ライフサイエンスコーパス: VSMC

1 VSMC DNA damage has minimal effects on atherogenesis, bu

2 VSMC senes cence promotes both atherosclerosis and featu

3 VSMC treatment with MG132, a proteasome inhibitor, indic

4 VSMC-derived exosomes were enriched with the tetraspanin

5 VSMC-expressed PDE3A deserves scrutiny as a therapeutic

6 VSMCs from male KO mice showed reduced contractility whe

7 In addition, VSMC proliferation may be beneficial throughout atheroge

8 In particular, it is not known whether all VSMCs proliferate and display plasticity or whether indi

9 ulate NF-kappaB activation, thereby altering VSMC sensitivity to IGF-I.

10 celerating DSB repair increased cap area and VSMC content.

11 , regulates several key endothelial cell and VSMC functions including cell growth, migration, surviva

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

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

14 whereas VSMC apoptosis, cell senescence, and VSMC-derived macrophage-like cells may promote inflammat

15 ced by ligating the left carotid artery, and VSMCs were pretreated with platelet-derived growth facto

16 anisms and interplay between damaged ECs and VSMCs that lead to activation of IL-1alpha and, thus, in

17 Cs could activate neighboring normal ECs and VSMCs, causing them to release inflammatory cytokines an

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

19 ults open new avenues for an innovative anti-VSMC foam cell-based strategy for the treatment of vascu

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

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

22 Consistent with these data, SM-ARKO VSMCs showed a reduction in Osterix mRNA expression.

23 lunted in VSMC-specific AR-ablated (SM-ARKO) VSMCs compared to WT.

24 nd sufficient to inhibit postinjury arterial VSMC proliferation, whereas membrane ERalpha largely reg

25 in (alphaSMA) double-immunostaining assessed VSMC differentiation and proliferation in endometria fro

26 roliferation is implicated in atherogenesis, VSMCs in advanced plaques and cultured from plaques show

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

28 ral imbalance stimulate exosome secretion by VSMCs, most likely by the activation of sphingomyelin ph

29 Vascular smooth muscle cell (VSMC) accumulation is a hallmark of atherosclerosis and

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

31 at LAPCs impair vascular smooth muscle cell (VSMC) and pericyte proliferation and migration producing

32 Vascular smooth muscle cell (VSMC) apoptosis occurs during the progression of atheros

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

34 )-induced mouse vascular smooth muscle cell (VSMC) calcification following either testosterone or dih

35 ycemia leads to vascular smooth muscle cell (VSMC) dedifferentiation and enhances responses to IGF-I.

36 the periportal vascular smooth muscle cell (VSMC) layer, which are apparent at embryonic day 18 and

37 t regulators of vascular smooth muscle cell (VSMC) membrane voltage.

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

39 CP1) stimulates vascular smooth muscle cell (VSMC) migration in vascular wall remodeling.

40 ey regulator of vascular smooth muscle cell (VSMC) phenotypes, including differentiation, proliferati

41 Vascular smooth muscle cell (VSMC) phenotypic conversion from a contractile to 'synth

42 ntion, in which vascular smooth muscle cell (VSMC) proliferation and activation of inflammation are t

43 Although vascular smooth muscle cell (VSMC) proliferation is implicated in atherogenesis, VSMC

44 m) in cultured vascular smooth muscle cells (VSMC) expressing an ALDH2 mutant that reduces GTN to NO

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

46 lcium entry in vascular smooth muscle cells (VSMC).

47 rat and human vascular smooth muscle cells (VSMC).

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

49 1 activator in vascular smooth muscle cells (VSMC).

50 m cell-derived vascular smooth muscle cells (VSMCs) and chondrocytes provided insights into molecular

51 in calcifying vascular smooth muscle cells (VSMCs) and in calcified vessels of patients with atheros

52 Hyperplasia of vascular smooth muscle cells (VSMCs) and infiltration of immune cells are the hallmark

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

54 its action on vascular smooth muscle cells (VSMCs) are not fully understood.

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

56 NC cells into vascular smooth muscle cells (VSMCs) by regulating Notch signaling.

57 receptors from vascular smooth muscle cells (VSMCs) caused a modest (approximately 7 mmHg) yet signif

58 regulators of vascular smooth muscle cells (VSMCs) contractility and arterial tone.

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

60 Vascular smooth muscle cells (VSMCs) cultured from shGRK2 knockdown mice show increase

61 orical view of vascular smooth muscle cells (VSMCs) in atherosclerosis is that aberrant proliferation

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

63 Studies with vascular smooth muscle cells (VSMCs) indicate a role for induction of dual specificity

64 that EPHB4 on vascular smooth muscle cells (VSMCs) is involved in blood pressure regulation.

