ライフサイエンスコーパス: VSMC

1 VSMC adhesion force to FN (+33%) and integrin alpha5 exp

2 VSMC remodeling is characterized by molecular rewiring o

3 VSMC treatment with MG132, a proteasome inhibitor, indic

4 VSMC-specific SCAP knockdown decreased the lipid accumul

5 VSMC-specific SCAP knockdown mice were generated by Cre/

6 VSMCs are more plastic than previously recognized and ca

7 VSMCs can switch back and forth between highly prolifera

8 xypropyl-beta-cyclodextrin inhibits AAA in a VSMC TFEB-dependent manner in mouse models.

9 In addition, VSMC stiffness (-46.6%) and ex vivo aortic ring contract

10 proaches, we determined that miR-128 affects VSMC proliferation, migration, differentiation, and cont

11 chanism through which SCAP signaling affects VSMC foam cell development.

12 tudy demonstrated that TFEB protects against VSMC apoptosis and AAA.

13 blocked the increase in cytosolic Ca(2+) and VSMC calcification.

14 giogenesis and increased HUVEC apoptosis and VSMC calcification; however, all these detrimental effec

15 nificant improvement in IHBD development and VSMC differentiation during the first week.

16 ole of this microRNA in EV-induced HUVEC and VSMC dysfunction.

17 ssed TGF-beta1-induced hyperpolarization and VSMC differentiation, but this effect was abolished by T

18 contraction force (-40.1%) were lowered and VSMC actin cytoskeletal orientation was reduced (-24.5%)

19 SIRT6 regulates telomere maintenance and VSMC lifespan and inhibits atherogenesis, all dependent

20 artially inhibited SOCs, VSMC migration, and VSMC proliferation.

21 ing molecular pathways that control Nox5 and VSMC-derived EVs provides potential targets to modulate

22 ondrial fission decreases ROS production and VSMC senescence.

23 sticity and summarize the roles of VSMCs and VSMC-derived cells in atherosclerotic plaque development

24 OX from nucleus to cytoplasm in both ECs and VSMCs, potentially facilitating SPM biosynthesis.

25 skeletal myocytes (Pax7(+) and MyoD(+)) and VSMCs (Prrx1(+) and NG2(+)) were analyzed via whole moun

26 sed this esterase in human primary VSMCs and VSMCs differentiated from hiPSCs and observed that the n

27 tration significantly supressed human aortic VSMC apoptosis (via activation of PI-3 kinase/Akt signal

28 ate-induced senescence versus healthy aortic VSMCs.

29 receptor genes was detected in murine aortic VSMCs, with the highest levels of LPA1, LPA2, LPA4, and

30 TGFbeta1-stimulated human aortic or arterial VSMCs which revealed large and consistent upregulation o

31 tro, SCAP knockdown in human coronary artery VSMCs by RNA interference reduced lipid accumulation and

32 ed SOCs in contractile rat mesenteric artery VSMCs.

33 ng TRPC1-based SOCs in rat mesenteric artery VSMCs.

34 ess of any therapeutic intervention aimed at VSMCs and their derivatives.

35 MIA3 expression may promote atheroprotective VSMC phenotypic transitions, including increased prolife

36 ens junctions (AJ) along the borders between VSMCs.

37 ion occurs after platelet internalization by VSMCs.

38 sed EV release and decreased phagocytosis by VSMCs.

39 ng, but inhibited STAT3 activity, and caused VSMC phenotypic switching to a similar extent as TGFbeta

40 Vascular smooth muscle cell (VSMC) activation in response to injury plays an importan

41 s in regulating vascular smooth muscle cell (VSMC) activity.

42 Vascular smooth muscle cell (VSMC) apoptosis precipitates AAA formation, whereas VSMC

43 on primary rat vascular smooth muscle cell (VSMC) biomechanics.

44 Vascular smooth muscle cell (VSMC) function is regulated by Nox-derived reactive oxyg

45 stimulation of vascular smooth muscle cell (VSMC) migration and proliferation.

