ライフサイエンスコーパス: smooth muscle cell

1 ard a mesenchymal cell (e.g., myofibroblast, smooth muscle cell).

2 lpha-SMA function within the cerebrovascular smooth muscle cell.

3 tor ROCKi significantly relax human ureteral smooth muscle cells.

4 ediated by the nuclear actions of ERalpha in smooth muscle cells.

5 arts owing to an increase in ventricular and smooth muscle cells.

6 racheal mesoderm containing chondrocytes and smooth muscle cells.

7 when COX1 was knocked out in ECs but not in smooth muscle cells.

8 to the electrical excitability of myometrial smooth muscle cells.

9 les did not increase near contact sites with smooth muscle cells.

10 sion of CD47 and other oncogenes in arterial smooth muscle cells.

11 tracellular Ca(2+) concentration in vascular smooth muscle cells.

12 and other arterial tissues, including medial smooth muscle cells.

13 rimary cortical neurons and primary cortical smooth muscle cells.

14 to longitudinal proliferation of arteriolar smooth muscle cells.

15 on of IL-2Rbeta on human and murine vascular smooth muscle cells.

16 ration and contraction of pulmonary arterial smooth muscle cells.

17 oked in both conduit and resistance arterial smooth muscle cells.

18 induced contraction in primary human uterine smooth muscle cells.

19 ECs released >10-fold more prostacyclin than smooth muscle cells.

20 3 and IL-4 in human bronchi and human airway smooth muscle cells.

21 y endothelial cells, pericytes, and vascular smooth muscle cells.

22 diomyocytes compared to neurons and vascular smooth muscle cells.

23 imary human airway epithelial progenitor and smooth muscle cells.

24 ed in lesional macrophages, endothelial, and smooth muscle cells.

25 ood vessels are comprised of endothelial and smooth muscle cells.

26 djacent to the PAA endothelium into vascular smooth muscle cells.

27 quired the presence of the underlying medial smooth muscle cells.

28 or (n = 28) microbleeds, both Abeta (4%) and smooth muscle cells (4%) were almost never present in th

29 neurons(1), cardiomyocytes(2-4) and vascular smooth muscle cells(5), where they are involved in the r

30 els associated with microinfarcts had intact smooth muscle cells (9%).

31 ic inflammation and remodeling via decreased smooth muscle cell activation and neutrophil transendoth

32 In primary vascular smooth muscle cells, aging reduced proliferation, wherea

33 -based patterning to mechanically controlled smooth muscle cell alignment and provide a mechanistic c

34 SCAP knockdown in vascular smooth muscle cells alleviates atherosclerosis plaque fo

35 elastic fiber disruption, and an increase in smooth muscle cell alpha-actin expression compared to un

36 his results in depolarization of the uterine smooth muscle cells and calcium entry, which may contrib

37 fication gene, highly expressed in arteries' smooth muscle cells and chondrocytes.

38 tin, MCP-1) in endothelial cells or vascular smooth muscle cells and decreased monocytes adhesion to

39 on PIP(2) as a regulator of ion channels in smooth muscle cells and endothelial cells-the two major

40 benign tumors characterized by hyperplastic smooth muscle cells and excessive deposition of extracel

41 controlled proliferation of pulmonary artery smooth muscle cells and fibroblasts.

42 HHIPL1 expression was detected in human smooth muscle cells and in smooth muscle within atherosc

43 n increase in lipid content and decreases in smooth muscle cells and macrophages, resulting in an exp

44 Mural cells (smooth muscle cells and pericytes) are integral componen

45 n endothelial cells and surrounding vascular smooth muscle cells and pericytes.

46 ings were accompanied with elevated vascular smooth muscle cells and reduced MMPs.

47 tures correlated with increased retention of smooth muscle cells and reduced vessel areas at the junc

48 jacent mesenchymal tissues, including airway smooth muscle cells and their extracellular protein prod

49 ion maps (~750 bases) in aortic endothelial, smooth muscle cells and THP-1 (human leukemia monocytic

50 where it regulates contractile pericytes and smooth muscle cells and thus blood flow.

