ライフサイエンスコーパス: vascular smooth muscle cell

1 ecialized processes (e.g. the contraction of vascular smooth muscle cells).

2 osphorylated Thr-172 in rat aortic and human vascular smooth muscle cells.

3 thelial colony-forming cells, pericytes, and vascular smooth muscle cells.

4 rease Adamts-1 expression in endothelial and vascular smooth muscle cells.

5 heterodimeric complexes in both HEK 293 and vascular smooth muscle cells.

6 cardiac fibroblasts, endothelial cells, and vascular smooth muscle cells.

7 own, promoted calcification of primary mouse vascular smooth muscle cells.

8 place astrocytic endfeet from endothelial or vascular smooth muscle cells.

9 ATPase expression is specific to contractile vascular smooth muscle cells.

10 7.5 heteromers are endogenously expressed in vascular smooth muscle cells.

11 e C (PKC) in response to vasoconstrictors in vascular smooth muscle cells.

12 e in regulating expression of other genes in vascular smooth muscle cells.

13 s of protein secretion by lipid-loaded human vascular smooth muscle cells.

14 4/7.5 channels exogenously expressed in A7r5 vascular smooth muscle cells.

15 n via activation of KATP channels located on vascular smooth muscle cells.

16 ding with modified proteoglycans secreted by vascular smooth muscle cells.

17 ility caused by mitochondrial dysfunction in vascular smooth muscle cells.

18 telet-derived growth factor receptor-beta on vascular smooth muscle cells.

19 myoblasts, adipocytes, ligament, tendon, or vascular smooth muscle cells.

20 lation of Ca(2+) handling and sensitivity in vascular smooth muscle cells.

21 ts that significantly alter the phenotype of vascular smooth muscle cells.

22 ninase controlled the production of 3-HAA in vascular smooth muscle cells.

23 by ischemia/reperfusion do not involve BK in vascular smooth muscle cells.

24 tion and integration of endothelial cell and vascular smooth muscle cells.

25 , in endothelial cells (ECs), HL1, H9C2, and vascular smooth muscle cells.

26 t ET-1 diminishes the dilatation capacity of vascular smooth muscle cells.

27 ng cardiac myocytes, cardiac fibroblasts and vascular smooth muscle cells.

28 mposed of hyperproliferative endothelial and vascular smooth-muscle cells.

29 an epithelial kidney cells (HEK 293) and rat vascular smooth muscle cells (A7r5), we correlate cell r

30 stinct from TRPC6 or KCNQ3, 4, or 5 to enact vascular smooth muscle cell activation and elevated vasc

31 In cultured human aortic vascular smooth muscle cells, AKT2 inhibited the express

32 However, both vascular smooth muscle cell and endothelial cell mPGES-1

33 Vascular smooth muscle cell and endothelial cell mPGES-1

34 Molecular mechanisms were probed in vessels/vascular smooth muscle cells and adipose tissue/adipocyt

35 ion in aortic tissues were reduced while the vascular smooth muscle cells and collagen increased in p

36 n the arterial adventitia are progenitors of vascular smooth muscle cells and contribute to neointima

37 opulations of bronchial smooth muscle cells, vascular smooth muscle cells and desmin(+) fibroblasts b

38 Deletion of COX-2 in vascular smooth muscle cells and endothelial cells coinc

39 esent study, selective depletion of COX-2 in vascular smooth muscle cells and endothelial cells depre

40 ts of enzyme depletion in macrophages versus vascular smooth muscle cells and endothelial cells.

41 ere used to identify the TMEM184A protein in vascular smooth muscle cells and endothelial cells.

42 scular maturation because of a deficiency of vascular smooth muscle cells and impaired myocardial tra

43 (Erk) signaling in Nf1(+/-) macrophages and vascular smooth muscle cells and in vivo evidence of Erk

44 KV1.5 is the major KV1 channel expressed in vascular smooth muscle cells and is abundantly localized

45 In vascular smooth muscle cells and macrophages, NLS peptid

46 e-rRNA processing and ribosome biogenesis in vascular smooth muscle cells and macrophages.