46 ) by increasing vascular smooth muscle cell (VSMC) osteogenic differentiation, ADAM17-induced renal a

47 Vascular smooth muscle cell (VSMC) phenotype switching from a contractile state to a

48 rns that define vascular smooth muscle cell (VSMC) phenotype.

49 role of YY1 in vascular smooth muscle cell (VSMC) phenotypic modulation both in vivo and in vitro.

50 major driver of vascular smooth muscle cell (VSMC) phenotypic switching, an important pathobiology in

51 Vascular smooth muscle cell (VSMC) remodeling is a pathological hallmark of chronic h

52 al dynamics and vascular smooth muscle cell (VSMC) senescence.

53 ate the role of vascular smooth muscle cell (VSMC) TFEB in the development of AAA and establish TFEB

54 ures in SE, and vascular smooth muscle cell (VSMC) TRPC3 channels participate in vasoconstriction.

55 ges, collagen, vascular smooth muscle cells (VSMC) and matrix metalloproteinases (MMPs).

56 F-1 actions in vascular smooth muscle cells (VSMC) are associated with accelerated arterial intima hy

57 is specific to vascular smooth muscle cells (VSMC), has histone methyl transferase activities, and ac

58 eralization of vascular smooth muscle cells (VSMC).

59 t) dynamics in vascular smooth muscle cells (VSMC).

60 1 activator in vascular smooth muscle cells (VSMC).

61 e cytoplasm of vascular smooth muscle cells (VSMCs) and tubular epithelial cells, with a median posit

62 Vascular smooth muscle cells (VSMCs) are a major cell type present at all stages of an

63 Vascular smooth muscle cells (VSMCs) are critical in the development of CAD.

64 and migratory vascular smooth muscle cells (VSMCs) are quite intricate with many channels contributi

65 Vascular smooth muscle cells (VSMCs) can be derived in large numbers from human induce

66 ells (ECs) and vascular smooth muscle cells (VSMCs) converted 17-HDHA to SPMs, including resolvin D1

67 re shared with vascular smooth muscle cells (VSMCs) derived from mesenchymal stem cell-like progenito

68 eral miRNAs in vascular smooth muscle cells (VSMCs) has been extensively characterized, the function

69 Vascular smooth muscle cells (VSMCs) in the normal arterial media continually express

70 orders between vascular smooth muscle cells (VSMCs) in the pressurized rat superior cerebellar artery

71 s migration of vascular smooth muscle cells (VSMCs) into the intima in mice as well as migration and

72 l formation in vascular smooth muscle cells (VSMCs) is poorly understood.

73 e of TSPANs in vascular smooth muscle cells (VSMCs) is unexplored.

74 ion of Plk1 in vascular smooth muscle cells (VSMCs) led to reduced arterial elasticity, hypotension,

75 d migration of vascular smooth muscle cells (VSMCs) or endothelial cell (ECs) promote or inhibit, res

76 regulators of vascular smooth muscle cells (VSMCs) phenotypic switch, one of the main events respons

77 Vascular smooth muscle cells (VSMCs) play critical roles in the stability and tonic re

78 ons applied to vascular smooth muscle cells (VSMCs) regulates mitochondrial network structure near th

79 Vascular smooth muscle cells (VSMCs) show a remarkable phenotypic plasticity, allowing

80 ells (ECs) and vascular smooth muscle cells (VSMCs) through the Notch pathway regulates arterial remo

81 In vascular smooth muscle cells (VSMCs), activation of Ca(2+) -permeable store-operated c

82 ABSTRACT: In vascular smooth muscle cells (VSMCs), stimulation of canonical transient receptor pote

83 In vascular smooth muscle cells (VSMCs), stimulation of SOCs composed of canonical transi

84 also stimulate vascular smooth muscle cells (VSMCs), thereby contributing to vasoregulation and remod

85 f striated and vascular smooth muscle cells (VSMCs), we performed lineage tracing studies in mice to

86 se (AADAC), in vascular smooth muscle cells (VSMCs).