51 endothelial cells with 2 abluminal layers of smooth muscles cells and matrix.

52 of granulocytes, proliferation of fibrocytes/smooth muscle cells, and basement membrane thickening.

53 Endothelial cells, smooth muscle cells, and cardiomyocytes derived from hyp

54 1 knockout mouse and HHIPL1 knockdown aortic smooth muscle cells, and hedgehog signaling was decrease

55 ding platelets, fibroblasts, endothelial and smooth muscle cells, and immune cells.

56 ysfunctional autophagy in endothelial cells, smooth muscle cells, and macrophages, plays a detrimenta

57 nd cell types, including platelets, vascular smooth muscle cells, and neuronal cells.

58 1alpha) was assessed in isolated rat aortic smooth muscle cells, and the mechanism of action of this

59 1) Treatments of human aortic smooth muscle cells (AoSMCs) with SIRT1 activators (SRT1

60 Prkg1(R177Q/+) aortas show increased smooth muscle cell apoptosis, elastin fiber breaks, and

61 ese results identify P2Y(2) receptors in RTN smooth muscle cells as requisite determinants of respira

62 We also identify P2Y(2) receptors in RTN smooth muscle cells as the substrate responsible for thi

63 Specialized pacemaker cells, termed atypical smooth muscle cells (ASMCs), are thought to drive the pe

64 eceptor to preferentially colonize at airway smooth muscle cells (ASMCs)-a rich source of collagen II

65 a direct impact on the contraction of airway smooth muscle cells (ASMCs).

66 es and evaluates the changes in rat vascular smooth muscle cell biomechanics following statin-mediate

67 blockade or genetic deletion of P2Y(2) from smooth muscle cells blunted the ventilatory response to

68 f blood outgrowth endothelial cells (BOECs), smooth muscle cells (BO-SMCs), and leukocytes were obtai

69 by differing cell types (e.g., activation by smooth muscle cells but not fibroblasts) within clinical

70 1 in human lung myofibroblasts, human airway smooth muscle cells but not lung mast cells.

71 relax the myosin cytoskeleton of the airway smooth muscle cells by acting as a receptor for extracel

72 ur work showing that IL-2 surrounds vascular smooth muscle cells by association with perlecan, led us

73 SV was detected in the arterial tunica media smooth muscle cells by immunohistochemistry, in situ hyb

74 gregated within the mitochondria of vascular smooth muscle cells can drive an hour-long disruption.

75 They produced keratinocytes, smooth muscle cells, cardiac muscle cells, neurons and g

76 r cells, like endothelial cells and vascular smooth muscle cells, cardiac myocytes and inflammatory c

77 directly on mouse and human coronary artery smooth muscle cells (caSMCs) and caECs, resulting in sol

78 In cultured coronary arterial smooth muscle cells (CASMCs) from Asah1(fl/fl)/SM(Cre) m

79 that abnormal proliferation of the vascular smooth muscle cells causes the marked tortuosity of reti

80 Hhipl1(-/-) mice were generated and aortic smooth muscle cells collected for phenotypic analysis an

81 e, mutant transgenic PDE3A overexpression in smooth muscle cells confirmed that mutant PDE3A causes h

82 ised intracellular Ca(2+) levels in arterial smooth muscle cells, constricted arterioles ex vivo and

83 s, and lesions were characterized by reduced smooth muscle cell content.

84 regulate spontaneous Ca(2+) oscillations in smooth muscle cells controlling renal arterial spontaneo

85 sistent with what we know of endothelial and smooth muscle cells cultured from blood vessels.

86 holesterol depletion remodels total vascular smooth muscle cell cytoskeletal orientation that may add

87 In contrast, loss of DGKzeta in airway smooth muscle cells decreased AHR but not airway inflamm

88 V4 channels at myoendothelial projections to smooth muscle cells decreases resting blood pressure in

89 ro-inflammatory actions of TWEAK on vascular smooth muscle cells, decreasing NF-kB activation, cytoki

90 gene encoding NOTCH3 and results in vascular smooth muscle cell degeneration, stroke, and dementia.

