PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 26862579-9 2016 The research provides information about the sequential events of NOX1/alpha1beta1 integrin/ILK/NOX2 in Ang II effects on VSMC. vsmc 121-125 angiotensinogen Homo sapiens 103-109 29127880-4 2018 Ang II significantly reduced the miR-145 compared with the control VSMC groups; all the tested flavonoids increased miR-145 in the 100 nM concentration. vsmc 67-71 angiotensinogen Homo sapiens 0-6 28814529-11 2017 Finally, we show that PD184161 blocked mitochondrial ROS (mtROS) production and cellular ATP levels, at the same time enhancing ascorbate availability in AngII-treated VSMC. vsmc 168-172 angiotensinogen Homo sapiens 154-159 26520903-5 2015 Ang II also stimulates ROS production in VSMC (140%) that is NOX1 dependent, being completely inhibited in NOX1 silenced cells. vsmc 41-45 angiotensinogen Homo sapiens 0-6 26520903-9 2015 Silencing of ILK blocked cell migration, AKT phosphorylation and the second peak of ROS, but partially inhibits (70%) VSMC proliferation induced by Ang II. vsmc 118-122 angiotensinogen Homo sapiens 148-154 26520903-8 2015 Corroborating the involvement of alpha1beta1 integrin, the pretreatment of VSMC with obtustatin impaired Ang II-induced FAK phosphorylation, AKT activation, p21 degradation and the increase of ILK expression. vsmc 75-79 angiotensinogen Homo sapiens 105-111 25496286-7 2015 RESULTS: VSMC migration was increased by Ang II (10(-10)-10(-7) mol/L) in a concentration-dependent manner, but not by aldosterone (10(-10)-10(-7) mol/L), and a synergistic effect of Ang II (10(-10) mol/L)/aldosterone (10(-10)mol/L) was also observed in VSMC migration. vsmc 9-13 angiotensinogen Homo sapiens 41-47 25496286-4 2015 We hypothesize that the D3 receptor has an inhibitory effect on angiotensin II (Ang II)/aldosterone-induced VSMC migration. vsmc 108-112 angiotensinogen Homo sapiens 64-78 25496286-4 2015 We hypothesize that the D3 receptor has an inhibitory effect on angiotensin II (Ang II)/aldosterone-induced VSMC migration. vsmc 108-112 angiotensinogen Homo sapiens 80-86 25496286-7 2015 RESULTS: VSMC migration was increased by Ang II (10(-10)-10(-7) mol/L) in a concentration-dependent manner, but not by aldosterone (10(-10)-10(-7) mol/L), and a synergistic effect of Ang II (10(-10) mol/L)/aldosterone (10(-10)mol/L) was also observed in VSMC migration. vsmc 9-13 angiotensinogen Homo sapiens 183-189 25496286-8 2015 The migratory effects of Ang II alone/with aldosterone were attenuated by the activation of D3 receptors (10(-10)-10(-7) mol/L), although a D3 receptor agonist, PD128907, by itself, had no effect on VSMC migration. vsmc 199-203 angiotensinogen Homo sapiens 25-31 24685565-10 2014 In this sense, leptin inhibits the angiotensin II-induced Ca(2+) increase, contraction and proliferation of VSMC through NO-dependent mechanisms. vsmc 108-112 angiotensinogen Homo sapiens 35-49 25088215-5 2014 In both VSMC phenotypes, cortisol markedly increased both angiotensinogen (AGT) and AT1-receptor (AT1R) mRNA levels. vsmc 8-12 angiotensinogen Homo sapiens 58-73 25088215-5 2014 In both VSMC phenotypes, cortisol markedly increased both angiotensinogen (AGT) and AT1-receptor (AT1R) mRNA levels. vsmc 8-12 angiotensinogen Homo sapiens 75-78 21148411-3 2011 To study cross-talk between G protein-coupled receptor- and integrin-induced signaling, we hypothesized that integrins are involved in AII-induced proliferation of VSMC. vsmc 164-168 angiotensinogen Homo sapiens 135-138 23846495-2 2013 Cyclophilin A (CyPA) is a ubiquitously expressed cytosolic protein that possesses peptidyl-prolyl