87 e of origin of vascular smooth muscle cells (VSMCs).

88 on molecule in vascular smooth muscle cells (VSMCs).

89 expression in vascular smooth muscle cells (VSMCs).

90 articularly in vascular smooth muscle cells (VSMCs).

91 is mediated by vascular smooth muscle cells (VSMCs).

92 recruitment of vascular smooth muscle cells; VSMCs) in the presence of enhanced flow.

93 ea that TRPC3 channels expressed by cerebral VSMCs contribute to the IHR during SE, which is a critic

94 'vulnerable plaque' hypotheses, contractile VSMCs recruited from the media undergo phenotypic conver

95 understood this allows normally contractile VSMCs to become proliferative following vessel injury, a

96 amatically enhanced formation of contractile VSMCs and increased systemic blood pressure as well as r

97 ng formation, and maintenance of contractile VSMCs in vivo.

98 P10 for controlling formation of contractile VSMCs.

99 We show here that contractile VSMCs are resistant to calcification and identify Nox5 a

100 inding protein A4) compared with contractile VSMCs.

101 In contrast, VSMC-derived cells generating the neointima after vascul

102 MKL1 and MKL2) and their role in controlling VSMC and EC proliferation and migration.

103 aming induced by Poldip2 deficiency controls VSMC differentiation.

104 ediated cholesterol depletion may coordinate VSMC migration and adhesion to different ECM proteins an

105 ular enhancer and SE repertoires in cultured VSMCs in vitro, ex vivo, and in AngII-infused mice aorta

106 Accordingly, knockdown of Homer1 in cultured VSMCs partially inhibited SOCs, VSMC migration, and VSMC

107 Consequently, Poldip2-deficient VSMC and mouse aorta express high levels of contractile

108 Mechanistically, Epac1 deficient VSMCs exhibited lower level of PI3K/AKT signaling and da

109 TRPC6-deficient VSMCs exhibited more polarized resting membrane potentia

110 TGF-beta signaling potential in CNC-derived VSMCs associated, in vivo, with increased Smad2/3 phosph

111 and excessive Smad signaling in CNC-derived VSMCs.

112 h on defective Smad signaling in SHF-derived VSMCs and excessive Smad signaling in CNC-derived VSMCs.

113 cardiac neural crest-derived (CNC-derived), VSMCs showed impaired Smad2/3 activation in response to

114 rise due to diabetes contribute to different VSMC behavior and thus vascular disease.

115 YY1 expression is induced in differentiated VSMCs in response to serum stimulation.

116 ntin knockout mice (VimKO) display disrupted VSMC differentiation and adverse remodeling in aortic ex

117 eless, removing one copy of Rumi from either VSMCs or hepatoblasts is sufficient to partially suppres

118 Thus, we identified the first VSMC-enriched and MYOCD/SRF and TGF-beta1/SMAD-dependent

119 myocardin (MYOCD) are potent activators for VSMC differentiation, we screened for TGF-beta1 and MYOC

120 In this Review, we present the evidence for VSMC plasticity and summarize the roles of VSMCs and VSM

121 essel pericyte coverage, and is required for VSMC recruitment during increased nitric oxide-mediated

122 nstream pathways activated by SIRT6, and how VSMC SIRT6 regulates atherogenesis.

123 We examined how VSMC phenotypic switching influences vascular calcificat

124 active mutant (SIRT6(H133Y)) shortened human VSMC lifespan and induced senescence, associated with te

125 Human VSMCs express Nox1, Nox4, Nox5 and Cav-1.

126 mouse atherosclerotic plaques, and in human VSMCs derived from plaques or undergoing replicative or

127 We examined SIRT6 expression in human VSMCs, the role, regulation, and downstream pathways act

128 wth factor (PDGF)-induced migration in human VSMCs.

129 ing the contractile gene expression in human VSMCs.