91 nhibition of TRPV4 channels mitigates aortic smooth muscle cell-dependent inflammatory cytokine produ

92 calcifications formed by calcifying vascular smooth muscle cell derived extracellular vesicles in the

93 sed a strategy whereby human endothelial and smooth muscle cells derived from blood progenitors from

94 Second, about half of all foam cells are smooth muscle cell-derived, retaining smooth muscle cell

95 e deacetylase (AADAC) expression in vascular smooth muscle cells (dVSMCs) differentiated from patient

96 uctions were associated with endothelial and smooth muscle cell dysfunction, rescued by enzastaurin t

97 ular calcium concentrations ([Ca(2+)](i)) in smooth muscle cells embedded in the walls of freshly iso

98 n arterial cell types: fibroblasts, vascular smooth muscle cells, endothelial cells (ECs), and immune

99 gans, lung lymphatic collecting vessels lack smooth muscle cells entirely, suggesting that forward ly

100 hich oxytocin may act to modulate myometrial smooth muscle cell excitability.

101 We now report that vascular smooth muscle cells express all three subunits of the IL

102 ith perlecan, led us to ask whether vascular smooth muscle cells express an IL-2R.

103 Smooth muscle cells express Kv7.4 and Kv7.5 voltage-depe

104 In mouse vascular smooth muscle cells expressing both alpha- and beta1-sub

105 Compared with renal vascular smooth muscle cells from Add3 transgenic rats, those fro

106 differentiated human macrophages, and aortic smooth muscle cells from humans with diabetes), MCC950 s

107 rrent in freshly isolated pulmonary arterial smooth muscle cells from Kcnk3-mutated rats.

108 3 (EYA3) are elevated in pulmonary arterial smooth muscle cells from patients with pulmonary arteria

109 e-expression of P2Y(2) receptors only in RTN smooth muscle cells fully rescued the CO(2)/H(+) chemore

110 ates signaling pathways and impacts vascular smooth muscle cell function.

111 imal and medial endothelial, macrophage, and smooth muscle cell function.

112 lic syndrome alters vascular endothelial and smooth muscle cell functions in the heart, brain, kidney

113 Vascular smooth muscle cells going from a proliferative and motil

114 R-145-5p was strongly associated with airway smooth muscle cell growth in vitro.

115 Tensin1 expression in cultured human airway smooth muscle cells (HASMCs) was evaluated using qRT-PCR

116 proliferation and migration of human aortic smooth muscle cells (HASMCs).

117 In current clamp, KO arterial smooth muscle cells have easily evoked Ca(2+) -dependent

118 links Ca(2+) influx in human coronary artery smooth muscle cells (hCASMCs) to 3',5'-cyclic adenosine

119 on in primary human coronary artery vascular smooth muscle cells (HCASMCs).

120 Human pulmonary artery smooth muscle cells (HPASMCs) demonstrated hypoxic induc

121 In human airway smooth muscle cells, IL-13 and IL-4, but not IL-5 and IL

122 rimentally by treating human coronary artery smooth muscle cells in an in vitro calcification assay.

123 Endothelial and smooth muscle cells in arterial tissue expressed CARD8 a

124 es promoted mineralization of human arterial smooth muscle cells in culture, as shown by Alizarin red

125 nd to be expressed predominantly on vascular smooth muscle cells in lesions of athero-prone Apoe(-/-)

126 well as the expression of CD47 from arterial smooth muscle cells in mice.

