ライフサイエンスコーパス: smooth muscle cell

1 stage, which contained both macrophages and smooth muscle cells.

2 disrupts TGF-beta-driven differentiation of smooth muscle cells.

3 ignificantly alter the phenotype of vascular smooth muscle cells.

4 ntrolled the production of 3-HAA in vascular smooth muscle cells.

5 l to map the fate of NG2(+)CD146(+) immature smooth muscle cells.

6 of intraluminal pressure in cerebral artery smooth muscle cells.

7 naling pathway in human kidney podocytes and smooth muscle cells.

8 diomyocytes, endothelial cells, and arterial smooth muscle cells.

9 ia/reperfusion do not involve BK in vascular smooth muscle cells.

10 n plaque macrophages, endothelial cells, and smooth muscle cells.

11 function of other cell types such as airway smooth muscle cells.

12 ry human T cell subtypes and coronary artery smooth muscle cells.

13 alization and extensive population by mature smooth muscle cells.

14 cells including epithelial, endothelial and smooth muscle cells.

15 integration of endothelial cell and vascular smooth muscle cells.

16 acylglycerol-stimulated rat pulmonary artery smooth muscle cells.

17 thelial cells (ECs), HL1, H9C2, and vascular smooth muscle cells.

18 crophage-like cells can also be derived from smooth muscle cells.

19 se (ROCK) increase in penile endothelial and smooth muscle cells.

20 minishes the dilatation capacity of vascular smooth muscle cells.

21 secondarily stimulated collagen synthesis in smooth muscle cells.

22 eage, but not endothelial, immune/myeloid or smooth muscle cells.

23 c myocytes, cardiac fibroblasts and vascular smooth muscle cells.

24 natively expressed in rat mesenteric artery smooth muscle cells.

25 mmation, and proliferation in fibroblast and smooth muscle cells.

26 y 45-fold higher in isolated cerebral artery smooth muscle cells.

27 ression was found in human and murine airway smooth muscle cells.

28 xylase domain activity were increased in PAH smooth muscle cells.

29 and an enhanced ability to differentiate to smooth muscle cells.

30 rentially expressed in vascular and visceral smooth muscle cells.

31 ein secretion by lipid-loaded human vascular smooth muscle cells.

32 crostructure including elastin, collagen and smooth muscle cells.

33 y artery endothelial cells, pulmonary artery smooth muscle cell, adventitial fibroblasts, and pulmona

34 apurinic/apyrimidinic endonuclease I protect smooth muscle cells against oxidant-induced cell death.

35 articles were safe to rat pulmonary arterial smooth muscle cell and to the lungs, as evidenced by the

36 r mechanisms were probed in vessels/vascular smooth muscle cells and adipose tissue/adipocytes and fo

37 ts due to this ACTA2 mutation in both aortic smooth muscle cells and adventitial fibroblasts may cont

38 rtic tissues were reduced while the vascular smooth muscle cells and collagen increased in plaques fr

39 II (30 nm) also increased TRPM4 currents in smooth muscle cells and constricted cerebral arteries fr

40 hritis, IL-26 is expressed by renal arterial smooth muscle cells and deposits in necrotizing lesions.

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

42 ity are strongly reduced in pulmonary artery smooth muscle cells and endothelial cells.

43 nternalized by endothelial cells relative to smooth muscle cells and fibroblasts, demonstrating a dir

44 h hyperpolarization to promote relaxation of smooth muscle cells and increase tissue blood flow.

45 the major KV1 channel expressed in vascular smooth muscle cells and is abundantly localized on the p

46 ocessing and ribosome biogenesis in vascular smooth muscle cells and macrophages.

47 lymph nodes originating from differentiated smooth muscle cells and myofibroblasts.