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

66 K1 activity in vascular smooth muscle cells (VSMCs) leads to decreased sodium-potassium ATPase activi

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

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

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

70 pericytes and vascular smooth muscle cells (VSMCs) regulating vascular stability and function.

71 uated in human vascular smooth muscle cells (VSMCs) stimulated with angiotensin II (Ang II).

72 ion of SFAs in vascular smooth muscle cells (VSMCs), are characteristic events in the development of

73 ), secreted by vascular smooth muscle cells (VSMCs), form the first nidus for mineralization and fetu

74 In vascular smooth muscle cells (VSMCs), stimulation of canonical transient receptor pote

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

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

77 Surprisingly, vascular smooth muscle cells (VSMCs), the predominant and often exclusive cell type of

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

79 1 proteins in vascular smooth muscle cells (VSMCs), which contribute to important cellular functions

80 articularly in vascular smooth muscle cells (VSMCs).

81 from necrotic vascular smooth muscle cells (VSMCs).

82 romultimers in vascular smooth muscle cells (VSMCs).

83 attractant for vascular smooth muscle cells (VSMCs).

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

85 expression in vascular smooth muscle cells (VSMCs).

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

87 and injury-induced neointima did not contain VSMC-derived cells expressing a different fluorescent re

88 In contrast, VSMC Akt1 inhibition in established atherosclerotic plaq

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

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

91 specifically regulated by NOTCH3 in cultured VSMCs and in mouse aortas.

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

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

94 proliferation and cell survival in cultured VSMCs.

95 migration assays were performed on cultured VSMCs treated with MPA or etonogestrel (ETO).

96 be primed by IL-1alpha from adjacent damaged VSMCs, and necrotic ECs could activate neighboring norma

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

98 locker, were selectively reduced in diabetic VSMCs.

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

100 SM22alpha-NBS1/apolipoprotein E(-/-) VSMCs showed enhanced DSB repair and decreased growth ar

101 SM22alpha-(DeltaC)NBS1/apolipoprotein E(-/-) VSMCs showed reduced DSB repair and increased growth arr

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

103 ized by bigger necrotic core areas, enhanced VSMC apoptosis, and reduced fibrous cap and collagen con

104 Transgenic mice expressing VSMC-specific TRF2(T188A) showed increased atheroscleros

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

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

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

108 nd the secretion of calcifying exosomes from VSMCs in vitro, and chemical inhibition of sphingomyelin

109 On the other hand, VSMCs and the extracellular matrix that they produce als

110 lating cell adhesion and migration highlight VSMC exosomes as potentially important communication mes

111 However, VSMC DNA damage reduced relative fibrous cap areas, wher

112 CR4 in a HeLa expression system and in human VSMC.

113 8-labeled fetuin-A was internalized by human VSMCs, trafficked via the endosomal system, and exocytos

114 s could be validated in Ang II-treated human VSMCs.

115 peutic targeting of these hyperproliferating VSMCs might effectively reduce vascular disease without

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

117 sary and sufficient for GTN bioactivation in VSMC.

118 he regulation, and role, of MV biogenesis in VSMC calcification.

119 sterone-induced calcification was blunted in VSMC-specific AR-ablated (SM-ARKO) VSMCs compared to WT.

120 Calcium stress induces dramatic changes in VSMC exosome composition and accumulation of phosphatidy

121 between Orai1, TRPC1, and CaV1.2 channels in VSMC, confirming that upon agonist stimulation, vessel c

122 alpha1A/B-AR:CXCR4 heteromeric complexes in VSMC and abolished phenylephrine-induced Ca(2+) fluxes a

123 ectly activated by cAMP isoform 1 (Epac1) in VSMC and to evaluate the potential of Epac1 as therapeut

124 (1) the selective inactivation of ERalpha in VSMC abrogates the neointimal hyperplasia protection ind

125 kdown inhibit alpha1-AR-mediated function in VSMC and that activation of CXCR4 enhances the potency o

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

127 ession of endothelin-1 and genes involved in VSMC contraction, higher systolic blood pressure, and si

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

129 phaSMA staining and fewer PCNA (+) nuclei in VSMC (P < 0.005).

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

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

132 f contractile markers and of endothelin-1 in VSMCs.

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

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

135 The absence of Akt1 in VSMCs during the progression of atherosclerosis results

136 The absence of Akt1 in VSMCs induces features of plaque vulnerability including

137 bodies that mimic heparin-induced changes in VSMCs were employed to support the hypothesis that hepar

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

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

140 Consistently, in VSMCs pretreated with PDGF-BB, calpastatin induction and

141 ular calcium transients and contractility in VSMCs.

142 at LTC4S knockdown inhibited LRC currents in VSMCs.

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

144 inflammation, the direct effects of DSBs in VSMCs seen in atherogenesis are unknown.