130 rms for Nox1 and Nox5 but not Nox4, in human VSMCs.

131 PDGFRbeta and contractile phenotype of human VSMCs.

132 In VSMC, Bbetaglucans prevented LPS- or uremic serum-induce

133 In VSMC, deleting IGF1R increases homodimers of IR, enhance

134 In VSMC, p42/p44 mitogen-activated protein kinase (MAPK) pa

135 The effect of changes in VSMC biomechanics on aortic function was assessed using

136 lammatory cytokine expression and changes in VSMC metabolism associated with senescence.

137 d role for PD184161 as an HIF-1 inhibitor in VSMC under nonhypoxic conditions.

138 to increase expression of genes involved in VSMC dysfunction, and could uncover novel therapies.

139 d assessed the role of these microdomains in VSMC ROS production and pro-contractile and growth signa

140 PA-IQGAP1 pathway plays an important role in VSMC migration and injury-induced vascular remodeling, a

141 ta show that IL11 plays an important role in VSMC phenotype switching, vascular inflammation and aort

142 ated well with activation of purified sGC in VSMC lysates and cGMP accumulation in intact porcine aor

143 or (SMIRKO) or IGF-1 receptor (SMIGF1RKO) in VSMC and in mice.

144 approaches to understand the role of TFEB in VSMC survival and explored the underlying mechanisms thr

145 um response factor (SRF)-regulated TSPANs in VSMC by using RNA-seq analyses and RNA-arrays.

146 The effects of BMP9/10 in VSMCs are mediated by different combinations of BMP type

147 (melanoma inhibitory activity protein 3) in VSMCs resulted in lower proliferation, consistent with h

148 y was to evaluate the role of miR-125a-5p in VSMCs phenotypic switch.

149 olved in the modulation of miRNA activity in VSMCs is unknown.

150 sitive to pressure and vasomotor agonists in VSMCs and support a functional role of N-cadherin AJs in

151 Deletion of Alk1 in VSMCs recapitulated the Bmp9/10 phenotype in pulmonary b

152 TFEB potently inhibits apoptosis in VSMCs, and transcriptome analysis revealed that TFEB reg

153 Furthermore, we found that autophagy in VSMCs was increased in SM22alpha-Cre:SCAP(flox/+):ApoE(-

154 e role of multiple Ca(2+) influx channels in VSMCs and are the first to show the role of Homer protei

155 nd Homer1 are present in the same complex in VSMCs and how Homer1 contributes to VSMC SOCs, prolifera

156 ular calcium transients and contractility in VSMCs.

157 and MYOCD, and reduced by SRF deficiency in VSMCs.

158 ctivation of RhoA and actomyosin dynamics in VSMCs in a mitosis-independent manner.

159 lar RNAs interacting with miRNAs enriched in VSMCs and modulating the cells' activity.

160 identified several circular RNAs enriched in VSMCs; however, only one, possessing multiple putative b

161 activate STIM/ORAI-mediated Ca(2+) entry in VSMCs.

162 PKCdelta was expressed in VSMCs, and selective PKCdelta inhibitory peptides and kn

163 gest that miR-125a-5p is highly expressed in VSMCs, but it is down-regulated after vascular injury in

164 we show that deletion of IRS-1 expression in VSMCs in non-diabetic mice results in dedifferentiation,

165 ings suggest that higher AADAC expression in VSMCs protects T2DM patients from CVD.

166 c mice by decreasing PDGFRbeta expression in VSMCs.

167 4, localize in cholesterol-rich fractions in VSMCs.

168 IL11 has an unknown function in VSMCs, which highly express the IL11 receptor alpha, sug

169 imal mitochondrial structure and function in VSMCs.

170 ive and pro-migratory MKL1/2 target genes in VSMCs but not in ECs.

171 ed that overexpress SIRT6 or SIRT6(H133Y) in VSMCs only.