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

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

50 hly isolated (not cultured) pulmonary artery smooth muscle cells and pulmonary artery endothelial cel

51 ntributes to dysfunction of pulmonary artery smooth muscle cells and pulmonary artery endothelial cel

52 r consists of a mesenchymal wall composed of smooth muscle cells and surrounding fibrocytes of the tu

53 profiling of perturbed human coronary artery smooth muscle cells and tissues to begin to identify cau

54 erformed on two cell lines: A7r5 (rat aortic smooth muscle cells) and SH-SY5Y (human neuroblastoma ce

55 differentiated cells, including adipocytes, smooth muscle cells, and endothelial cells (EC).

56 luripotent stem cell-derived cardiomyocytes, smooth muscle cells, and endothelial cells (in a 2:1:1 r

57 otency to differentiate into cardiomyocytes, smooth muscle cells, and endothelial cells in vitro.

58 hen seeded the scaffold with cardiomyocytes, smooth muscle cells, and endothelial cells that had been

59 adjacent epithelial cells, stromal cells and smooth muscle cells, and soluble and cell-associated gro

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

61 Pericytes and smooth muscle cells are integral components of the brain

62 mited wire-induced injury response, existing smooth muscle cells are the primary contributors to neoi

63 NF-kappaB-dependent allergen-induced airway smooth muscle cell (ASMC) hyperproliferation and cyclin

64 Activated CD4 T cells connect to airway smooth muscle cells (ASMCs) in vitro via lymphocyte-deri

65 Airway smooth muscle cells (ASMCs) were isolated from smooth mu

66 portant in regulating healthy primary airway smooth muscle cells (ASMCs), whereas changed expression

67 is driven by excessive contraction of airway smooth muscle cells (ASMCs).

68 ay and inhibiting Fgf10 expression in airway smooth muscle cells (ASMCs).

69 equency of Ca(2+) oscillations within airway smooth muscle cells (ASMCs).

70 is driven by excessive contraction of airway smooth muscle cells (ASMCs).

71 molecular mechanisms responsible for airway smooth muscle cells' (aSMCs) contraction and proliferati

72 steady-state pHi persisted only in vascular smooth muscle cells but not endothelial cells.

73 odest reduction of proliferation in vascular smooth muscle cells, but given low proliferative capacit

74 of hyperglycemia on vascular endothelial and smooth muscle cells, but the underlying mechanisms are n

75 pidly activated RhoA, ERK, and Akt in airway smooth-muscle cells, but only in the presence of TSG-6.

76 th muscle alpha-actin filaments in wild-type smooth muscle cells by various mechanisms activates nucl

77 , DRP1 inhibition attenuated mouse and human smooth muscle cell calcification.

78 revealed that the origin of aortic vascular smooth muscle cells can be traced back to progenitor cel

79 ted Ca(2+) channels in the adjacent vascular smooth muscle cells, causing vasoconstriction.

80 These mice exhibit lung eosinophilia; smooth muscle cell, collagen, and goblet cell hyperplasi

81 rtner polypeptides in regulation of vascular smooth-muscle cell contractility.

82 kinase inhibition directly attenuates airway smooth muscle cell contraction independent of its protec

83 and VN-PAH, we found enrichment in vascular smooth muscle cell contraction pathways and greater gene

84 Smooth muscle cell contraction significantly increased t

85 force microscopy, changes in single vascular smooth muscle cell cortical actin are observed to remode

86 vates the bleedings and severely compromises smooth muscle cell coverage of the vasculature leading t

87 In cardiomyocytes and smooth muscle cells, cyclic AMP (cAMP) and subsequent ca

88 , decreased hydrogen sulfide production, and smooth muscle cell dedifferentiation in vitro.

89 ndent mechanism, possibly through a vascular smooth muscle cell-dependent mechanism, and methacholine

90 , SRF alone is not sufficient for regulating smooth muscle cell development.

91 (PROCR, rs867186 (p.Ser219Gly)) and vascular smooth muscle cell differentiation (LMOD1, rs2820315).