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

146 the molecular level, the absence of EPHB4 in VSMCs resulted in compromised signaling from Ca(2+)/calm

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

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

149 Akt1 expression in VSMCs influences early and late stages of atherosclerosi

150 up-regulation of LTC4S protein expression in VSMCs.

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

152 a reduction in KV-mediated currents (IKv) in VSMCs from a high fat diet (HFD) mouse model of type 2 d

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

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

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

156 ghts discrete roles for NOTCH2 and NOTCH3 in VSMCs and connects these roles to specific upstream regu

157 lated ERK1/2 phosphorylation are observed in VSMCs derived from 6-week-old shGRK2 mice prior to the d

158 sing NBS1 or C-terminal deleted NBS1 only in VSMCs, and crossed them with apolipoprotein E(-/-) mice.

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

160 ion of the KV2.1 subunit mRNA and protein in VSMCs/arteries isolated from HFD mice.

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

162 est that direct actions of AT1A receptors in VSMCs are essential for regulation of renal blood flow b

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

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

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

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

167 ment in heparin-induced signaling as seen in VSMCs.

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

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

170 s obligatory for activation of TRPC1 SOCs in VSMCs, and the present study investigates if the classic

171 novel activation mechanism for TRPC1 SOCs in VSMCs, in which store depletion induces formation of TRP

172 ns enhancing Akt1 expression specifically in VSMCs may lessen plaque progression.

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

174 beta-activated transcription factor STAT1 in VSMCs alleviates inflammation of the arterial wall and r

175 ession of proteins that protect telomeres in VSMCs derived from human plaques and normal vessels.

176 ated T cells (NFAT) nuclear translocation in VSMCs.

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

178 ve fibrous cap area in plaques and increases VSMC apoptosis.

179 n, suggesting that proliferation-independent VSMC migration does not make a major contribution to VSM

180 also revealed that the progeny of individual VSMCs contributes to both alpha smooth muscle actin (aSm

181 and the phenotypic changes within individual VSMCs, which underlie vascular disease, remain unresolve

182 ever, the mechanisms underlying MCP1-induced VSMC migration have not been understood.

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

184 Calpains influence VSMC proliferation and collagen synthesis.

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

186 LTC4S and Orai3 knockdown inhibited VSMC migration in vitro with no effect on proliferation.

187 l endometrial vessel formation by inhibiting VSMC proliferation and migration.

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

189 Aorta rings and isolated VSMC obtained from wild type or smooth muscle-selective

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

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

192 and migration responses in shGRK2 knockdown VSMCs when cultured from mice that are either 3 months o

193 sults in less-differentiated forms that lack VSMC markers including macrophage-like cells, and this s

194 -1 is functioning constitutively to maintain VSMCs in their differentiated state and, thereby, inhibi

195 s that PRDM6 plays a key role in maintaining VSMCs in an undifferentiated stage in order to promote t

196 vity was suppressed in neointimal and medial VSMCs from injured vessels at 2 weeks postinjury but was

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

198 EPHB4 to EFNB2 (reverse signaling) modulated VSMC contractility.

199 ter occlusion by dedifferentiated neointimal VSMC.

200 s were up-regulated in medial and neointimal VSMCs after vascular injury and that Orai3 knockdown inh

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

202 and morphology; however, the consequences of VSMC senescence or the mechanisms underlying VSMC senesc

203 (MLC) 2 phosphorylation, and contraction of VSMC upon alpha1-AR activation.

204 therosclerosis, the specific contribution of VSMC Akt1 remains poorly characterized.

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

206 s and cultured from plaques show evidence of VSMC senescence and DNA damage.

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

208 To trigger neointimal hyperplasia of VSMC, we used a mouse model of femoral arterial injury.

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

210 inhibited the proliferation and migration of VSMC and EC.

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

212 te that direct pharmacological modulation of VSMC Kv7 channel activity can influence blood vessel con

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

214 elling evidence that a full understanding of VSMC behavior in atherosclerosis is critical to identify

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

216 Microarray analysis of VSMCs identified several MPA- and ETO-altered transcript

217 ction, leading to increased calcification of VSMCs in response to calcifying conditions.

218 augmented the osteogenic differentiation of VSMCs by phosphorylating SMAD1/5/8 via direct interactio

219 o activation of Notch and differentiation of VSMCs.

220 en the pro- and anti-inflammatory effects of VSMCs and their extracellular matrix versus the strength

221 der the inflammatory and immune functions of VSMCs and how they may lead to medial immunoprivilege or

222 more intense leukocytic infiltrates, loss of VSMCs, and destruction of the extracellular matrix archi

223 uppressed the proliferation and migration of VSMCs and collagen synthesis, and reduced expression of

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

225 ching, the evidence for different origins of VSMCs, and the role of individual processes that VSMCs u

226 e modulation of the contractile phenotype of VSMCs via transforming growth factor-beta1-signaling inh

227 eas that there is a homogenous population of VSMCs within the plaque, that can be identified separate

228 ed beta-catenin signalling, proliferation of VSMCs and pathological arterial remodelling.

