ライフサイエンスコーパス: vascular smooth muscle

1 stiffness of individual elastic lamellae and vascular smooth muscle.

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

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

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

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

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

7 the parotid, which was not myoepithelial or vascular smooth muscle.

8 ncover the mechanism of action of RhoBTB1 in vascular smooth muscle.

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

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

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

12 ulating the variant were differentiated into vascular smooth muscle and endothelial cells that demons

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

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

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

16 uch hyperpolarization decreases pericyte and vascular smooth muscle [Ca(2+)](i) levels, thereby relax

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

18 Vascular smooth muscle cell (SMC) composes the majority

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

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

21 Vascular smooth muscle cell (SMC) proliferation and endo

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

23 Vascular smooth muscle cell (VSMC) activation in respons

24 established a role for miRNAs in regulating vascular smooth muscle cell (VSMC) activity.

25 Vascular smooth muscle cell (VSMC) apoptosis occurs duri

26 Vascular smooth muscle cell (VSMC) apoptosis precipitate

27 diated cholesterol management on primary rat vascular smooth muscle cell (VSMC) biomechanics.

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

29 tudy aimed to determine the role of SIRT1 in vascular smooth muscle cell (vSMC) calcification within

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

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

32 Vascular smooth muscle cell (VSMC) function is regulated

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 es vascular calcification (VC) by increasing vascular smooth muscle cell (VSMC) osteogenic differenti

37 Vascular smooth muscle cell (VSMC) phenotype switching f

38 ontrols gene expression patterns that define vascular smooth muscle cell (VSMC) phenotype.

39 Vascular smooth muscle cell (VSMC) phenotypic conversion

40 tudy, we aim to determine the role of YY1 in vascular smooth muscle cell (VSMC) phenotypic modulation

41 actor beta-1 (TGFbeta1) is a major driver of vascular smooth muscle cell (VSMC) phenotypic switching,

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

43 Vascular smooth muscle cell (VSMC) remodeling is a patho

44 the link between mitochondrial dynamics and vascular smooth muscle cell (VSMC) senescence.

45 his study, we aim to investigate the role of vascular smooth muscle cell (VSMC) TFEB in the developme

46 al to the propagation of seizures in SE, and vascular smooth muscle cell (VSMC) TRPC3 channels partic

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

48 emonstrates and evaluates the changes in rat vascular smooth muscle cell biomechanics following stati

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

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

51 ediated cholesterol depletion remodels total vascular smooth muscle cell cytoskeletal orientation tha

52 he human gene encoding NOTCH3 and results in vascular smooth muscle cell degeneration, stroke, and de

53 to microcalcifications formed by calcifying vascular smooth muscle cell derived extracellular vesicl

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

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

56 L-2 initiates signaling pathways and impacts vascular smooth muscle cell function.

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

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

59 ne model lacks the key anatomical feature of vascular smooth muscle cell loss seen in HGPS patients,

60 ediated cholesterol depletion may coordinate vascular smooth muscle cell migration and adhesion to di

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

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

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

64 nd that expression of IL-2Ralpha varies with vascular smooth muscle cell phenotype.

65 ine circulations in terms of endothelial and vascular smooth muscle cell plasticity.

66 signaling is associated with an increase in vascular smooth muscle cell proliferation and changes in

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 (2)S (CBS, CSE and 3MST) showed reduction of vascular smooth muscle cell proliferation.

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

71 pelling evidence of coordinated reduction in vascular smooth muscle cell stiffness and actin cytoskel

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

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

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

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

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

77 lacetamide deacetylase (AADAC) expression in vascular smooth muscle cells (dVSMCs) differentiated fro

78 -regulation in primary human coronary artery vascular smooth muscle cells (HCASMCs).

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

80 gk-Cul3Delta9) and the other specifically in vascular smooth muscle cells (SM22-Cul3Delta9).