92 P/TAZ provides the positional cue and allows smooth muscle cell differentiation induced by Hedgehog s

93 GAS5) suppresses TGF-beta/Smad3 signaling in smooth muscle cell differentiation of mesenchymal progen

94 metalloproteinase-3 expression and vascular smooth muscle cell elastin production, both important fa

95 s, which are expressed by endothelial cells, smooth muscles cells, epithelial cells, and hematopoieti

96 real-time imaging was performed in vascular smooth muscle cells expressing a FRET-biosensor comprisi

97 wered blood pressure, which was dependent on smooth muscle cell expression of Panx1 and independent o

98 capacity and beating rate and suppressed the smooth muscle cell formation.

99 A discrete population of smooth muscle cells forms in the embryo and is postnatal

100 Phenotypic switching of vascular smooth muscle cells from a contractile to a synthetic st

101 ctivity promotes the phenotypic switching of smooth muscle cells from a contractile to a synthetic st

102 Aortic tissue and explanted smooth muscle cells from Acta2(-/-) aortas show increase

103 s were markedly reduced in isolated vascular smooth muscle cells from CAD arterioles, although mRNA o

104 In smooth muscle cells from cerebral arteries, increasing i

105 teins and cocaine was confirmed in pulmonary smooth muscle cells from cocaine injected HIV-transgenic

106 o the ureteric epithelium and differentiated smooth muscle cells from E16.5 onwards.

107 Airway smooth muscle cells from healthy and severe asthmatic su

108 of myosin light-chain kinases (MLCK) in the smooth muscle cells from internal anal sphincter (IAS-SM

109 Smooth-muscle cells from mouse tracheas were assayed in

110 and explain why R179H disrupts even visceral smooth muscle cell function where the SM alpha-actin iso

111 Airway smooth muscle cells generated pro-MMP-1, which was prote

112 In response to arterial injuries, existing smooth muscle cells give rise to neointima, but on exten

113 In vascular smooth muscle cells, GPR75-20-HETE pairing is associated

114 ar cell functions, including endothelial and smooth muscle cell growth, proliferation, and migration;

115 and degradation in facilitating human aortic smooth muscle cell (HASMC) proliferation.

116 In addition, studies on human aortic smooth muscle cells (HASMCs) demonstrated membrane hyper

117 o, knockdown of T-cadherin from human aortic smooth muscle cells (HASMCs) with synthetic phenotype si

118 In cultured human airway smooth muscle cells (hASMCs), TGF-beta pre-treatment enh

119 r leukemia-associated RhoGEF in human aortic smooth muscle cells (HASMCs).

120 tractile markers in co-cultured human aortic smooth muscle cells (HASMCs).

121 Oxidant challenge studies show that vascular smooth muscle cells have an intrinsic ability to reduce

122 sts, and Dox-sensitive human coronary artery smooth muscle cells (HCASM).

123 ription factor Nrf2 in human coronary artery smooth muscle cells (HCASMC) and cardiac myocytes (HCM),

124 GC led to reduced migration only in vascular smooth muscle cells homozygous for the nonrisk allele.

125 Histopathologic findings of smooth muscle cell hypertrophy and stroma-like cells, co

126 Loss of smooth muscle cell hypoxia inducible factor-1alpha under

127 se, releases various vasodilators that relax smooth muscle cells in a process termed flow-mediated di

128 h in atherosclerotic plaques and in vascular smooth muscle cells in culture.

129 this study was to determine whether vascular smooth muscle cells in cultured microvascular networks m

130 pA protein expression restricted to vascular smooth muscle cells in healthy human kidney tissue but p

131 e of the ischemic cascade: selective loss of smooth muscle cells in juveniles but not adults shortly

132 x18 selectively marks pericytes and vascular smooth muscle cells in multiple organs of adult mouse.

133 he transplanted cells were made from colonic smooth muscle cells in recipient mice.