127 ated PAH microvascular endothelial cells and smooth muscle cells in vitro, and in diverse PAH rat mod

128 acemaker cells (previously termed 'atypical' smooth muscle cells) in the murine and cynomolgus monkey

129 ition requires that the uterine (myometrial) smooth muscle cells increase their excitability, althoug

130 Distinct loss of function of IDO in smooth muscle cells, inflammatory cells, or cardiomyocyt

131 y, while inhibition of HDAC9 in human aortic smooth muscle cells inhibited calcification and enhanced

132 caspase-1 secretion and attenuated leukocyte-smooth muscle cell interactions under high glucose or li

133 ing through activation of nuclear ERalpha in smooth muscle cells, inviting to revisit the mechanisms

134 cepted role of the protein Kv2.1 in arterial smooth muscle cells is to form K(+) channels in the sarc

135 involved ongoing proliferation of intestinal smooth muscle cells (ISMC) with expression of platelet-d

136 duced vascular endothelial cells (iVECs) and smooth muscle cells (iSMCs) by direct reprogramming of h

137 or.Methods: Microvascular endothelial cells, smooth muscle cells isolated from distal pulmonary arter

138 otype of microvascular endothelial cells and smooth muscle cells isolated from patients with PAH.

139 studied glomeruli and primary renal vascular smooth muscle cells isolated from these rats.

140 A is widely expressed, including in vascular smooth muscle cells, kidney, myocardium and brain.

141 amining the mesenchymal components including smooth muscle cells, laminin, and elastin in airway and

142 lacks the key anatomical feature of vascular smooth muscle cell loss seen in HGPS patients, our data

143 ssion, CD31(+) microvessel growth, and media smooth muscle cell loss, compared with those from Apoe(-

144 Multiple subtypes were observed for smooth muscle cells, macrophages, and T lymphocytes, sug

145 ell populations including endothelial cells, smooth muscle cells, mast cells, B cells, myeloid cells,

146 holesterol depletion may coordinate vascular smooth muscle cell migration and adhesion to different e

147 Smooth muscle cell migration is essential for many diver

148 Abi1 knockdown by shRNA reduced human airway smooth muscle cell migration, which was restored by Abi1

149 e examined the effects of red blood cells on smooth muscle cell mineralization and vascular calcifica

150 partly a result of changes in the myometrial smooth muscle cell (MSMC) resting membrane potential.

151 isms that regulate PKD2 channels in arterial smooth muscle cells (myocytes).

152 l proline-rich repeat 3 (SPRR3), in vascular smooth muscle cells of atheromas.

153 intercellular Ca(2+) waves are generated in smooth muscle cells of colonic longitudinal muscles (LSM

154 prepared from the kidney and renal vascular smooth muscle cells of FHH rats was associated with the

155 Spontaneous Ca(2+) fluctuations in smooth muscle cells of p66Shc knockout (p66ShcKO) rats h

156 Adaptor protein p66Shc is overexpressed in smooth muscle cells of renal resistance vessels of hyper

157 Spontaneous cytosolic Ca(2+) oscillations in smooth muscle cells of renal vessels mediate their spont

158 gene signatures of mesangial cells, vascular smooth muscle cells of the afferent and efferent arterio

159 Smooth muscle cells of the muscularis mucosa, in close p

160 ously released endothelin-1 were recorded in smooth muscle cells of the renal arteries.

161 Genetic disruption of autophagy in smooth muscle cells of young mice exposed to hyperlipide

162 reviously reported enhanced proliferation of smooth muscle cells on the combined exposure of HIV prot

163 ed in mice harboring specific endothelial or smooth muscle cells or cardiomyocyte or myeloid cell def

164 that IL-2 and IL-2Rbeta-deficient mice lose smooth muscle cells over time, eventually resulting in a

165 Altered metabolism in pulmonary artery smooth muscle cells (PASMCs) and endothelial cells (PAEC

166 d apoptosis resistance of pulmonary arterial smooth muscle cells (PASMCs) and pulmonary arterial endo

167 ound FPN to be present in pulmonary arterial smooth muscle cells (PASMCs) and regulated by hepcidin c

168 Ca(2+) signaling in pulmonary arterial smooth muscle cells (PASMCs) plays an important role in

169 with marked accumulation of pulmonary artery smooth muscle cells (PASMCs) represents one of the major

170 the abnormal phenotype of pulmonary arterial smooth muscle cells (PASMCs), a major contributor of PAH

171 HPV is intrinsic to pulmonary artery smooth muscle cells (PASMCs).

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

173 onmyocyte cardiac lineages, such as vascular smooth muscle cells, pericytes, and fibroblasts.