81 ole in early stage of atherosclerosis and on vascular smooth muscle cells (SMC) remain to be fully el

82 Vascular smooth muscle cells (SMCs) and endothelial cell

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

84 In response to various stimuli, vascular smooth muscle cells (SMCs) can de-differentiate

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

86 In vascular smooth muscle cells (SMCs) grown under calcifyi

87 Vascular smooth muscle cells (SMCs) produce the layered

88 Vascular smooth muscle cells (SMCs) synthesize extracell

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

90 ay arise from a subset of "dedifferentiated" vascular smooth muscle cells (SMCs) which proliferate in

91 he Cygb-mediated NO dioxygenation process in vascular smooth muscle cells (SMCs), and the requisite r

92 tors of contractility and differentiation in vascular smooth muscle cells (SMCs), but the specific fu

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

94 ritical splicing regulator in differentiated vascular smooth muscle cells (SMCs).

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

96 ust encourage the infiltration and growth of vascular smooth muscle cells (SMCs).

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

98 In vascular smooth muscle cells (VMSCs), stimulation of Ca(

99 amined by IHC against macrophages, collagen, vascular smooth muscle cells (VSMC) and matrix metallopr

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

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

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

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

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

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

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

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

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

109 Vascular smooth muscle cells (VSMCs) are a major cell ty

110 Vascular smooth muscle cells (VSMCs) are critical in the

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

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

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

114 Vascular smooth muscle cells (VSMCs) can be derived in l

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

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

117 )PDGFRbeta(+) cells, a signature shared with vascular smooth muscle cells (VSMCs) derived from mesenc

118 Although the role of several miRNAs in vascular smooth muscle cells (VSMCs) has been extensivel

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

120 Vascular smooth muscle cells (VSMCs) in the normal arter

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

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

123 PLD2 deficiency inhibits migration of vascular smooth muscle cells (VSMCs) into the intima in

124 tion between SCAP and foam cell formation in vascular smooth muscle cells (VSMCs) is poorly understoo

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

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

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

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

129 Vascular smooth muscle cells (VSMCs) play critical roles

130 extent of mechanical fluctuations applied to vascular smooth muscle cells (VSMCs) regulates mitochond

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

132 Vascular smooth muscle cells (VSMCs) show a remarkable p

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

134 ignaling between endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) through the Notch p

135 lytic activity in the aneurysmal tissues and vascular smooth muscle cells (vSMCs) was observed with D

136 In vascular smooth muscle cells (VSMCs), activation of Ca(2

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

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

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

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

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

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

143 cribed as a hybrid phenotype of striated and vascular smooth muscle cells (VSMCs), we performed linea

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

145 mutation depend on the lineage of origin 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 crystals in the vessel wall, is mediated by vascular smooth muscle cells (VSMCs).

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

150 erase, arylacetamide deacetylase (AADAC), in vascular smooth muscle cells (VSMCs).

151 SCAP knockdown in vascular smooth muscle cells alleviates atherosclerosis

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

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

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

155 , E-selectin, MCP-1) in endothelial cells or vascular smooth muscle cells and decreased monocytes adh

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

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

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

161 on between endothelial cells and surrounding vascular smooth muscle cells and pericytes.

162 hese findings were accompanied with elevated vascular smooth muscle cells and reduced MMPs.

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

164 ed with our work showing that IL-2 surrounds vascular smooth muscle cells by association with perleca

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

166 at has aggregated within the mitochondria of vascular smooth muscle cells can drive an hour-long disr

167 othesized that abnormal proliferation of the vascular smooth muscle cells causes the marked tortuosit

168 We now report that vascular smooth muscle cells express all three subunits

169 ciation with perlecan, led us to ask whether vascular smooth muscle cells express an IL-2R.

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

171 In mouse vascular smooth muscle cells expressing both alpha- and

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

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

174 Compared with renal vascular smooth muscle cells from Add3 transgenic rats,

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

176 Vascular smooth muscle cells going from a proliferative

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

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

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

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

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

182 p was found to be expressed predominantly on vascular smooth muscle cells in lesions of athero-prone

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

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

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

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

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

188 We also studied glomeruli and primary renal vascular smooth muscle cells isolated from these rats.

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

192 fractions prepared from the kidney and renal vascular smooth muscle cells of FHH rats was associated

193 enes and gene signatures of mesangial cells, vascular smooth muscle cells of the afferent and efferen

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 osed of circumferentially arranged layers of vascular smooth muscle cells that are separated by conce

198 TRPC6 regulates phenotypic switching of vascular smooth muscle cells through plasma membrane pot

199 nts of the Kv7.4 and Kv7.5 alpha-subunits in vascular smooth muscle cells to determine which componen