134 fibroblasts, endothelial cells, and vascular smooth muscle cells in the absence of serum.

135 localized on endothelial cells and synthetic smooth muscle cells in the aortic intima.

136 Neointimal endothelium and smooth muscle cells in the injured arteries were of mous

137 Extensive proliferation of immature smooth muscle cells in the primitive embryonic dorsal ao

138 xpression in glucose-stimulated human aortic smooth muscle cells in vitro.

139 Nitrovasodilators relax vascular smooth-muscle cells in part by modulating the interactio

140 ic differentiation of primary human vascular smooth muscle cells increased DRP1 expression.

141 on of smooth muscle alpha-actin filaments in smooth muscle cells increases reactive oxygen species le

142 lved in the transdifferentiation of vascular smooth muscle cells into osteoblast-like cells, we inves

143 s likely that in its absence, contraction of smooth muscle cells is impaired.

144 ells, which encompass pericytes and vascular smooth muscle cells, is a hallmark of CADASIL and other

145 in vascular endothelial cells and bronchial smooth muscle cells, leading to lethal vascular leakage

146 rd transient cation currents that depolarize smooth muscle cells, leading to vasoconstriction.

147 ies revealed that loss of YY1AP1 in vascular smooth muscle cells leads to cell cycle arrest with decr

148 differentiate primarily into endothelial and smooth muscle cell lineages in vitro, and contribute ext

149 ary human T cell subsets and coronary artery smooth muscle cells link variants associated with autoim

150 and evidence of higher biological activity (smooth muscle cell loss and fibrin deposition) in the FP

151 , dissection, heightened ROS generation, and smooth muscle cell loss.

152 integrity or on the intimal accumulation of smooth muscle cells, macrophages, and anti-donor antibod

153 om different origins, including endothelial, smooth muscle cells, macrophages, hepatocytes, adipocyte

154 T2 line revealed that pericytes and vascular smooth muscle cells maintained their identity in aging a

155 In vivo, vascular smooth muscle cell/mesangial cell-specific overexpressio

156 s levels substantially attenuated BI-induced smooth muscle cell migration and proliferation, resultin

157 llular phenotypes was analyzed with vascular smooth muscle cell migration assays and platelet aggrega

158 ome P450 (CYP) 1B1 is implicated in vascular smooth muscle cell migration, proliferation, and hyperte

159 ABSTRACT: Smooth muscle cells (myocytes) of resistance-size arteri

160 pha and auxiliary beta1 subunits in arterial smooth muscle cells (myocytes).

161 ) channel isoforms are expressed in arterial smooth muscle cells (myocytes).

162 ong with increased fibrous cap thickness and smooth muscle cell numbers.

163 ells in a manner not seen in Young MAs or in smooth muscle cells of either age.

164 We show that ECs, but not smooth muscle cells, of small mesenteric arteries have K

165 c increase in the proliferation of pulmonary smooth muscle cells on exposure to HIV-proteins and/or c

166 orylated SMAD2/3 in human pulmonary arterial smooth muscle cells on treatment with cocaine and Tat.

167 endogenous Kv7.5 channels in A7r5 rat aortic smooth muscle cells or through Kv7.4/Kv7.5 heteromeric c

168 bronchial epithelial (P = 0.0002) and airway smooth muscle cells (P = 0.0352) of patients with asthma

169 Endothelial and smooth muscle cells participate in atherogenesis, but it

170 characterized by excessive pulmonary artery smooth muscle cell (PASMC) proliferation, migration, and

171 signaling induces abnormal pulmonary artery smooth muscle cell (PASMC) survival patterns to promote

172 as in pulmonary artery and pulmonary artery smooth muscle cells (PASMC) exposed to hypoxia.

173 stressful conditions, pulmonary artery (PA) smooth muscle cells (PASMCs) exhibit a "cancer-like" pro

174 In parallel, pulmonary arterial smooth muscle cells (PASMCs) from Cox4i2(-/-) mice showe

175 , the role of HIF-1alpha in pulmonary artery smooth muscle cells (PASMCs) remains controversial.