174 xpression of IL-2Ralpha varies with vascular smooth muscle cell phenotype.

175 lar physiology, regulating vascular tone and smooth-muscle cell phenotype.

176 tics allow the investigation of pericyte and smooth muscle cell physiology and their role in regulati

177 g is associated with an increase in vascular smooth muscle cell proliferation and changes in vessel m

178 clerosis plaques, through promoting arterial smooth muscle cell proliferation and maintaining the mol

179 at enhances hedgehog signaling and regulates smooth muscle cell proliferation and migration.

180 Furthermore, IgG antibodies enhanced smooth muscle cell proliferation in vitro in an Fc recep

181 ith asthma and additionally increases airway smooth muscle cell proliferation.

182 function-selective ERK inhibitors on airway smooth muscle cell proliferation.

183 o, IL-6 activates STAT3 and induces human PA smooth muscle cell proliferation.

184 und healing, with increased angiogenesis and smooth muscle cell proliferation.

185 IL-6 levels, STAT3 activation, and human PA smooth muscle cell proliferation.

186 g (i) binding to fibrin, (ii) stimulation of smooth-muscle cell proliferation, and (iii) stimulation

187 ncreased expression of HDAC9 in human aortic smooth muscle cells promoted calcification and reduced c

188 ssion of Akt1E17K to endothelial, cardiac or smooth muscle cells resulted in viable offspring and rem

189 lta9) and the other specifically in vascular smooth muscle cells (SM22-Cul3Delta9).

190 occurs for intact vessels or differs between smooth muscle cell (SMC) and endothelial cell (EC) layer

191 sected advanced atherosclerotic lesions with smooth muscle cell (SMC) and endothelial lineage tracing

192 Rapamycin decreased smooth muscle cell (SMC) and macrophage proliferation; r

193 Formation of AAA was driven by increased smooth muscle cell (SMC) apoptosis and oxidative stress

194 It has been thought that smooth muscle cell (SMC) degeneration at the site of art

195 chanisms of aortic delamination arising from smooth muscle cell (SMC) dysfunction or apoptosis, degra

196 formation in MFS may be related to distinct smooth muscle cell (SMC) embryologic lineages.

197 erosclerotic plaque development by promoting smooth muscle cell (SMC) investment.

198 ssection (AAD), caused by progressive aortic smooth muscle cell (SMC) loss and extracellular matrix d

199 ule-1 (ICAM-1), endothelial dysfunction, and smooth muscle cell (SMC) proliferation in the grafted ve

200 sm development and identified a key role for smooth muscle cell (SMC) reprogramming into a mesenchyma

201 Smooth muscle cell (SMC)-specific RyR2 knockout (KO) or

202 aneurysms and dissections (AADs) induced by smooth muscle cell (SMC)-specific, postnatal deletion of

203 Network is that detrimental reprogramming of smooth muscle cells (SMC) and other ACTA2+ fibrous cap c

204 Smooth muscle cells (SMC) play a critical role in athero

205 rly stage of atherosclerosis and on vascular smooth muscle cells (SMC) remain to be fully elucidated.

206 iously collected transcriptomes from primary smooth muscle cells (SMC), interstitial cells of Cajal (

207 an, external to which lie contraction-primed smooth muscle cells (SMC).

208 ing neurons, Schwann cells, melanocytes, and smooth muscle cells (SMC).

209 In addition, smooth muscle cells (SMCs) along the renal arterioles tr

210 Neointima arises from smooth muscle cells (SMCs) and not endothelium.

211 ous excitability and contractions of colonic smooth muscle cells (SMCs) are normally suppressed by in

212 Smooth muscle cells (SMCs) are the most affected cells i

213 g extra domain A (Fn-EDA) is associated with smooth muscle cells (SMCs) following vascular injury.

214 In vascular smooth muscle cells (SMCs) grown under calcifying condit

215 mmuno-SERS (iSERS) microscopy for imaging of smooth muscle cells (SMCs) in atherosclerotic plaques.