172 Mice lacking Klf5 in VSMCs exacerbate vascular senescence and progression of

173 SCAP knockdown in VSMCs reduced oxidative stress and increased AMPK phosph

174 part of a novel mechanosensory mechanism in VSMCs and plays an active role in both the arteriolar my

175 and inhibited proliferation and migration in VSMCs but not EC.

176 lcification, proliferation, and migration in VSMCs isolated from 151 multiethnic heart transplant don

177 AP1 blocks ruffle formation and migration in VSMCs, which are rescued by expression of the exogenous

178 unterbalancing the functions of the miRNA in VSMCs.

179 ed nuclear-translocation of MKL1 and MKL2 in VSMCs but not ECs.

180 the reactive oxygen species/AMPK pathway in VSMCs, and consequently alleviated atherosclerosis plaqu

181 gration and is crucial in PDGF-BB pathway in VSMCs.

182 induces a highly differentiated phenotype in VSMCs through a mechanism that involves regulation of me

183 d show that Ca(2+) induces ROS production in VSMCs via Nox5.

184 d a significant reduction of MIA3 protein in VSMCs in thin fibrous caps of late-stage atherosclerotic

185 first to show the role of Homer proteins in VSMCs and its importance in neointima formation.

186 not mRNA, expression was markedly reduced in VSMCs in human and mouse atherosclerotic plaques, and in

187 ing requires STIM1, which is up-regulated in VSMCs from hypertensive rats.

188 Here, we show that Klf5 down-regulation in VSMCs is correlated with rupture of abdominal aortic ane

189 mer assembles SOC complexes, but its role in VSMCs is not well understood.

190 n different cell types; however, its role in VSMCs is still unknown.

191 fficiently glucosylated, and loss of Rumi in VSMCs results in increased levels of full-length JAG1 an

192 Conditional deletion of Rumi in VSMCs results in progressive arborization of the IHBD tr

193 activation mechanism of TRPC1-based SOCs in VSMCs, and a novel role for STIM1, in which store-operat

194 activation mechanism of TRPC1-based SOCs in VSMCs, and a novel role for STIM1, where store-operated

195 Also, US28 facilitates HCMV spreading in VSMCs in vitro.

196 ated by an altered DNA methylation status in VSMCs, and among the hits, we selected miR-128.

197 d tripartite motif-containing 27 (TRIM27) in VSMCs.

198 indicate that LPA causes vasoconstriction in VSMCs, mediated by LPA1-, Gi-, and COX1-dependent autocr

199 ntly observed that TFEB deficiency increases VSMC apoptosis and promotes AAA formation in different m

200 signaling reduced TGFbeta1- or ANGII-induced VSMC phenotypic switching, placing IL11 activity downstr

201 KLF4, a transcription factor that induces VSMC dedifferentiation, was up-regulated in IRS-1(-/-) m

202 by TFEB and is required for TFEB to inhibit VSMC apoptosis.

203 sTie2 and sFlt1 both inhibited VSMC recruitment (both 0%), and VEGF inhibition increase

204 raction of all SOC components in the injured VSMCs, where Homer1 interacts with Orai1 and various TRP

205 ies of N-cadherin adhesion sites in isolated VSMCs.

206 in (EGFP) on the plasma membrane of isolated VSMCs, whereas treatment with PE (10(-5) m) or sodium ni

207 dependent upon epigenetic regulation of key VSMC differentiation genes; notably, Kruppel-like factor

208 m (SNP) rs67180937 was associated with lower VSMC MIA3 expression and lower proliferation.

209 iated cholesterol depletion (-27.8%) lowered VSMC migration distance on a fibronectin (FN)-coated sur

210 -1 is functioning constitutively to maintain VSMCs in their differentiated state and, thereby, inhibi

211 However, enhancers/SEs mediating VSMC dysfunction remain uncharacterized.

212 on programs that can be targeted to modulate VSMC phenotype during vascular diseases.

213 promoted proliferation and lifespan of mouse VSMCs, and prevented senescence-associated metabolic cha

214 ter occlusion by dedifferentiated neointimal VSMC.

