ライフサイエンスコーパス: vascular smooth muscle

1 CaV) channel type in myocytes in cardiac and vascular smooth muscle.

2 (AVPR)2 in the kidney and AVP receptor 1A in vascular smooth muscle.

3 cle vessels lack the normal association with vascular smooth muscle.

4 riety of cell lineages, including airway and vascular smooth muscle.

5 ns with alpha1-adrenergic receptors (ARs) in vascular smooth muscle.

6 r of the function and expression of Kv7.4 in vascular smooth muscle.

7 ting the function and expression of Kv7.4 in vascular smooth muscle.

8 f ATP-sensitive potassium (KATP) channels in vascular smooth muscle.

9 stiffness of individual elastic lamellae and vascular smooth muscle.

10 onent of total stiffness not attributable to vascular smooth muscle activation, is severalfold lower

11 Mutations in vascular smooth muscle alpha-actin (SM alpha-actin), enc

12 Point mutations in vascular smooth muscle alpha-actin (SM alpha-actin), enc

13 nsistent with incomplete development of both vascular smooth muscle and compact myocardium at later d

14 tides promote migration and proliferation of vascular smooth muscle and endothelial cells via P1 and

15 ariants at this locus in primary cultures of vascular smooth muscle and endothelial cells.

16 Epac increases STOC activity in contractile vascular smooth muscle and show that a critical step is

17 s that migrate normally, but fail to produce vascular smooth muscle, and Notch target genes such as J

18 R-133b, and miR-211 have direct roles in the vascular smooth muscle calcification induced by high pho

19 on include pancreatic beta- and delta-cells, vascular smooth muscle, cardiac atrium, gastric antrum/p

20 Vascular smooth muscle cell (SMC) composes the majority

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

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

23 Vascular smooth muscle cell (SMC) proliferation and endo

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

25 Vascular smooth muscle cell (VSMC) activation in respons

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

27 Vascular smooth muscle cell (VSMC) apoptosis occurs duri

28 Vascular smooth muscle cell (VSMC) apoptosis precipitate

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

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

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

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

33 9 expression, and thinning of the periportal vascular smooth muscle cell (VSMC) layer, which are appa

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

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

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

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

38 Vascular smooth muscle cell (VSMC) phenotypic conversion

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

57 Meanwhile, vascular smooth muscle cell lymphotoxin beta receptors (

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 Vascular smooth muscle cell-specific overexpression of R

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

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

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

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

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

83 Vascular smooth muscle cells (SMCs) and endothelial cell

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

120 Vascular smooth muscle cells (VSMCs) cultured from shGRK

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 In vascular smooth muscle cells and renal tubular epithelia

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

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

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

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

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

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

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

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

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

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

173 Vascular smooth muscle cells from chr4(Delta70kb/Delta70

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

198 2 in endothelial cells and angiopoietin-1 in vascular smooth muscle cells through nuclear factor-kapp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

237 7.5 heteromers are endogenously expressed in vascular smooth muscle cells.

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

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

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

241 4/7.5 channels exogenously expressed in A7r5 vascular smooth muscle cells.

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

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

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

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

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

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

248 (8.6 +/- 1.3% of vessels with recruitment of vascular smooth muscle cells; VSMCs) in the presence of

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

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

251 ely active ZIPK is involved in regulation of vascular smooth muscle contraction through direct phosph

252 l adhesion, transforming growth factor-beta, vascular smooth muscle contraction, and the hedgehog and

253 Vascular smooth muscle contraction-related genes were en

254 esponsible for lysophosphatidic acid-induced vascular smooth muscle contraction.

255 show that CD146 is transiently expressed in vascular smooth muscle development.

256 of adenosine, suggesting that distension of vascular smooth muscles does not explain blunted sympath

257 sium (BKCa) channels are key determinants of vascular smooth muscle excitability.