cis-trans isomerase activity, scaffold function, and significantly enhances AngII-induced ROS production in VSMC. vsmc 206-210 angiotensinogen Homo sapiens 174-179 21470202-7 2012 PVAT-derived angiotensin II, angiotensin 1-7, reactive oxygen species, complement component 3, NO and H(2) S have a paracrine action on VSMC contraction, endothelial or fibroblast function; however, their paracrine actions on VSMC growth remain to be directly verified. vsmc 136-140 angiotensinogen Homo sapiens 13-27 21148411-10 2011 This work demonstrates roles for specific integrins (most likely alpha(5)beta(1) and alpha(1)beta(1)) in AII-induced proliferation of VSMC. vsmc 134-138 angiotensinogen Homo sapiens 105-108 21148411-6 2011 AII significantly induced proliferation in VSMC grown on collagen I or fibronectin, and this effect was blocked by the ERK inhibitor PD-98059, suggesting that AII-induced proliferation requires ERK activity. vsmc 43-47 angiotensinogen Homo sapiens 0-3 21148411-6 2011 AII significantly induced proliferation in VSMC grown on collagen I or fibronectin, and this effect was blocked by the ERK inhibitor PD-98059, suggesting that AII-induced proliferation requires ERK activity. vsmc 43-47 angiotensinogen Homo sapiens 159-162 21148411-7 2011 VSMC grown on collagen I or on fibronectin demonstrated approximately three- and approximately sixfold increases in ERK phosphorylation after stimulation with 100 nM AII, respectively, whereas VSMC grown on poly-d-lysine demonstrated no significant ERK activation, supporting the importance of integrin-mediated adhesion. vsmc 0-4 angiotensinogen Homo sapiens 166-169 17379189-4 2007 Upon angiotensin-II treatment of cultured VSMC, immunoprecipitated 12-LO was found bound to alpha-actin, a component of the cytoplasmic myofilaments. vsmc 42-46 angiotensinogen Homo sapiens 5-19 20601126-8 2010 Furthermore, an increase in VSMC growth was attenuated by PTP-1B antisense only in the presence of both Ang II and insulin. vsmc 28-32 angiotensinogen Homo sapiens 104-110 17275785-2 2007 The proliferative actions of insulin and angiotensin-II (A-II) in VSMC are mediated in part by ERK1/2. vsmc 66-70 angiotensinogen Homo sapiens 41-55 17275785-2 2007 The proliferative actions of insulin and angiotensin-II (A-II) in VSMC are mediated in part by ERK1/2. vsmc 66-70 angiotensinogen Homo sapiens 57-61 10559511-8 1999 Ang II and TNF-alpha induced the expression of IP-10 (1.5 and 3.4-fold) and MCP-1 (2.4 and 4-fold) in VSMC. vsmc 102-106 angiotensinogen Homo sapiens 0-6 15297771-3 2004 We found that L-NAC and D-NAC both inhibited Ang II-induced c-Jun N-terminal kinase and p38 mitogen-activated protein kinase activation and [(3)H]-thymidine incorporation in VSMC. vsmc 174-178 angiotensinogen Homo sapiens 45-51 12695657-4 2003 Recent studies demonstrate that hypertrophic signals, such as those elicited by Angiotensin II, abrogate the mechanisms of control of M phase in VSMC and induce cell cycle re-entry and polyploidization. vsmc 145-149 angiotensinogen Homo sapiens 80-94 12573135-3 2002 Ang II induced a quick and transient increase of dichlorodihydrofluorescein (DCHF) fluorescence in VSMC, an effect that was completely abolished by catalase and by diethyldithiocarbamate, a cell-permeable superoxide dismutase inhibitor. vsmc 99-103 angiotensinogen Homo sapiens 0-6 12088869-5 2002 These data indicate that hyperglycemia contributes to abnormal proliferation of VSMC by two mechanisms; the induction of NF-kappaB activation by Ang II, which facilitates transcription of certain growth factors, and the augmentation of E2F-1 in response to growth factors. vsmc 