215 highly plastic VSMCs results in the observed VSMC accumulation after injury and in atherosclerotic pl

216 restenosis after angioplasty, how control of VSMC phenotypic switching is dysregulated in pathologic

217 RyR on the intracellular calcium dynamics of VSMC and to understand how variation in protein levels t

218 injury generally retained the expression of VSMC markers and the upregulation of Mac3 was less prono

219 identify targets for specific inhibition of VSMC migration and proliferation.

220 s an important and unrecognized inhibitor of VSMC senescence and atherosclerosis.

221 inhibited the proliferation and migration of VSMC and EC.

222 ues and down-regulated in in vitro models of VSMC phenotypic modulation.

223 on dedifferentiation of VSMCs, prevention of VSMC-mediated excessive repair remains poorly understood

224 LCCB-induced promotion of VSMC remodeling requires STIM1, which is up-regulated in

225 Lrp6 hindered miR-145-mediated regulation of VSMC migration, proliferation, and differentiation.

226 tion and identify Nox5 as a key regulator of VSMC phenotypic switching.

227 mouse AAA models, we determined the role of VSMC TFEB and a TFEB activator in AAA in vivo.

228 enhanced sensitivity to IGF-I stimulation of VSMC proliferation and a hyperproliferative response to

229 n vascular quality control by fine-tuning of VSMC phenotypic switching.

230 arly antigen was detected in less than 5% of VSMCs, tubular epithelial cells, interstitial endotheliu

231 studies have focused on dedifferentiation of VSMCs, prevention of VSMC-mediated excessive repair rema

232 s facilitated contractile differentiation of VSMCs through plasma membrane hyperpolarization.

233 restimated both the content and functions of VSMCs in plaques and have thus challenged our view on th

234 miR-128 is a critical modulator of VSMCs and is regulated by epigenetic modifications upon

235 apidly declined postnatally as the number of VSMCs necessary for ductus contraction increased.

236 pressed differentiation and proliferation of VSMCs and reiterated defects observed in adult Bmp9/10 d

237 , whereas a direct role in the regulation of VSMCs was not investigated.

238 ay and is therefore a potential regulator of VSMCs phenotypic switch.

239 laining the strikingly different response of VSMCs and ECs to cAMP elevation.

240 have thus challenged our view on the role of VSMCs in atherosclerosis.

241 r VSMC plasticity and summarize the roles of VSMCs and VSMC-derived cells in atherosclerotic plaque d

242 Although abnormal phenotypic switching of VSMCs is a hallmark of vascular disorders such as athero

243 Treatment of VSMCs with Ca(2+) loaded extracellular vesicles (EVs) le

244 K2i showed significant inhibitory effects on VSMC migration through down-regulated phosphorylation of

245 etic variants have significant influences on VSMC function relevant to the development of atheroscler

246 nstrates that BMP9 and BMP10 act directly on VSMCs for induction and maintenance of their contractile

247 ignificant loci associated with at least one VSMC phenotype.

248 rotein E (Apoe)-knockout mice overexpressing VSMC-specific Aadac showed amelioration of atherosclerot

249 nificantly decreased in AADAC-overexpressing VSMCs.

250 tion of TRPC6 channel activity in pathologic VSMCs could be a rational strategy to maintain vascular

251 dulate the methylation status of the pivotal VSMC gene myosin heavy chain 11 (Myh11).

252 ession was reduced in human and mouse plaque VSMCs and by palmitate in a p38- and c-Jun N-terminal ki

253 ression is reduced in human and mouse plaque VSMCs and is positively regulated by CHIP.

254 ration of a low proportion of highly plastic VSMCs results in the observed VSMC accumulation after in

255 Intact small arteries and primary VSMCs from humans were studied.

256 ry infiltrates, and glomerular cells.Primary VSMCs were infected with green fluorescent protein-tagge

257 overexpressed this esterase in human primary VSMCs and VSMCs differentiated from hiPSCs and observed

258 and formation of membrane ruffles in primary VSMCs.