258 Acquisition and maintenance of vascular smooth muscle fate are essential for the morpho

259 ggest impairment in BKCa channel function in vascular smooth muscle from diabetic patients through un

260 whether similar alterations occur in native vascular smooth muscle from humans with type 2 diabetes

261 In this study, we evaluated BKCa function in vascular smooth muscle from small resistance adipose art

262 as biaxial tests for identifying changes in vascular smooth muscle function.

263 KATP channels in vascular smooth muscle have a well-defined role in regul

264 a role in controlling membrane potential in vascular smooth muscle, have certain members that are re

265 t the 12 new loci point to genes involved in vascular smooth muscle (IGFBP3, KCNK3, PDE3A and PRDM6)

266 Pressure-induced changes in global vascular smooth muscle intracellular Ca(2+) (using Fura-

267 Selective expression of TSPAN2 in vascular smooth muscle is independently regulated by TGF

268 dominant mutations in the NOTCH3 receptor in vascular smooth muscle, is a genetic paradigm of small v

269 gnal transduction-mediated responsiveness of vascular smooth muscle Kv7 channel subunits to cAMP/PKA

270 between NO and O2 (-) production seen by the vascular smooth muscle layer of terminal arterioles.

271 y malformed blood vessels that lack a mature vascular smooth muscle layer.

272 'gliotransmitters' which act on neurons and vascular smooth muscle, led to the idea that astrocytes

273 y differentiated pericytes, but by a coat of vascular smooth muscle-like cells and a thickened basal

274 drogenic programs, alkaline phosphatase, and vascular smooth muscle lineage calcification.

275 LRP6 restrains vascular smooth muscle lineage noncanonical signals that

276 ein receptor-related protein 6 (LRP6) in the vascular smooth muscle lineage of male low-density lipop

277 not USF2 supports OPN expression in LRP6-VKO vascular smooth muscle lineage, and immunoprecipitation

278 Vascular smooth muscle NOX4, the common denominator of i

279 Kv1.5 channels in vascular smooth muscle play a critical role in coupling

280 perglycemia results in hypercontractility of vascular smooth muscle possibly due to increased activat

281 iption factor Runx2, increased expression of vascular smooth muscle protein 22-alpha, and restored ao

282 rpolarization of the endothelium coordinates vascular smooth muscle relaxation along resistance arter

283 n directly activated by cAMP (Epac), induces vascular smooth muscle relaxation by increasing the acti

284 yosin cross-bridging and force generation in vascular smooth muscle required for physiological vasore

285 , as well as changes in both endothelial and vascular smooth muscle signalling, differ in muscle of d

286 dissections (TAAD) are missense mutations in vascular smooth muscle (SM) alpha-actin encoded by ACTA2

287 y developed mice that overexpress p22phox in vascular smooth muscle, tg(sm/p22phox), which have incre

288 Similarly, adaptations of the vascular smooth muscle that occur with advancing age are

289 widely mammalian cells, including epithelia, vascular smooth muscle tissue, electrically excitable ce

290 releases vasoactive compounds that regulate vascular smooth muscle tone.

291 characterize the dynamics and mechanisms of vascular smooth muscle turnover from the earliest stages

292 RATIONALE: Vascular smooth muscle turnover has important implicatio

293 ator-induced second messenger cAMP can relax vascular smooth muscle via its effector, exchange protei

294 RATIONALE: Decreasing Ca(2+) sensitivity of vascular smooth muscle (VSM) allows for vasodilation wit

295 rge to increase phosphorylation of myosin in vascular smooth muscle (VSM) cells, causing persistent c

296 Vascular smooth muscle (VSM) expresses calcium/calmoduli

297 nase II delta-isoform (CaMKIIdelta) promotes vascular smooth muscle (VSM) proliferation, migration, a

298 eceptor tyrosine kinases highly expressed in vascular smooth muscle (VSM).

299 In vascular smooth muscle, which controls blood flow by con

300 F-1 augments synthesis of collagen type I in vascular smooth muscle, which may play an important role