176 ute to the proliferation of pulmonary artery smooth muscle cells (PASMCs), and inhibition of phosphod

177 excessive proliferation of pulmonary artery smooth muscle cells (PASMCs).

178 dases, ADAM10 and ADAM17 in pulmonary artery smooth muscle cells (PASMCs).

179 red apoptosis of pulmonary arterial vascular smooth muscle cells (PAVSMCs) are key pathophysiologic c

180 1.5 protein expression were decreased in PAH smooth muscle cells (primary culture).

181 egulating the adhesion of monocytic cells to smooth muscle cells producing an inflammatory matrix.

182 vasculoprotective effect of NOD by reducing smooth muscle cell proliferation and inflammation-induce

183 sults identify SMILR as a driver of vascular smooth muscle cell proliferation and suggest that modula

184 PHD2-deficient endothelial cells promoted smooth muscle cell proliferation in part through hypoxia

185 developed less neointimal hyperplasia, less smooth muscle cell proliferation, and had fewer infiltra

186 l functions, including platelet aggregation, smooth muscle cell proliferation, and immune regulation.

187 utic application for selective inhibition of smooth muscle cell proliferation, enhancement of endothe

188 In human aortic smooth muscle cells, prostaglandin E2 (PGE2) stimulates

189 A7 expression and pHi regulation in vascular smooth muscle cells provides an insight into the molecul

190 ctors that preferentially influence vascular smooth muscle cells rather than endothelial cells.

191 Uterine smooth muscle cells remain quiescent throughout most of

192 Knock-down of Csrp2bp in smooth muscle cells resulted in reduced smooth muscle ge

193 n and pharmacological inhibition in vascular smooth muscle cells reveal that cytochrome b5 reductase

194 Other false IVOCT TCFA causes included smooth muscle cell-rich fibrous tissue (12%) and loose c

195 ological sGC heme iron reductase in vascular smooth muscle cells, serving as a critical regulator of

196 Incubation of S1P with airway smooth muscle cells significantly increased contractilit

197 itro studies revealed that in mouse vascular smooth muscle cells, siRNA knockdown of GRIP1, which is

198 restingly, ADAMTS-4 was directly involved in smooth muscle cell (SMC) apoptosis.

199 Vascular smooth muscle cell (SMC) composes the majority of the va

200 ng to thoracic aortic disease either disrupt smooth muscle cell (SMC) contraction or adherence to an

201 elect in vivo A20 targets in human and mouse smooth muscle cell (SMC) cultures.

202 Smooth muscle cell (SMC) death contributes to plaque des

203 In mice, Foxe3 deficiency reduced smooth muscle cell (SMC) density and impaired SMC differ

204 Smooth muscle cell (SMC) differentiation is essential fo

205 vivo fate-mapping approaches combined with a smooth muscle cell (SMC) epigenetic lineage mark, we rep

206 vivo fate-mapping approaches combined with a smooth muscle cell (SMC) epigenetic lineage mark, we rep

207 ics, we measured primary human aortic single smooth muscle cell (SMC) forces using nanonet force micr

208 We established expandable cell lines under smooth muscle cell (SMC) growth conditions that retained

209 romal cell (MSC) differentiation towards the smooth muscle cell (SMC) lineage but not in combination.

210 s associated with marked changes in vascular smooth muscle cell (SMC) phenotype and function.