80-84 angiotensinogen Homo sapiens 145-151 10699963-18 2000 To determine the effect of homocysteine on the ability of VSMC to react to potent agonist such as angiotensin II, VSMC were pretreated with homocysteine and exposed to a range of angiotensin II concentrations which normally have no effect on intracellular Ca(2+). vsmc 58-62 angiotensinogen Homo sapiens 98-112 10699963-19 2000 After homocysteine pretreatment, VSMC were extremely responsive to angiotensin II at concentrations well below the physiologic range. vsmc 33-37 angiotensinogen Homo sapiens 67-81 16081869-3 2005 Treatment with a lower dose of Aldo (10(-12) mol/L) and with a lower dose of Ang II (10(-10) mol/L) significantly enhanced DNA synthesis, whereas Aldo or Ang II alone at these doses did not affect VSMC proliferation. vsmc 197-201 angiotensinogen Homo sapiens 77-83 15680482-3 2005 Several reports suggested that VSMC growth induced by Ang II was elicited by oxidative stress. vsmc 31-35 angiotensinogen Homo sapiens 54-60 15797645-6 2005 In addition, AII (10(-7) mol/L) increased the release of 12- and 15-hydroxyeicosatetraenoic acid from VSMC within 10 min approximately 3-fold (P = .03) and 50% (P < .05), respectively. vsmc 102-106 angiotensinogen Homo sapiens 13-16 12763029-1 2003 Many of the signaling events in VSMC stimulated by angiotensin II (AngII) are mediated by members of the mitogen-activated protein kinase (MAPK) family, including p38 MAPK. vsmc 32-36 angiotensinogen Homo sapiens 51-65 12763029-1 2003 Many of the signaling events in VSMC stimulated by angiotensin II (AngII) are mediated by members of the mitogen-activated protein kinase (MAPK) family, including p38 MAPK. vsmc 32-36 angiotensinogen Homo sapiens 67-72 12074579-6 2002 VSMC migration induced by AngII was also inhibited not only by an EGFR inhibitor but also by BiPS. vsmc 0-4 angiotensinogen Homo sapiens 26-31 9535424-5 1998 Combining Ang II and 50 micromol/L oleic acid doubled thymidine incorporation and VSMC number. vsmc 82-86 angiotensinogen Homo sapiens 10-16 11228745-8 1999 Thus, endogenous noncyclooxygenase arachidonic acid metabolites mediate angiotensin II-stimulated protein synthesis in cultured VSMC by activating the NADH/NADPH oxidase, providing mechanistic evidence for redox control of VSMC hypertrophy. vsmc 128-132 angiotensinogen Homo sapiens 72-86 11228745-8 1999 Thus, endogenous noncyclooxygenase arachidonic acid metabolites mediate angiotensin II-stimulated protein synthesis in cultured VSMC by activating the NADH/NADPH oxidase, providing mechanistic evidence for redox control of VSMC hypertrophy. vsmc 223-227 angiotensinogen Homo sapiens 72-86 9176147-5 1997 Incubation of permeabilized VSMC with anti-PLC-beta 1 or anti-Gq alpha antibodies inhibited ANG II-dependent inositol polyphosphate (IP) formation, while anti-PLC-gamma 1 antibodies did not inhibit ANG II-regulated IP formation. vsmc 28-32 angiotensinogen Homo sapiens 92-98 9357768-4 1997 For example, a 50% reduction was observed after exposure to 50 ng/ml EGF for 24 h. Incubation of cultured VSMC with 50 ng/ml EGF for 24 h resulted in a 77% reduction in ANG II-stimulated inositol phosphate formation. vsmc 106-110 angiotensinogen Homo sapiens 169-175 9176147-5 1997 Incubation of permeabilized VSMC with anti-PLC-beta 1 or anti-Gq alpha antibodies inhibited ANG II-dependent inositol polyphosphate (IP) formation, while anti-PLC-gamma 1 antibodies did not inhibit ANG II-regulated IP formation. vsmc 28-32 angiotensinogen Homo sapiens 198-204 7723594-2 1995 ANG II stimulated DNA synthesis of VSMC in a dose-dependent manner as estimated by 3H-Tdr