ライフサイエンスコーパス: muscle cell

1 retion by lipid-loaded human vascular smooth muscle cells.

2 positioning of the mitochondrial network in muscle cells.

3 ading through gap junctions into neighboring muscle cells.

4 , and reduced percentage of severely damaged muscle cells.

5 causes damage to motor neurons and skeletal muscle cells.

6 and regulates SLO-1 function in neurons and muscle cells.

7 cture including elastin, collagen and smooth muscle cells.

8 ivergent isoforms expressed predominantly in muscle cells.

9 RNA AK017368 is highly expressed in skeletal muscle cells.

10 hat SPARC might serve a specific role within muscle cells.

11 on and enhances glucose uptake into skeletal muscle cells.

12 o inosine (A to I) RNA editing of Ctn RNA in muscle cells.

13 anslocation and glucose uptake into skeletal muscle cells.

14 which contained both macrophages and smooth muscle cells.

15 gy, and the regenerative capacity of primary muscle cells.

16 ts TGF-beta-driven differentiation of smooth muscle cells.

17 antly alter the phenotype of vascular smooth muscle cells.

18 d the production of 3-HAA in vascular smooth muscle cells.

19 p the fate of NG2(+)CD146(+) immature smooth muscle cells.

20 raluminal pressure in cerebral artery smooth muscle cells.

21 pathway in human kidney podocytes and smooth muscle cells.

22 ytes, endothelial cells, and arterial smooth muscle cells.

23 hibit contractility in demembranated cardiac muscle cells.

24 rfusion do not involve BK in vascular smooth muscle cells.

25 e macrophages, endothelial cells, and smooth muscle cells.

26 cells of nonhematopoietic lineage, including muscle cells.

27 on of other cell types such as airway smooth muscle cells.

28 apid cytoskeletal rearrangement, even in non-muscle cells.

29 n T cell subtypes and coronary artery smooth muscle cells.

30 ey moiety disrupting the physiology of heart muscle cells.

31 on and extensive population by mature smooth muscle cells.

32 including epithelial, endothelial and smooth muscle cells.

33 tPs function to antagonize IFN induction in muscle cells.

34 receptors (AChRs) in Caenorhabditis elegans muscle cells.

35 nals known as puffs in neurons and sparks in muscle cells.

36 , and proliferation in fibroblast and smooth muscle cells.

37 ld higher in isolated cerebral artery smooth muscle cells.

38 ion and relaxation, respectively, in colonic muscle cells.

39 was found in human and murine airway smooth muscle cells.

40 bunit p41ARC is a PAK1 substrate in skeletal muscle cells.

41 ctly the effect of MTM1 mutations on patient muscle cells.

42 domain activity were increased in PAH smooth muscle cells.

43 enhanced ability to differentiate to smooth muscle cells.

44 ly expressed in vascular and visceral smooth muscle cells.

45 ay a role in nuclear positioning in skeletal muscle cells [8-12].

46 c/apyrimidinic endonuclease I protect smooth muscle cells against oxidant-induced cell death.

47 ed macrophages is critical for both skeletal muscle cell and hBD-MSCs death in PIRI-CLI.

48 methods can predict the state of the cardiac muscle cell and its metabolic conditions during ischemia

49 om activated macrophages is critical in both muscle cell and stem cell death, we evaluated the recove

50 s were safe to rat pulmonary arterial smooth muscle cell and to the lungs, as evidenced by the cytoto

51 to this ACTA2 mutation in both aortic smooth muscle cells and adventitial fibroblasts may contribute

52 nm) also increased TRPM4 currents in smooth muscle cells and constricted cerebral arteries from both

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

54 tify the TMEM184A protein in vascular smooth muscle cells and endothelial cells.

55 t shock protein (HspB8) in ischemic skeletal muscle cells and enhanced ischemic muscle autophagic flu

56 ized by endothelial cells relative to smooth muscle cells and fibroblasts, demonstrating a direct rol

57 polarization to promote relaxation of smooth muscle cells and increase tissue blood flow.

58 jor KV1 channel expressed in vascular smooth muscle cells and is abundantly localized on the plasma m

59 Mural cells (vascular smooth muscle cells and pericytes) play an essential role in th

60 filament, which is specifically expressed in muscle cells and serves as a skeletal muscle differentia

61 rize individual motoneuron outputs to single muscle cells and show that the strength and reliability

62 sts of a mesenchymal wall composed of smooth muscle cells and surrounding fibrocytes of the tunica ad

63 d on two cell lines: A7r5 (rat aortic smooth muscle cells) and SH-SY5Y (human neuroblastoma cells).

64 entiated cells, including adipocytes, smooth muscle cells, and endothelial cells (EC).

