexin43.	bmcs	0-4	gap junction protein, alpha 1	Mus musculus	179-189
17724223-2	2007	METHODS: Adult RPE cells were cocultured with green fluorescence protein (GFP)-labeled stem cell antigen-1 positive (Sca-1(+)) BMCs for 1, 2, and 3 weeks.	bmcs	127-131	lymphocyte antigen 6 complex, locus A	Mus musculus	87-106
17724223-2	2007	METHODS: Adult RPE cells were cocultured with green fluorescence protein (GFP)-labeled stem cell antigen-1 positive (Sca-1(+)) BMCs for 1, 2, and 3 weeks.	bmcs	127-131	lymphocyte antigen 6 complex, locus A	Mus musculus	117-125
17312179-6	2007	BMCs isolated from human corneal stroma showed a chemotactic response to MCP-1/CCL2 in the Boyden chamber assay.	bmcs	0-4	C-C motif chemokine ligand 2	Homo sapiens	73-78
17312179-6	2007	BMCs isolated from human corneal stroma showed a chemotactic response to MCP-1/CCL2 in the Boyden chamber assay.	bmcs	0-4	C-C motif chemokine ligand 2	Homo sapiens	79-83
17312179-8	2007	This is the first work on constitutive expression of CCR2 by BMCs from the corneal stroma and MCP-1/CCL2 by keratocytes/epithelial cells.	bmcs	61-65	chemokine (C-C motif) receptor 2	Mus musculus	53-57
17312179-9	2007	Our findings suggest that the interaction between MCP-1/CCL2 and CCR2 determines the distribution of constitutive BMCs in normal human corneal stroma.	bmcs	114-118	C-C motif chemokine ligand 2	Homo sapiens	50-55
17312179-9	2007	Our findings suggest that the interaction between MCP-1/CCL2 and CCR2 determines the distribution of constitutive BMCs in normal human corneal stroma.	bmcs	114-118	C-C motif chemokine ligand 2	Homo sapiens	56-60
17312179-9	2007	Our findings suggest that the interaction between MCP-1/CCL2 and CCR2 determines the distribution of constitutive BMCs in normal human corneal stroma.	bmcs	114-118	C-C motif chemokine receptor 2	Homo sapiens	65-69
17158356-5	2007	Of note, treatment of BMCs derived from S1P3-/- mice with S1P did not rescue blood flow recovery.	bmcs	22-26	sphingosine-1-phosphate receptor 3	Mus musculus	40-44
17158356-5	2007	Of note, treatment of BMCs derived from S1P3-/- mice with S1P did not rescue blood flow recovery.	bmcs	22-26	sphingosine-1-phosphate receptor 1	Mus musculus	40-43
16920925-7	2006	Conversely, thymus weight and cell number were decreased in the reverse graft setting in WT to db/db BMCs, indicating that expression of the leptin receptor in the environment is important for T cell development.	bmcs	101-105	leptin receptor	Mus musculus	141-156