200 related changes in migration and adhesion of vascular smooth muscle cells to extracellular matrix pro

201 of the transcriptional control of CPI-17 in vascular smooth muscle cells under inflammatory conditio

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

203 n external tensile force was applied to live vascular smooth muscle cells using a fibronectin-functio

204 g CD31(+) endothelial cells and alpha-SMA(+) vascular smooth muscle cells were detected within all ce

205 mRNA and protein expression, pretreatment of vascular smooth muscle cells with the FoxO inhibitor dec

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

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

208 In primary vascular smooth muscle cells, aging reduced proliferatio

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

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

211 tissues and cell types, including platelets, vascular smooth muscle cells, and neuronal cells.

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

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

214 n vascular cells, like endothelial cells and vascular smooth muscle cells, cardiac myocytes and infla

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

216 hed the pro-inflammatory actions of TWEAK on vascular smooth muscle cells, decreasing NF-kB activatio

217 f the main arterial cell types: fibroblasts, vascular smooth muscle cells, endothelial cells (ECs), a

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

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

220 AVPR1A is widely expressed, including in vascular smooth muscle cells, kidney, myocardium and bra

221 ng into nonmyocyte cardiac lineages, such as vascular smooth muscle cells, pericytes, and fibroblasts

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 he inhibition of CaN phosphatase activity in vascular smooth muscle cells, which express MKK7gamma mR

226 ses in intracellular Ca(2+) concentration in vascular smooth muscle cells.

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

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

229 capillary endothelial cells, pericytes, and vascular smooth muscle cells.

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

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

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

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

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

235 ms in cardiomyocytes compared to neurons and vascular smooth muscle cells.

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

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

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

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

240 d cells adjacent to the PAA endothelium into vascular smooth muscle cells.

241 (8.6 +/- 1.3% of vessels with recruitment of vascular smooth muscle cells; VSMCs) in the presence of

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

243 othelin-like 1 (SMTNL1) protein in mediating vascular smooth muscle contractile responses to intralum

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

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

246 Vascular smooth muscle contraction-related genes were en

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

248 d myosin light chain, which is essential for vascular smooth muscle contraction.

249 ugs that can reduce inflammation and inhibit vascular smooth muscle contraction.

250 Pannexin 1 (PANX1)-mediated ATP release in vascular smooth muscle coordinates alpha1-adrenergic rec

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

252 imal hyperplasia, diseases linked to loss of vascular smooth muscle differentiation.

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

254 de that RhoBTB1 protected from hypertension, vascular smooth muscle dysfunction, and arterial stiffne

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

256 sing PPARgamma dominant negative mutation in vascular smooth muscle exhibit RhoBTB1-deficiency and hy

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

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

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

260 ependent dilation, as well as alterations in vascular smooth muscle function, directly contribute to

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

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

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

264 We show that Poldip2 deficiency in vascular smooth muscle in vitro and in vivo induces the

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

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

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

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

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

270 ribed various aspects of the endothelial and vascular smooth muscle layers in these diseases, the out

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

272 LRP6 restrains vascular smooth muscle lineage noncanonical signals that

273 ed to exaggerated calcium signaling and high vascular smooth muscle mechanosensitivity, which could e

274 Vascular smooth muscle NOX4, the common denominator of i

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

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

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

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

279 ne 3',5'-monophosphate (cGMP) and subsequent vascular smooth muscle relaxation.

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

281 ffect the responses to capsaicin revealing a vascular smooth muscle-restricted signalling mechanism.

282 ated that gain-of-function KATP mutations in vascular smooth muscle resulted in cardiac remodeling.

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

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

285 calcification genes (proteins) to the human vascular smooth muscle-specific protein-protein interact

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

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

288 releases vasoactive compounds that regulate vascular smooth muscle tone.

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

290 RATIONALE: Vascular smooth muscle turnover has important implicatio

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

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

293 H-related protein] receptor) is expressed in vascular smooth muscle (VSM) and increased VSM PTH1R sig

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

295 Vascular smooth muscle (VSM) expresses calcium/calmoduli

296 e SUR2 and Kir6.1 subunits, respectively, of vascular smooth muscle (VSM) KATP channels.

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 ponses were mediated at the level of uterine vascular smooth muscle, whereas, in pregnant rats, PVAT-

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