65 ent stem cell-derived cardiomyocytes, smooth muscle cells, and endothelial cells (in a 2:1:1 ratio) t

66 ded the scaffold with cardiomyocytes, smooth muscle cells, and endothelial cells that had been differ

67 t epithelial cells, stromal cells and smooth muscle cells, and soluble and cell-associated growth and

68 d RRV infection in stromal cells, especially muscle cells, and that this controls local inflammation

69 ration and pathogenesis of adult human heart muscle cells, and this concept may be expanded to maturi

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

71 Muscle cells are a syncytium in which the many nuclei ar

72 Thus, sphincter muscle cells are bona fide, albeit unconventional, photo

73 Pericytes and smooth muscle cells are integral components of the brain microv

74 that the enhanced force observed when heart muscle cells are maximally activated by calcium is due t

75 ire-induced injury response, existing smooth muscle cells are the primary contributors to neointima f

76 tivated CD4 T cells connect to airway smooth muscle cells (ASMCs) in vitro via lymphocyte-derived mem

77 Airway smooth muscle cells (ASMCs) were isolated from smooth muscle bu

78 in regulating healthy primary airway smooth muscle cells (ASMCs), whereas changed expression has bee

79 en by excessive contraction of airway smooth muscle cells (ASMCs).

80 inhibiting Fgf10 expression in airway smooth muscle cells (ASMCs).

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

82 lar mechanisms responsible for airway smooth muscle cells' (aSMCs) contraction and proliferation in a

83 channel SLO-2 currents in native neurons and muscle cells between worm strains with and without BKIP-

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

85 eduction of proliferation in vascular smooth muscle cells, but given low proliferative capacity, a si

86 ctivated RhoA, ERK, and Akt in airway smooth-muscle cells, but only in the presence of TSG-6.

87 rglycemia on vascular endothelial and smooth muscle cells, but the underlying mechanisms are not full

88 nsulin-stimulated glucose uptake in skeletal muscle cells by implicating p41ARC as a new component of

89 le alpha-actin filaments in wild-type smooth muscle cells by various mechanisms activates nuclear fac

90 inhibition attenuated mouse and human smooth muscle cell calcification.

91 ed that the origin of aortic vascular smooth muscle cells can be traced back to progenitor cells that

92 2+) channels in the adjacent vascular smooth muscle cells, causing vasoconstriction.

93 le of the Abs in the pathology, we performed muscle cell coculture with the Abs.

94 al intercellular communication between local muscle cell compartments, such as PAX7 positive cells, a

95 olypeptides in regulation of vascular smooth-muscle cell contractility.

96 inhibition directly attenuates airway smooth muscle cell contraction independent of its protective im

97 Smooth muscle cell contraction significantly increased the rati

98 We monitor muscle cell contractions elicited by single motoneurons

99 icroscopy, changes in single vascular smooth muscle cell cortical actin are observed to remodel follo

100 he bleedings and severely compromises smooth muscle cell coverage of the vasculature leading to embry

101 In cardiomyocytes and smooth muscle cells, cyclic AMP (cAMP) and subsequent calcium (

102 rete AGE-albumin, which induced the skeletal muscle cell death and injected hBD-MSCs in PIRI-CLI thro

103 ased hydrogen sulfide production, and smooth muscle cell dedifferentiation in vitro.

104 ed current in Xenopus oocytes, or C. elegans muscle cells, depends on NRAP-1 and that recombinant NRA

105 lone is not sufficient for regulating smooth muscle cell development.

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

107 variants act through a mechanism of impaired muscle cell differentiation and tissue formation during

108 rovides the positional cue and allows smooth muscle cell differentiation induced by Hedgehog signalin

109 uppresses TGF-beta/Smad3 signaling in smooth muscle cell differentiation of mesenchymal progenitor ce

110 e activity is necessary for each step of the muscle cell differentiation program in vitro.

111 During C2C12 muscle cell differentiation, nesprin-1 levels are increa

112 n factor ZNF148 plays a direct role in human muscle cell differentiation.

113 COUP-TFII expression is required for proper muscle cell differentiation.

114 main microtubule-organizing center (MTOC) in muscle cells due to the accumulation of centrosomal prot

115 vironments, and that it is highly induced in muscle cells during systemic inflammation.

116 etazoan-specific traits, such as neurons and muscle cells, either evolved once along the metazoan ste

117 oproteinase-3 expression and vascular smooth muscle cell elastin production, both important factors i

118 ime imaging was performed in vascular smooth muscle cells expressing a FRET-biosensor comprising the

119 lood pressure, which was dependent on smooth muscle cell expression of Panx1 and independent of NR3C2

120 atory network determines cardiac or skeletal muscle cell fates.