47 ed that Tbx18 is expressed in renal capsule, vascular smooth muscle cells and pericytes and glomerula

48 Mural cells (MCs) consisting of vascular smooth muscle cells and pericytes cover the end

49 Mural cells (vascular smooth muscle cells and pericytes) play an esse

50 In vascular smooth muscle cells and renal tubular epithelia

51 lar labile zinc in hypoxia-exposed pulmonary vascular smooth muscle cells and their proliferation in

52 Nox2 transgenic ECs (but not vascular smooth muscle cells) and aortas had greater sec

53 es such as endothelial and epithelial cells, vascular smooth muscle cells, and certain leukocyte subs

54 with impaired proliferation and apoptosis of vascular smooth muscle cells, and hyperlipidemia.

55 tes, cardiac fibroblasts, endothelial cells, vascular smooth muscle cells, and macrophages.

56 of activating FcgammaR in endothelial cells, vascular smooth muscle cells, and monocytes/macrophages

57 including renal epithelial, intestinal, and vascular smooth muscle cells, and neurons in trigeminal

58 Astrocytes, vascular smooth muscle cells, and pericytes are importan

59 ensitive Kv channel current in patch-clamped vascular smooth muscle cells, and similar concentrations

60 VEGF-C, expressed mainly in vascular smooth muscle cells, and VEGFR3 in lymphatic en

61 Accordingly, Lmna(G609G/+) vascular smooth muscle cells are defective for the produ

62 Finally, Alk1 levels in vascular smooth muscle cells are not directly upregulate

63 ck phospholamban phosphorylation and exhibit vascular smooth muscle cell arrest in the synthetic stat

64 We have identified pulmonary vascular smooth muscle cells as the source responsible f

65 Here, we investigated a role for lncRNAs in vascular smooth muscle cell biology and pathology.

66 In cultured vascular smooth muscle cells, both the NO donor S-nitros

67 ptake and steady-state pHi persisted only in vascular smooth muscle cells but not endothelial cells.

68 only of the cardiomyocytes, endothelium, and vascular smooth muscle cells, but also of interstitial c

69 ts in a modest reduction of proliferation in vascular smooth muscle cells, but given low proliferativ

70 empt to specifically reduce proliferation of vascular smooth muscle cells, but not endothelial cells.

71 tween KLF6 and specificity protein 1, and in vascular smooth muscle cells by an EC-vascular smooth mu

72 mice, ShcA was deleted in cardiomyocytes and vascular smooth muscle cells by crossing ShcA flox mice

73 ain key to the initiation and progression of vascular smooth muscle cell calcification in CKD.

74 subsequently blocked Runx2 transactivity and vascular smooth muscle cell calcification.

75 AKT phosphorylation, which in turn enhanced vascular smooth muscle cell calcification.

76 periments revealed that the origin of aortic vascular smooth muscle cells can be traced back to proge

77 oltage-gated Ca(2+) channels in the adjacent vascular smooth muscle cells, causing vasoconstriction.

78 Cs induced greater Erk1/2 phosphorylation in vascular smooth muscle cells compared with wild-type con

79 th, collagen composition, and macrophage and vascular smooth muscle cell content were unchanged.

80 ulum Ca2+ -ATPase synergistically induce the vascular smooth muscle cell contractile phenotype.

81 on in an angioplasty rat model by preventing vascular smooth muscle cell contractile to synthetic phe

82 hatase partner polypeptides in regulation of vascular smooth-muscle cell contractility.

83 en VR-PAH and VN-PAH, we found enrichment in vascular smooth muscle cell contraction pathways and gre

84 latelet-derived growth factor B (PDGF-BB) in vascular smooth muscle cells, contributing to vessel mat

85 g atomic force microscopy, changes in single vascular smooth muscle cell cortical actin are observed

86 OS-independent mechanism, possibly through a vascular smooth muscle cell-dependent mechanism, and met

87 ammation (PROCR, rs867186 (p.Ser219Gly)) and vascular smooth muscle cell differentiation (LMOD1, rs28

88 ibitor of metalloproteinase-3 expression and vascular smooth muscle cell elastin production, both imp