229 osclerosis is that aberrant proliferation of VSMCs promotes plaque formation, but that VSMCs in advan

230 ivation of beta-catenin and proliferation of VSMCs were observed after blood-pressure elevation, whic

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

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

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

234 review the effect of embryological origin on VSMC behavior in atherosclerosis, the role, regulation a

235 PDGF receptor beta (PDGFRbeta) activation on VSMCs have not been studied in the context of atheroscle

236 We conclude that plaque VSMC senescence in atherosclerosis is associated with lo

237 Plaque VSMCs showed reduced expression and telomere binding of

238 Human atherosclerotic plaque VSMCs show increased DNA damage, including DSBs and DNA

239 Human atherosclerotic plaque VSMCs showed increased expression of multiple DNA damage

240 stress-induced DSBs were increased in plaque VSMCs, but DSB repair was maintained.

241 In particular, plaque VSMCs show shortening of telomeres, which can directly i

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

243 cessary and sufficient to inhibit postinjury VSMC proliferation.

244 sphingomyelin phosphodiesterase 3 prevented VSMC calcification.

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

246 dult global Akt2KO mice triggers progressive VSMC apoptosis.

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

248 S and Orai3 altered Akt signaling to promote VSMC migration and neointima formation.

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

250 hat Epac1 plays important roles in promoting VSMC proliferation and phenotypic switch in response to

251 on retarding VSMC apoptosis whilst promoting VSMC proliferation.

252 ta show that NOTCH3, but not NOTCH2 protects VSMCs from apoptosis and apoptosis mediators degrade NOT

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

254 ooth muscle cell lymphotoxin beta receptors (VSMC-LTbetaRs) protected against atherosclerosis by main

255 Both MPA and ETO reduce VSMC proliferation and migration (P < 0.001).

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

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

258 4-to-EFNB reverse signaling, which regulated VSMC contractility, based on siRNA gene knockdown studie

259 tification of signalling pathways regulating VSMC exosome secretion, including activation of SMPD3 an

260 on and, thereby, Notch signalling regulating VSMC maintenance.

261 ession in Akt-deficient endothelium restores VSMC coverage.

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

263 ly, endothelial Akt deletion induces retinal VSMC loss and basement membrane deterioration resulting

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

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

266 ls (particularly macrophages) using standard VSMC and macrophage immunohistochemical markers.

267 ine production and enhanced IGF-I-stimulated VSMC proliferation.

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

269 tion of exosomes is a feature of 'synthetic' VSMCs and that exosomes are novel players in vascular re

270 rta T cell homeostasis during aging and that VSMC-LTbetaRs participate in atherosclerosis protection

271 prising the plaque, and the causal role that VSMC senescence plays in atherogenesis.

272 Comparative proteomics showed that VSMC-derived exosomes were compositionally similar to ex

273 Recent data showing that VSMC exosomes are loaded with proteins and miRNA regulat

274 etic lineage tracing studies have shown that VSMC phenotypic switching results in less-differentiated

275 of VSMCs promotes plaque formation, but that VSMCs in advanced plaques are entirely beneficial, for e

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

277 s, and the role of individual processes that VSMCs undergo in atherosclerosis in regard to plaque for

278 distinguish between the endothelial- and the VSMC-specific actions of E2.

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

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

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

282 ibited an increase in SIK1 expression in the VSMCs layer of the aorta, whereas the sik1(-/-) mice exh

283 cture, cellularity, and size of ATLOs though VSMC-LTbetaRs did not affect secondary lymphoid organs:

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

285 ration does not make a major contribution to VSMC accumulation in vascular disease.

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

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

288 cing ascorbate availability in AngII-treated VSMC.

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

290 rated the calcification in phosphate-treated VSMCs and aortic rings and in vitamin D3-treated mice.

291 ased expression of PDK4 in phosphate-treated VSMCs induced mitochondrial dysfunction followed by apop

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

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

294 VSMC senescence or the mechanisms underlying VSMC senescence in atherosclerosis are mostly unknown.

295 upregulated in balloon-injured vs. uninjured VSMCs.

296 interacts with Orai1 and TRPC1 in untreated VSMC.

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

298 s, and not just in advanced lesions, whereas VSMC apoptosis, cell senescence, and VSMC-derived macrop

299 and necrotic core formation in vivo, whereas VSMC-specific TRF2 increased the relative fibrous cap an

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