121 y and beating rate and suppressed the smooth muscle cell formation.

122 A discrete population of smooth muscle cells forms in the embryo and is postnatally sust

123 Aortic tissue and explanted smooth muscle cells from Acta2(-/-) aortas show increased produ

124 markedly reduced in isolated vascular smooth muscle cells from CAD arterioles, although mRNA or total

125 In smooth muscle cells from cerebral arteries, increasing intralum

126 nd cocaine was confirmed in pulmonary smooth muscle cells from cocaine injected HIV-transgenic rats a

127 reteric epithelium and differentiated smooth muscle cells from E16.5 onwards.

128 Airway smooth muscle cells from healthy and severe asthmatic subjects

129 Smooth-muscle cells from mouse tracheas were assayed in vitro f

130 Mechanistically, the inefficient muscle cell fusion correlates well with the transcriptio

131 At the cellular level, heart muscle cells generate higher force when stretched, but d

132 Airway smooth muscle cells generated pro-MMP-1, which was proteolytica

133 sponse to arterial injuries, existing smooth muscle cells give rise to neointima, but on extensive da

134 In vascular smooth muscle cells, GPR75-20-HETE pairing is associated with G

135 functions, including endothelial and smooth muscle cell growth, proliferation, and migration; angiog

136 radation in facilitating human aortic smooth muscle cell (HASMC) proliferation.

137 In addition, studies on human aortic smooth muscle cells (HASMCs) demonstrated membrane hyperpolariz

138 kdown of T-cadherin from human aortic smooth muscle cells (HASMCs) with synthetic phenotype significa

139 In cultured human airway smooth muscle cells (hASMCs), TGF-beta pre-treatment enhanced t

140 e markers in co-cultured human aortic smooth muscle cells (HASMCs).

141 mia-associated RhoGEF in human aortic smooth muscle cells (HASMCs).

142 challenge studies show that vascular smooth muscle cells have an intrinsic ability to reduce oxidize

143 to reduced migration only in vascular smooth muscle cells homozygous for the nonrisk allele.

144 Histopathologic findings of smooth muscle cell hypertrophy and stroma-like cells, consisten

145 Loss of smooth muscle cell hypoxia inducible factor-1alpha underlies in

146 herosclerotic plaques and in vascular smooth muscle cells in culture.

147 udy was to determine whether vascular smooth muscle cells in cultured microvascular networks maintain

148 e ischemic cascade: selective loss of smooth muscle cells in juveniles but not adults shortly after o

149 n identified spinal motoneurons and skeletal muscle cells in larval zebrafish.

150 ectively marks pericytes and vascular smooth muscle cells in multiple organs of adult mouse.

151 Nitrovasodilators relax vascular smooth-muscle cells in part by modulating the interaction of th

152 splanted cells were made from colonic smooth muscle cells in recipient mice.

153 The vast majority of Hofstenia muscle cells in regions tested express PCGs, suggesting

154 chondrial morphology of mouse C2C12 skeletal muscle cells in response to heat acclimation and heat sh

155 asts, endothelial cells, and vascular smooth muscle cells in the absence of serum.

156 ed on endothelial cells and synthetic smooth muscle cells in the aortic intima.

157 Extensive proliferation of immature smooth muscle cells in the primitive embryonic dorsal aorta est

158 a single origin of the gut, nerve cells, and muscle cells in the stem lineage of eumetazoans (bilater

159 on in glucose-stimulated human aortic smooth muscle cells in vitro.

160 d monoclonal antibodies (DMAbs), produced by muscle cells in vivo, potentially allow the prevention o

161 clonal antibodies (DMAbs) can be produced by muscle cells in vivo, potentially allowing prevention or

162 ell myogenesis (transformation into skeletal muscle cells) includes several stages characterized by t

163 s argued that the functional response of the muscle cell, including the speed of its contraction and

164 erentiation of primary human vascular smooth muscle cells increased DRP1 expression.

165 mooth muscle alpha-actin filaments in smooth muscle cells increases reactive oxygen species levels, a

166 ate muscle catabolism via activating TLR4 on muscle cells independent of immune responses.

167 In primary human skeletal muscle cells, inhibition and overexpression strategies d

168 the transdifferentiation of vascular smooth muscle cells into osteoblast-like cells, we investigated

169 y that in its absence, contraction of smooth muscle cells is impaired.

170 Contraction of skeletal muscle cells is initiated by a well-known signaling path

171 reover, mechanical integrity of vascular and muscle cells is partly dependent on caveolae [13-15].

172 hich encompass pericytes and vascular smooth muscle cells, is a hallmark of CADASIL and other SVDs, i

173 sient cation currents that depolarize smooth muscle cells, leading to vasoconstriction.