89 e, we generated mice deficient in mPGES-1 in vascular smooth muscle cells, endothelial cells, and mye

90 own of CypA in ECs abolished the increase in vascular smooth muscle cell Erk1/2 phosphorylation confe

91 dditional thrombin receptor, PAR-4, in human vascular smooth muscle cells exposed to high glucose and

92 binding, real-time imaging was performed in vascular smooth muscle cells expressing a FRET-biosensor

93 pression was altered in human saphenous vein vascular smooth muscle cells following stimulation with

94 deletion of NFATc1 prevented the capacity of vascular smooth muscle cells for MCP-1-induced activatio

95 Phenotypic switching of vascular smooth muscle cells from a contractile to a syn

96 Phenotypic modulation or switching of vascular smooth muscle cells from a contractile/quiescen

97 ) currents were markedly reduced in isolated vascular smooth muscle cells from CAD arterioles, althou

98 Vascular smooth muscle cells from chr4(Delta70kb/Delta70

99 ive aortic calcification, and primary aortic vascular smooth muscle cells from these progeroid animal

100 In vascular smooth muscle cells, GPR75-20-HETE pairing is a

101 ion of receptor-mediated MAPK activation and vascular smooth muscle cell growth were differentially o

102 HODS AND Oxidant challenge studies show that vascular smooth muscle cells have an intrinsic ability t

103 tion of sGC led to reduced migration only in vascular smooth muscle cells homozygous for the nonrisk

104 rn increases the expression of LRP1 in human vascular smooth muscle cells (hVSMCs).

105 lated by a molecular actin switch within the vascular smooth muscle cell in the wall of the vein.

106 rial membrane potential, is downregulated in vascular smooth muscle cells in culture exposed to monot

107 ition both in atherosclerotic plaques and in vascular smooth muscle cells in culture.

108 ctive of this study was to determine whether vascular smooth muscle cells in cultured microvascular n

109 found DbpA protein expression restricted to vascular smooth muscle cells in healthy human kidney tis

110 factor Tbx18 selectively marks pericytes and vascular smooth muscle cells in multiple organs of adult

111 face for fibroblasts, endothelial cells, and vascular smooth muscle cells in the absence of serum.

112 flow after label-free optical activation of vascular smooth muscle cells in the intact brain.

113 and accumulation of proliferating synthetic vascular smooth muscle cells in the lumen of small arter

114 se to cardiomyocytes, endothelial cells, and vascular smooth muscle cells in vitro at a clonal level.

115 Nitrovasodilators relax vascular smooth-muscle cells in part by modulating the i

116 n of endogenous extracellular ATP, acting on vascular smooth muscle cells, in controlling vascular to

117 Osteogenic differentiation of primary human vascular smooth muscle cells increased DRP1 expression.

118 ehind this assay is the magnetic printing of vascular smooth muscle cells into 3D rings that function

119 are involved in the transdifferentiation of vascular smooth muscle cells into osteoblast-like cells,

120 r that the actin cytoskeleton of contractile vascular smooth muscle cells is a dynamic structure reac

121 This defect in progerin-expressing vascular smooth muscle cells is associated with increase

122 We show that ZIP12 expression in pulmonary vascular smooth muscle cells is hypoxia dependent and th

123 types; whereas targeting cardiomyocytes and vascular smooth muscle cells is required for LT-induced

124 f mural cells, which encompass pericytes and vascular smooth muscle cells, is a hallmark of CADASIL a

125 In vascular smooth muscle cells, large-conductance Ca(2+)-

126 e Hb into interstitial spaces, including the vascular smooth muscle cell layer of rat and pig coronar

127 ular studies revealed that loss of YY1AP1 in vascular smooth muscle cells leads to cell cycle arrest

128 At the single vascular smooth muscle cell level, atomic force microsco

129 Meanwhile, vascular smooth muscle cell lymphotoxin beta receptors (

130 x18-CreERT2 line revealed that pericytes and vascular smooth muscle cells maintained their identity i

131 In vivo, vascular smooth muscle cell/mesangial cell-specific over

132 pe and cellular phenotypes was analyzed with vascular smooth muscle cell migration assays and platele

133 tion of human breast cancer and mouse aortic vascular smooth muscle cell migration by ATX.