259 essing neointima formation and proliferative VSMC accumulation in neointima area.

260 Additionally, MMP-7 promotes VSMC apoptosis by cleavage of N-cadherin.

261 on retarding VSMC apoptosis whilst promoting VSMC proliferation.

262 In addition, by presenting PS, VSMC exosomes can also provide the catalytic surface for

263 h from synthetic to contractile in pulmonary VSMCs.

264 together with analysis of isolated pulmonary VSMCs to unravel phenotypic and transcriptomic changes i

265 Its overexpression is sufficient to reduce VSMCs proliferation and migration, and it is able to pro

266 f matrix-metalloproteinase-7 (Mmp-7) reduced VSMC apoptosis in mouse atherosclerotic plaques.

267 us improving HUVEC angiogenesis and reducing VSMC calcification.

268 Nox5 itself regulated VSMC phenotype as siRNA knockdown of Nox5 increased cont

269 metabolism; however, its role in regulating VSMC senescence and atherosclerosis is unclear.

270 studies should therefore focus on retarding VSMC apoptosis whilst promoting VSMC proliferation.

271 et-derived microRNA-223 (miRNA-223) reverses VSMC dedifferentiation.

272 able to promote the expression of selective VSMCs markers such as alpha smooth muscle actin, myosin

273 ects recapitulated in Cav-1 silenced (siRNA) VSMCs.

274 in cultured VSMCs partially inhibited SOCs, VSMC migration, and VSMC proliferation.

275 We stretched VSMCs in culture with cycle-by-cycle variability in area

276 tional studies showed that TSPAN2 suppresses VSMC proliferation and migration.

277 ROS production in synthetic VSMCs was cytosolic Ca(2+)-dependent, in line with it be

278 f ROS and Ca(2+)-dependent Nox5 in synthetic VSMCs.

279 In vitro cultures of synthetic VSMCs showed decreased expression of contractile markers

280 icolor lineage labeling, we demonstrate that VSMCs in injury-induced neointimal lesions and in athero

281 were shown to be upregulated and mediate the VSMC contractile marker gene and PDGFRbeta expression in

282 ia-initiated signaling as key element of the VSMC differentiation programs that can be targeted to mo

283 anges in vascular tone and diminution of the VSMC layer with attenuated contractility and decreased s

284 nced green fluorescent protein (EGFP) on the VSMC surface.

285 ced a localized mechanical response from the VSMCs that opposed the pulling.

286 ced a localized mechanical response from the VSMCs that opposed the pulling.

287 mplex in VSMCs and how Homer1 contributes to VSMC SOCs, proliferation, and migration leading to neoin

288 The addition of 1 mum GTN to VSMC expressing either wild-type or C301S/C303S ALDH2 re

289 Mac3+ cell population, which is specific to VSMC-derived plaque cells.

290 oD(-)/Prrx1(+)/NG2(+) progenitors similar to VSMCs prior to postnatal day 10 (P10), and from a previo

291 cing ascorbate availability in AngII-treated VSMC.

292 bitor, is an HIF-1 blocker in Ang II-treated VSMC.

293 ild-type VSMCs, and was absent in TRPC1(-/-) VSMCs.

294 otein kinase B (Akt) activity than wild-type VSMCs in response to TGF-beta1 stimulation.

295 STIM1 short hairpin RNA (shRNA) in wild-type VSMCs, and was absent in TRPC1(-/-) VSMCs.

296 upregulated in balloon-injured vs. uninjured VSMCs.

297 Using VSMC-selective Tfeb knockout mice and different mouse AA

298 poptosis precipitates AAA formation, whereas VSMC proliferation repairs the vessel wall.

299 ease in migration and proliferation, whereby VSMCs are termed synthetic.

300 ose expression is intimately associated with VSMC differentiation and negatively correlated with vasc