211 Smooth muscle cell (SMC) phenotypic conversion from a co

212 Vascular smooth muscle cell (SMC) proliferation and endothelial c

213 etalloproteinase 9 expression and neointimal smooth muscle cell (SMC) proliferation were assessed by

214 sions of hyperglycemic ApoE(-/-) mice; also, smooth muscle cell (SMC), macrophage and leukocyte abund

215 Here we demonstrate that smooth muscle cell (SMC)-specific conditional knockout o

216 elial cell (BmxCreER(T2)-driven)-specific or smooth muscle cell (SMC, SmmhcCreER(T2)- or TaglnCre-dri

217 because voltage-dependent Ca(2+) channels in smooth muscle cells (SMC) provide the Ca(2+) that trigge

218 BB)-stimulated proliferation of human venous smooth muscle cells (SMC) was measured by a DNA-binding

219 90% of cells in HMGA2-uterine leiomyoma were smooth muscle cells (SMC) with HMGA2 overexpression.

220 Kir2 channels was observed in ICC but not in smooth muscle cells (SMC).

221 Vascular smooth muscle cells (SMCs) and endothelial cells (ECs) a

222 es, inhibited proliferation and migration of smooth muscle cells (SMCs) and promoted the tube formati

223 crest (NC) only differentiates into vascular smooth muscle cells (SMCs) around those aortic arches de

224 Vascular smooth muscle cells (SMCs) can resist and repair artery

225 he Rho GTPase-activating protein ARHGAP42 in smooth muscle cells (SMCs) controls blood pressure by in

226 Smooth muscle cells (SMCs) in normal blood vessels exist

227 expression could be resolved in ICC but not smooth muscle cells (SMCs) in the IAS and rectum.

228 Loss and dysfunction of smooth muscle cells (SMCs) in the vasculature may cause

229 n vitro differentiation into fibroblasts and smooth muscle cells (SMCs) is also described.

230 In mice, MR deficiency in smooth muscle cells (SMCs) protected against kidney IR i

231 Our MFS-hiPSC-derived smooth muscle cells (SMCs) recapitulated the pathology s

232 ted cellular contraction in primary vascular smooth muscle cells (SMCs) that were isolated from renal

233 In an in vitro model, primary smooth muscle cells (SMCs) were stimulated with elevated

234 A microarrays on the phenotypically distinct smooth muscle cells (SMCs) within the rat anorectrum, we

235 demonstrated TLR7 expression in macrophages, smooth muscle cells (SMCs), and endothelial cells from m

236 rcumferential layers of elastic lamellae and smooth muscle cells (SMCs), and many arterial diseases a

237 Moreover, indatraline induced autophagy in smooth muscle cells (SMCs); further, it exhibited therap

238 expression of 5-HTT induced proliferation of smooth muscle cells (SMCs); however, this phenotype coul

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

240 Gene-targeted mice with a cardiomyocyte- or smooth muscle cell-specific deletion of the BK (CMBK or

241 Generation of transgenic mice with smooth muscle cell-specific expression of either USP20 o

242 Lgr6(+) cells comprise a subpopulation of smooth muscle cells surrounding airway epithelia and pro

243 d integration site) signaling and regulating smooth muscle cell survival, as well as differentiation

244 plaques through inhibition of APC, ensuring smooth muscle cell survival.

245 In human primary vascular endothelial and smooth muscle cells that endogenously express RXFP1, ML2

246 tassium channels (Kv ) in pulmonary arterial smooth muscle cells that is mediated by the inhibition o

247 aorta establishes the long-lived lineages of smooth muscle cells that make up the wall of the adult a

248 In airway smooth muscle cells, these Ca(2+) oscillations are cause

249 Our investigation concludes that vascular smooth muscle cell TNF augments resistance artery myogen

250 fect in the capacity of the Cdkn2b-deficient smooth muscle cell to support the developing neovessel.

251 Exposure of human coronary artery smooth muscle cells to cigarette smoke extract led to in

252 ion, which reflects the intrinsic ability of smooth muscle cells to contract in response to increases

253 nted Sox10(+) stem cells differentiated into smooth muscle cells to stabilize functional microvessels

254 ameters vary throughout differentiation of a smooth muscle cell type in intact Caenorhabditis elegans

255 ntiation to multiple neural, pancreatic, and smooth muscle cell types.