134 Using this system, we have tracked vascular smooth muscle cell migration in vitro and quant

135 have implicated ADAMTS7 in the regulation of vascular smooth muscle cell migration, but a role for an

136 Cytochrome P450 (CYP) 1B1 is implicated in vascular smooth muscle cell migration, proliferation, an

137 iated reactive oxygen species production and vascular smooth muscle cell migration.

138 bly, reactive oxygen species production, and vascular smooth muscle cell migration.

139 ogical inhibition of IKK2 markedly decreased vascular smooth muscle cell MLC phosphorylation, suggest

140 by the AT1 receptor using HEK293 and primary vascular smooth muscle cell models.

141 1.2) are the primary Ca(2+) entry pathway in vascular smooth muscle cells (myocytes).

142 ression to allow NCCs to develop into mature vascular smooth muscle cells of cerebral vessels.

143 strongly upregulated in endothelial (EC) and vascular smooth muscle cells of mouse femoral arteries a

144 d promotes the expression of KV1 channels in vascular smooth muscle cells of the cerebral (cVSMCs) ci

145 stimuli or cell-specific calcium uncaging in vascular smooth muscle cells or astrocytes.

146 and in vascular smooth muscle cells by an EC-vascular smooth muscle cell paracrine communication duri

147 ic shift to glycolysis of pulmonary arterial vascular smooth muscle cells (PAVSMCs) are key pathophys

148 and impaired apoptosis of pulmonary arterial vascular smooth muscle cells (PAVSMCs) are key pathophys

149 subcellular localization studies in cultured vascular smooth muscle cells placed ADAMTS7 at the cytop

150 -deficient macrophages less potently induced vascular smooth muscle cell proliferation and migration

151 to protect against endothelial dysfunction, vascular smooth muscle cell proliferation and migration,

152 These results identify SMILR as a driver of vascular smooth muscle cell proliferation and suggest th

153 in have been documented to include decreased vascular smooth muscle cell proliferation following decr

154 induced inflammation, lipid accumulation and vascular smooth muscle cell proliferation.

155 (p16 and p14) and CDKN2B (p15) and increased vascular smooth muscle cell proliferation.

156 e on SLC4A7 expression and pHi regulation in vascular smooth muscle cells provides an insight into th

157 active factors that preferentially influence vascular smooth muscle cells rather than endothelial cel

158 nary vasculogenesis associated with impaired vascular smooth muscle cell recruitment and reduced inva

159 knockdown and pharmacological inhibition in vascular smooth muscle cells reveal that cytochrome b5 r

160 ncubation with CypA augmented Ang II-induced vascular smooth muscle cell ROS production.

161 ied physiological sGC heme iron reductase in vascular smooth muscle cells, serving as a critical regu

162 er time points, and primary Adamts7 knockout vascular smooth muscle cells showed reduced migration in

163 In vitro studies revealed that in mouse vascular smooth muscle cells, siRNA knockdown of GRIP1,

164 Vascular smooth muscle cell (SMC) composes the majority

165 ression is associated with marked changes in vascular smooth muscle cell (SMC) phenotype and function

166 on mitochondrial respiration that regulates vascular smooth muscle cell (SMC) proliferation after ar

167 Vascular smooth muscle cell (SMC) proliferation and endo

168 Vascular smooth muscle cells (SMCs) and endothelial cell

169 Vascular smooth muscle cells (SMCs) arise from diverse d

170 t neural crest (NC) only differentiates into vascular smooth muscle cells (SMCs) around those aortic

171 Vascular smooth muscle cells (SMCs) can resist and repai

172 Previous studies revealed loss of vascular smooth muscle cells (SMCs) in the media of larg

173 ia characterized by abnormal accumulation of vascular smooth muscle cells (SMCs) is a hallmark of occ

174 ts in proliferation and dedifferentiation of vascular smooth muscle cells (SMCs) is an important cont

175 and promoted cellular contraction in primary vascular smooth muscle cells (SMCs) that were isolated f