216 f21 is required for phenotypic modulation of smooth muscle cells (SMCs) in atherosclerotic tissues an

217 erations in extracellular matrix and loss of smooth muscle cells (SMCs) in the medial layer of the ao

218 most abundant junctophilin isotype in native smooth muscle cells (SMCs) isolated from cerebral arteri

219 Smooth muscle cells (SMCs) play significant roles in ath

220 communication between endothelial cells and smooth muscle cells (SMCs) plays a critical role not onl

221 Vascular smooth muscle cells (SMCs) produce the layered elastic l

222 Vascular smooth muscle cells (SMCs) synthesize extracellular matr

223 H(2) O(2) -induced death was greater in smooth muscle cells (SMCs) than endothelial cells (ECs)

224 phages (in the absence of serum or HDL) onto smooth muscle cells (SMCs) that had been metabolically l

225 se vasodilatory factors that act directly on smooth muscle cells (SMCs) to induce arterial dilation a

226 llular histone H4-mediated membrane lysis of smooth muscle cells (SMCs) triggers arterial tissue dama

227 from a subset of "dedifferentiated" vascular smooth muscle cells (SMCs) which proliferate in a clonal

228 ediated NO dioxygenation process in vascular smooth muscle cells (SMCs), and the requisite reducing s

229 ontractility and differentiation in vascular smooth muscle cells (SMCs), but the specific function of

230 uman atherosclerotic plaques associated with smooth muscle cells (SMCs), inflammation, extracellular

231 c motor neurons and SIP syncytium, including smooth muscle cells (SMCs), interstitial cells of Cajal

232 tional cells of the SIP syncytium, including smooth muscle cells (SMCs), interstitial cells of Cajal

233 erentiate into cardiac fibroblasts (CFs) and smooth muscle cells (SMCs), whereas THY1(-) cells were p

234 ty and contractility in bladder and urethral smooth muscle cells (SMCs).

235 interstitial cells of Cajal (ICC) but not by smooth muscle cells (SMCs).

236 plicing regulator in differentiated vascular smooth muscle cells (SMCs).

237 PAH resulting from LRP1 deletion in vascular smooth muscle cells (SMCs).

238 x proteins suggested increased production by smooth muscle cells (SMCs).

239 rage the infiltration and growth of vascular smooth muscle cells (SMCs).

240 in fully differentiated contractile vascular smooth muscle cells (SMCs).

241 investigated two GPCRs that characterize IAS smooth muscle cells (SMCs): thromboxane A(2) and angiote

242 Smooth muscle cell-specific overexpression of Smad7 comp

243 vidence of coordinated reduction in vascular smooth muscle cell stiffness and actin cytoskeletal orie

244 from fish that transgenically express GFP on smooth muscle cells (Tg[acta2:GFP]), to visualize the be

245 ircumferentially arranged layers of vascular smooth muscle cells that are separated by concentrically

246 Contractility of the nonmuscle and smooth muscle cells that comprise biological tubing is r

247 crine prostaglandin E(2) signaling in airway smooth muscle cells that eventually triggered cAMP/PKA-d

248 rations in extracellular matrix, and loss of smooth muscle cells, they are distinct diseases.

249 6 regulates phenotypic switching of vascular smooth muscle cells through plasma membrane potential-de

250 e Kv7.4 and Kv7.5 alpha-subunits in vascular smooth muscle cells to determine which components are es

251 hanges in migration and adhesion of vascular smooth muscle cells to extracellular matrix proteins fib

252 ls are smooth muscle cell-derived, retaining smooth muscle cell transcripts rather than transdifferen

253 ogy, adhesion, and migration of human airway smooth muscle cells transfected with PKAc variants conta

254 yte membranes were reduced in human arterial smooth muscle cells treated with the NO scavenger 2-phen

255 rive the peristaltic contractions of typical smooth muscle cells (TSMCs) in the renal pelvis.