256 DRP1 inhibition in human smooth muscle cells undergoing osteogenic differentiatio

257 upregulation is observed in endothelial and smooth muscle cells upon culture conditions, yielding a

258 Experiments were performed with aortic smooth muscle cells using inhibitor screening, small int

259 othelial denudation showed that antagonizing smooth muscle cell USP20 activity increased NFkappaB act

260 Vascular smooth muscle cell (VSMC) accumulation is a hallmark of

261 Vascular smooth muscle cell (VSMC) activation in response to inju

262 Vascular smooth muscle cell (VSMC) apoptosis precipitates AAA for

263 ion, and thinning of the periportal vascular smooth muscle cell (VSMC) layer, which are apparent at e

264 bunits, are important regulators of vascular smooth muscle cell (VSMC) membrane voltage.

265 in pathophysiologic stimulation of vascular smooth muscle cell (VSMC) migration and proliferation.

266 ncentrations (</=1 mum) in cultured vascular smooth muscle cells (VSMC) expressing an ALDH2 mutant th

267 nuclear protein that is specific to vascular smooth muscle cells (VSMC), has histone methyl transfera

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

269 one, as a potent HIF-1 activator in vascular smooth muscle cells (VSMC).

270 the main route for calcium entry in vascular smooth muscle cells (VSMC).

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

272 antly expressed in the cytoplasm of vascular smooth muscle cells (VSMCs) and tubular epithelial cells

273 OCs) in proliferative and migratory vascular smooth muscle cells (VSMCs) are quite intricate with man

274 nd differentiation of NC cells into vascular smooth muscle cells (VSMCs) by regulating Notch signalin

275 us vein endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) converted 17-HDHA to SPMs, i

276 The historical view of vascular smooth muscle cells (VSMCs) in atherosclerosis is that a

277 ions (AJ) along the borders between vascular smooth muscle cells (VSMCs) in the pressurized rat super

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

279 Specific ablation of Plk1 in vascular smooth muscle cells (VSMCs) led to reduced arterial elas

280 Proliferation and migration of vascular smooth muscle cells (VSMCs) or endothelial cell (ECs) pr

281 MicroRNAs are key regulators of vascular smooth muscle cells (VSMCs) phenotypic switch, one of th

282 NAs were further evaluated in human vascular smooth muscle cells (VSMCs) stimulated with angiotensin

283 that induces tissue factor (TF) in vascular smooth muscle cells (vSMCs), although the precise mechan

284 ABSTRACT: In vascular smooth muscle cells (VSMCs), stimulation of canonical tr

285 In vascular smooth muscle cells (VSMCs), stimulation of SOCs compose

286 indicate that it may also stimulate vascular smooth muscle cells (VSMCs), thereby contributing to vas

287 ptor potential (TRPC) 1 proteins in vascular smooth muscle cells (VSMCs), which contribute to importa

288 ajor cell-cell adhesion molecule in vascular smooth muscle cells (VSMCs).

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

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

291 1.3% of vessels with recruitment of vascular smooth muscle cells; VSMCs) in the presence of enhanced

292 hallenge, and bronchoscopy, and their airway smooth muscle cells were grown in culture.

293 In vitro analyses of human aortic smooth muscle cells were performed to test the effect of

294 Human endothelial and smooth muscle cells were treated with pro-inflammatory c

295 as well as in vascular networks layered with smooth muscle cells when compared with the control group

296 scovered globin expressed in fibroblasts and smooth muscle cells with unknown function.

297 hat neoarterioles were aberrantly covered by smooth muscle cells, with increased interprocess spacing

298 nerve terminals and electrically coupled to smooth muscle cells within the gastric musculature.

299 donors revealed that a substantial amount of smooth muscle cells within the obliterative tissue was o

300 hus potentiating AngII signaling in vascular smooth muscle cells without an increase in the exogenous