176 Vascular smooth muscle cells (SMCs), a major structural

177 d K(+) (BK) channel, expressed abundantly in vascular smooth muscle cells (SMCs), is a key determinan

178 In non-placental vascular smooth muscle cells (SMCs), K(+) channels regul

179 RXR heterodimers have beneficial effects in vascular smooth muscle cells (SMCs).

180 luence of ET-1 on the dilatation capacity of vascular smooth muscle cells (sodium nitroprusside; SNP)

181 Vascular smooth muscle cell-specific overexpression of R

182 2a) and alterations in Ca(2+) homeostasis in vascular smooth muscle cells that stimulate proliferatio

183 2 in endothelial cells and angiopoietin-1 in vascular smooth muscle cells through nuclear factor-kapp

184 Our investigation concludes that vascular smooth muscle cell TNF augments resistance arte

185 or sphingosine kinase 1, we demonstrate that vascular smooth muscle cell TNF drives the elevation of

186 including leukocytes, endothelial cells, and vascular smooth muscle cells, toward diverse attractants

187 Our results show that vascular smooth muscle cells undergo durotaxis on mechan

188 tic arteries or in the O-GlcNAcase knockdown vascular smooth muscle cell upregulated expression of th

189 ar stiffness in freshly isolated contractile vascular smooth muscle cells using magnetic microneedle

190 orticoid receptor (GR) in cardiomyocytes and vascular smooth muscle cells using smooth muscle protein

191 halofuginone produced greater inhibition of vascular smooth muscle cell versus endothelial cell prol

192 rticularly impacted on the earliest stage of vascular smooth muscle cell vessel coverage and subseque

193 id was present, stimulation of astrocytes or vascular smooth muscle cells via ex vivo Ca(2+) uncaging

194 Vascular smooth muscle cell (VSMC) accumulation is a hal

195 Vascular smooth muscle cell (VSMC) activation in respons

196 We hypothesize that LAPCs impair vascular smooth muscle cell (VSMC) and pericyte prolifer

197 Vascular smooth muscle cell (VSMC) apoptosis occurs duri

198 Vascular smooth muscle cell (VSMC) apoptosis precipitate

199 ealed increased phosphate (Pi)-induced mouse vascular smooth muscle cell (VSMC) calcification followi

200 Changes in the vascular smooth muscle cell (VSMC) contractile phenotype

201 Hyperglycemia leads to vascular smooth muscle cell (VSMC) dedifferentiation and

202 active agonists to induce dynamic changes in vascular smooth muscle cell (VSMC) elasticity and adhesi

203 rins have been shown to be key regulators of vascular smooth muscle cell (vSMC) function in vitro.

204 9 expression, and thinning of the periportal vascular smooth muscle cell (VSMC) layer, which are appa

205 alpha-subunits, are important regulators of vascular smooth muscle cell (VSMC) membrane voltage.

206 resulting in pathophysiologic stimulation of vascular smooth muscle cell (VSMC) migration and prolife

207 cyte chemotactic protein 1 (MCP1) stimulates vascular smooth muscle cell (VSMC) migration in vascular

208 Our prior studies on adult mice deficient in vascular smooth muscle cell (vSMC) Notch signaling revea

209 ne the actions of D-series resolvin (RvD) on vascular smooth muscle cell (VSMC) phenotype and vascula

210 Notch signaling is a key regulator of vascular smooth muscle cell (VSMC) phenotypes, including

211 own of the mechanisms driving age-associated vascular smooth muscle cell (VSMC) phenotypic change.

212 Vascular smooth muscle cell (VSMC) phenotypic conversion

213 vascular percutaneous intervention, in which vascular smooth muscle cell (VSMC) proliferation and act

214 ce recapitulated this phenotype of increased vascular smooth muscle cell (VSMC) proliferation and pla

215 lecule indirubin-3'-monoxime (I3MO) prevents vascular smooth muscle cell (VSMC) proliferation by sele

216 Although vascular smooth muscle cell (VSMC) proliferation is impl

217 Lesional myeloid cells were depleted and vascular smooth muscle cell (VSMC) proliferation, as ref

218 ptional mechanisms by which KCa3.1 regulates vascular smooth muscle cell (VSMC) proliferation.