incorporation (control; 2993 +/- 486 cpm, 10(-8)M; 3360 +/- 350 cpm, 10(-7)M; 3474 +/- 516 cpm, 10(-6)M; 4889 +/- 320 cpm, P < 0.01). vsmc 35-39 angiotensinogen Homo sapiens 0-6 7706254-3 1995 A novel transcriptionally regulated phosphatase, MAP kinase phosphatase-1 (MKP-1), is induced by angiotensin II in VSMC and selectively dephosphorylates MAP kinase in vitro. vsmc 115-119 angiotensinogen Homo sapiens 97-111 7723594-5 1995 Furthermore, DUP 753 decreased 10(-7) M ANG II-stimulated 3H-Tdr incorporation of VSMC in a dose-dependent manner (control; 2627 +/- 256 cpm, 10(-9) M; 2145 +/- 143 cpm, 10(-8) M; 1047 +/- 543 cpm, 10(-7) M; 639 +/- 169 cpm, 10(-6) M; 642 +/- 59 cpm, P < 0.01). vsmc 82-86 angiotensinogen Homo sapiens 40-46 8385175-10 1993 EXP3174 and losartan abolished the angiotensin II-induced formation of inositolphosphates in VSMC. vsmc 93-97 angiotensinogen Homo sapiens 35-49 7512570-2 1994 A potent vasoconstrictor, angiotensin II (Ang II), which causes a rapid phospholipase C-mediated phosphoinositide hydrolysis via the Ang II type 1 (AT1) receptor in VSMC, by itself did not stimulate the production of nitrite, a stable metabolite of NO, but dose dependently inhibited the IL-1 beta-induced nitrite production. vsmc 165-169 angiotensinogen Homo sapiens 26-40 7512570-2 1994 A potent vasoconstrictor, angiotensin II (Ang II), which causes a rapid phospholipase C-mediated phosphoinositide hydrolysis via the Ang II type 1 (AT1) receptor in VSMC, by itself did not stimulate the production of nitrite, a stable metabolite of NO, but dose dependently inhibited the IL-1 beta-induced nitrite production. vsmc 165-169 angiotensinogen Homo sapiens 42-48 7512570-2 1994 A potent vasoconstrictor, angiotensin II (Ang II), which causes a rapid phospholipase C-mediated phosphoinositide hydrolysis via the Ang II type 1 (AT1) receptor in VSMC, by itself did not stimulate the production of nitrite, a stable metabolite of NO, but dose dependently inhibited the IL-1 beta-induced nitrite production. vsmc 165-169 angiotensinogen Homo sapiens 133-139 8125929-3 1994 Angiotensin II induced a 2-3-fold increase in the phosphorylation of eIF-4E in VSMC. vsmc 79-83 angiotensinogen Homo sapiens 0-14 8125929-7 1994 Together, these observations indicate that angiotensin II induces phosphorylation of eIF-4E in a protein kinase C-dependent manner and suggest that this pathway may play an important role in the mechanism by which angiotensin II causes hypertrophy of VSMC. vsmc 251-255 angiotensinogen Homo sapiens 43-57 8125929-7 1994 Together, these observations indicate that angiotensin II induces phosphorylation of eIF-4E in a protein kinase C-dependent manner and suggest that this pathway may play an important role in the mechanism by which angiotensin II causes hypertrophy of VSMC. vsmc 251-255 angiotensinogen Homo sapiens 214-228 1332716-10 1992 Additionally, as found for Ang II, preincubation of VSMC with either phorbol 12-myristate, 13-acetate, forskolin or 8-bromo-cyclic GMP inhibited LDL- and HDL-induced accumulation of [3H]-inositol monophosphate. vsmc 52-56 angiotensinogen Homo sapiens 27-33 1326443-2 1992 When extracts of ang II-stimulated VSMC were fractionated by Mono Q anion-exchange column chromatography, three peaks of the activities which in vitro activate inactive MAP kinases were detected. vsmc 35-39 angiotensinogen Homo sapiens 17-23 3023395-4 1986 In addition, it was found that alpha 1 receptor-mediated Na/H exchange in VSMC was increased by angiotensin II and inhibited by 12-O-tetradecanoyl phorbol-13-acetate (TPA). vsmc 74-78 angiotensinogen Homo sapiens 96-110