256 ranscriptional control of CPI-17 in vascular smooth muscle cells under inflammatory conditions and su

257 cellular vesicles secreted by human coronary smooth muscle cells upon exposure to atherogenic conditi

258 l tensile force was applied to live vascular smooth muscle cells using a fibronectin-functionalized a

259 In vascular smooth muscle cells (VMSCs), stimulation of Ca(2+) -perm

260 hed a role for miRNAs in regulating vascular smooth muscle cell (VSMC) activity.

261 olesterol management on primary rat vascular smooth muscle cell (VSMC) biomechanics.

262 d to determine the role of SIRT1 in vascular smooth muscle cell (vSMC) calcification within the diabe

263 Vascular smooth muscle cell (VSMC) function is regulated by Nox-d

264 ar calcification (VC) by increasing vascular smooth muscle cell (VSMC) osteogenic differentiation, AD

265 Vascular smooth muscle cell (VSMC) phenotype switching from a con

266 ene expression patterns that define vascular smooth muscle cell (VSMC) phenotype.

267 aim to determine the role of YY1 in vascular smooth muscle cell (VSMC) phenotypic modulation both in

268 a-1 (TGFbeta1) is a major driver of vascular smooth muscle cell (VSMC) phenotypic switching, an impor

269 Vascular smooth muscle cell (VSMC) remodeling is a pathological h

270 between mitochondrial dynamics and vascular smooth muscle cell (VSMC) senescence.

271 , we aim to investigate the role of vascular smooth muscle cell (VSMC) TFEB in the development of AAA

272 propagation of seizures in SE, and vascular smooth muscle cell (VSMC) TRPC3 channels participate in

273 IHC against macrophages, collagen, vascular smooth muscle cells (VSMC) and matrix metalloproteinases

274 Insulin and IGF-1 actions in vascular smooth muscle cells (VSMC) are associated with accelerat

275 and on osteoblast mineralization of vascular smooth muscle cells (VSMC).

276 Vascular smooth muscle cells (VSMCs) are a major cell type presen

277 Vascular smooth muscle cells (VSMCs) are critical in the developm

278 Vascular smooth muscle cells (VSMCs) can be derived in large numb

279 a(+) cells, a signature shared with vascular smooth muscle cells (VSMCs) derived from mesenchymal ste

280 hough the role of several miRNAs in vascular smooth muscle cells (VSMCs) has been extensively charact

281 Vascular smooth muscle cells (VSMCs) in the normal arterial media

282 D2 deficiency inhibits migration of vascular smooth muscle cells (VSMCs) into the intima in mice as w

283 een SCAP and foam cell formation in vascular smooth muscle cells (VSMCs) is poorly understood.

284 Vascular smooth muscle cells (VSMCs) play critical roles in the s

285 mechanical fluctuations applied to vascular smooth muscle cells (VSMCs) regulates mitochondrial netw

286 Vascular smooth muscle cells (VSMCs) show a remarkable phenotypic

287 between endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) through the Notch pathway re

288 ivity in the aneurysmal tissues and vascular smooth muscle cells (vSMCs) was observed with DAPT (P <

289 In vascular smooth muscle cells (VSMCs), activation of Ca(2+) -perme

290 a hybrid phenotype of striated and vascular smooth muscle cells (VSMCs), we performed lineage tracin

291 ylacetamide deacetylase (AADAC), in vascular smooth muscle cells (VSMCs).

292 depend on the lineage of origin of vascular smooth muscle cells (VSMCs).

293 in the vessel wall, is mediated by vascular smooth muscle cells (VSMCs).

294 endothelial cells and alpha-SMA(+) vascular smooth muscle cells were detected within all cellular zo

295 ated from human lung tissue and human airway smooth muscle cells were treated for 2 and 1 day(s), res

296 activation and increased proliferation of PA smooth muscle cells, which contributes to remodeling of

297 tion of CaN phosphatase activity in vascular smooth muscle cells, which express MKK7gamma mRNA, enhan

298 r-272) was localized in centrosomes of human smooth muscle cells, which regulated centrosome maturati

299 14) is a GPCR also expressed on human airway smooth muscle cells, which signals to intracellular [Ca(

300 protein expression, pretreatment of vascular smooth muscle cells with the FoxO inhibitor decreased sG