219 ow GTN concentrations (</=1 mum) in cultured vascular smooth muscle cells (VSMC) expressing an ALDH2

220 0), is a central regulator of macrophage and vascular smooth muscle cells (VSMC) function.

221 ncodes a nuclear protein that is specific to vascular smooth muscle cells (VSMC), has histone methyl

222 h CXCR4 on the cell surface of rat and human vascular smooth muscle cells (VSMC).

223 rnative splice variants in the cell cycle of vascular smooth muscle cells (VSMC).

224 racellular calcium ([Ca(2+)]cyt) dynamics in vascular smooth muscle cells (VSMC).

225 tive hormone, as a potent HIF-1 activator in vascular smooth muscle cells (VSMC).

226 TCC) are the main route for calcium entry in vascular smooth muscle cells (VSMC).

227 tionally in myeloid cells (Mac-mPGES-1-KOs), vascular smooth muscle cells (VSMC-mPGES-1-KOs), or endo

228 ro analyses of mesenchymal stem cell-derived vascular smooth muscle cells (VSMCs) and chondrocytes pr

229 ns do not discriminate between proliferating vascular smooth muscle cells (VSMCs) and endothelial cel

230 x phosphorylation is increased in calcifying vascular smooth muscle cells (VSMCs) and in calcified ve

231 Hyperplasia of vascular smooth muscle cells (VSMCs) and infiltration of

232 Perivascular cells, including vascular smooth muscle cells (vSMCs) and pericytes, are

233 mesangial cells have a distinct origin from vascular smooth muscle cells (VSMCs) and the pathways th

234 ant cellular constituent of the vessel wall, vascular smooth muscle cells (VSMCs) and their functions

235 predominantly expressed in the cytoplasm of vascular smooth muscle cells (VSMCs) and tubular epithel

236 e networks induced by cell-cell contact with vascular smooth muscle cells (vSMCs) and vSMC-associated

237 Ca2+-activated chloride currents (CaCCs) in vascular smooth muscle cells (VSMCs) are candidates for

238 Vascular smooth muscle cells (vSMCs) are key in the regu

239 ut the molecular mechanisms of its action on vascular smooth muscle cells (VSMCs) are not fully under

240 annels (SOCs) in proliferative and migratory vascular smooth muscle cells (VSMCs) are quite intricate

241 Vascular smooth muscle cells (VSMCs) associate with larg

242 atory for native TRPC1 channel activation in vascular smooth muscle cells (VSMCs) but how PKC and PI(

243 artery and differentiation of NC cells into vascular smooth muscle cells (VSMCs) by regulating Notch

244 ile properties or changes in the identity of vascular smooth muscle cells (vSMCs) can result in struc

245 ound that elimination of AT1A receptors from vascular smooth muscle cells (VSMCs) caused a modest (ap

246 ted K(+) (KV) channels are key regulators of vascular smooth muscle cells (VSMCs) contractility and a

247 Activation of Na(+),HCO3(-) cotransport in vascular smooth muscle cells (VSMCs) contributes to intr

248 n saphenous vein endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) converted 17-HDHA t

249 Vascular smooth muscle cells (VSMCs) cultured from shGRK

250 The role of Drosha in vascular smooth muscle cells (VSMCs) has not been well a

251 The historical view of vascular smooth muscle cells (VSMCs) in atherosclerosis

252 Vascular smooth muscle cells (VSMCs) in human atheroscle

253 Proliferation of vascular smooth muscle cells (VSMCs) in response to vasc

254 ens junctions (AJ) along the borders between vascular smooth muscle cells (VSMCs) in the pressurized

255 Studies with vascular smooth muscle cells (VSMCs) indicate a role for

256 uating transcriptomic responses to Ang II in vascular smooth muscle cells (VSMCs) is important to und

257 This work presents evidence that EPHB4 on vascular smooth muscle cells (VSMCs) is involved in bloo

258 The importance of TSPANs in vascular smooth muscle cells (VSMCs) is unexplored.

259 Lower SIK1 activity in vascular smooth muscle cells (VSMCs) leads to decreased

260 Specific ablation of Plk1 in vascular smooth muscle cells (VSMCs) led to reduced arte

261 Vascular smooth muscle cells (VSMCs) of the G/G genotype

262 Proliferation and migration of vascular smooth muscle cells (VSMCs) or endothelial cell

263 MicroRNAs are key regulators of vascular smooth muscle cells (VSMCs) phenotypic switch,

264 Proinflammatory chemokines released by vascular smooth muscle cells (VSMCs) play a critical rol

265 terventional state, we exposed primary human vascular smooth muscle cells (vSMCs) pretreated with ure

266 or sustained interactions with pericytes and vascular smooth muscle cells (VSMCs) regulating vascular

267 ated lncRNAs were further evaluated in human vascular smooth muscle cells (VSMCs) stimulated with ang

268 Vascular smooth muscle cells (VSMCs) undergo phenotypic

269 Calcification was induced in vascular smooth muscle cells (VSMCs) with therapeutic le

270 etabolite that induces tissue factor (TF) in vascular smooth muscle cells (vSMCs), although the preci

271 , and the subsequent accumulation of SFAs in vascular smooth muscle cells (VSMCs), are characteristic

272 In arterial vascular smooth muscle cells (VSMCs), beta1-subunits are

273 Matrix vesicles (MVs), secreted by vascular smooth muscle cells (VSMCs), form the first nid

274 the adult vasculature, and in particular in vascular smooth muscle cells (VSMCs), is currently unkno

275 ABSTRACT: In vascular smooth muscle cells (VSMCs), stimulation of can

276 In vascular smooth muscle cells (VSMCs), stimulation of can

277 In vascular smooth muscle cells (VSMCs), stimulation of SOC

278 We recently showed, in primary vascular smooth muscle cells (VSMCs), that the platelet-

279 Surprisingly, vascular smooth muscle cells (VSMCs), the predominant an

280 evidence indicate that it may also stimulate vascular smooth muscle cells (VSMCs), thereby contributi

281 Pericytes and vascular smooth muscle cells (VSMCs), which are recruite

282 ient receptor potential (TRPC) 1 proteins in vascular smooth muscle cells (VSMCs), which contribute t

283 with Smad2 mRNA overexpression in aneurysmal vascular smooth muscle cells (VSMCs), which is dependent

284 sel inflammation after release from necrotic vascular smooth muscle cells (VSMCs).

285 ls encoded by Orai1/Orai3 heteromultimers in vascular smooth muscle cells (VSMCs).

286 (PDGF) is a mitogen and chemoattractant for vascular smooth muscle cells (VSMCs).

287 ll upon osteo/chondrocytic transformation of vascular smooth muscle cells (VSMCs).

288 is the major cell-cell adhesion molecule in vascular smooth muscle cells (VSMCs).

289 ting and pro-inflammatory gene expression in vascular smooth muscle cells (VSMCs).

290 hat comprise the plaque, but particularly in vascular smooth muscle cells (VSMCs).

291 (8.6 +/- 1.3% of vessels with recruitment of vascular smooth muscle cells; VSMCs) in the presence of

292 fferentiation of mesodermal derivatives into vascular smooth muscle cells was not defective.

293 In primary vascular smooth muscle cells, we find that the arrestin

294 subtype; its location on endothelial (EC) or vascular smooth muscle cells; whether ADO acts on KATP c

295 rb-Cre expressing mural cells (pericytes and vascular smooth muscle cells), which wrap around the end

296 crest proliferation and differentiation into vascular smooth muscle cells, while proliferation of pha

297 ed that suppression of TGF-beta signaling in vascular smooth muscle cells will ameliorate aortic dise

298 ings and membrane hyperpolarization in human vascular smooth muscle cells, with potency similar or su

299 The contractility of vascular smooth muscle cells within the walls of arterie

300 ession, thus potentiating AngII signaling in vascular smooth muscle cells without an increase in the

301 ve KCNQ3, 4, and 5 channels are expressed in vascular smooth muscle cells, XE991-sensitive K+ current