174 dothelial communication to mesenteric vessel muscle cells, leading to vasoconstriction.

175 ut that loss of all Tln forms from the heart-muscle cell leads to myocyte instability and a dilated c

176 ealed that loss of YY1AP1 in vascular smooth muscle cells leads to cell cycle arrest with decreased p

177 an T cell subsets and coronary artery smooth muscle cells link variants associated with autoimmune an

178 hesized that insulin resistance in lymphatic muscle cells (LMCs) affects cell bioenergetics and signa

179 idence of higher biological activity (smooth muscle cell loss and fibrin deposition) in the FP-PES co

180 erent origins, including endothelial, smooth muscle cells, macrophages, hepatocytes, adipocytes, skel

181 Personalized heart muscle cells made from stem cells in the laboratory coul

182 revealed that pericytes and vascular smooth muscle cells maintained their identity in aging and dive

183 otor nerve triggers an action potential in a muscle cell membrane, a transient increase of intracellu

184 In vivo, vascular smooth muscle cell/mesangial cell-specific overexpression of No

185 s substantially attenuated BI-induced smooth muscle cell migration and proliferation, resulting in re

186 phenotypes was analyzed with vascular smooth muscle cell migration assays and platelet aggregation an

187 ABSTRACT: Smooth muscle cells (myocytes) of resistance-size arteries expr

188 auxiliary beta1 subunits in arterial smooth muscle cells (myocytes).

189 el isoforms are expressed in arterial smooth muscle cells (myocytes).

190 We show that muscle cells of syndapin III KO mice show severe reducti

191 n fibroblastic, epithelial, endothelial, and muscle cells of the human intestinal tract and is activa

192 ase in the proliferation of pulmonary smooth muscle cells on exposure to HIV-proteins and/or cocaine

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

194 Neurons pass signals to other neurons, muscle cells, or gland cells at specialized junctions, t

195 MSTN-edited fry had more muscle cells (p < 0.001) than controls, and the mean bod

196 al epithelial (P = 0.0002) and airway smooth muscle cells (P = 0.0352) of patients with asthma, with

197 terized by excessive pulmonary artery smooth muscle cell (PASMC) proliferation, migration, and apopto

198 ful conditions, pulmonary artery (PA) smooth muscle cells (PASMCs) exhibit a "cancer-like" pro-prolif

199 In parallel, pulmonary arterial smooth muscle cells (PASMCs) from Cox4i2(-/-) mice showed no hy

200 ole of HIF-1alpha in pulmonary artery smooth muscle cells (PASMCs) remains controversial.

201 the proliferation of pulmonary artery smooth muscle cells (PASMCs), and inhibition of phosphodiestera

202 ADAM10 and ADAM17 in pulmonary artery smooth muscle cells (PASMCs).

203 Here, we combine single-cell PCR, whole muscle cell patch clamp, motility phenotyping (Worminato

204 cle dystrophies reduced the ability of human muscle cell precursors to adapt to substrates of differe

205 NC complexes are crucial for the response of muscle cell precursors to the rigidity of their environm

206 tein expression were decreased in PAH smooth muscle cells (primary culture).

207 ng the adhesion of monocytic cells to smooth muscle cells producing an inflammatory matrix.

208 ped less neointimal hyperplasia, less smooth muscle cell proliferation, and had fewer infiltrating ce

209 plication for selective inhibition of smooth muscle cell proliferation, enhancement of endothelial re

210 RT6 depletion in cardiac as well as skeletal muscle cells promotes myostatin (Mstn) expression.

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

212 ession and pHi regulation in vascular smooth muscle cells provides an insight into the molecular mech

213 nd knockdown of their receptor in pharyngeal muscle cells reduces growth.

214 cruitment to the plasma membrane of skeletal muscle cells requires F-actin remodeling.

215 mouse DUX and human DUX4 in mouse and human muscle cells, respectively, activate genes associated wi

216 Knock-down of Csrp2bp in smooth muscle cells resulted in reduced smooth muscle gene expr

217 harmacological inhibition in vascular smooth muscle cells reveal that cytochrome b5 reductase 3 expre

218 l sGC heme iron reductase in vascular smooth muscle cells, serving as a critical regulator of cGMP pr

219 Incubation of S1P with airway smooth muscle cells significantly increased contractility.

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

221 Vascular smooth muscle cell (SMC) composes the majority of the vascular

222 horacic aortic disease either disrupt smooth muscle cell (SMC) contraction or adherence to an impaire

223 Smooth muscle cell (SMC) death contributes to plaque destabiliz

224 Smooth muscle cell (SMC) differentiation is essential for vascu

225 te-mapping approaches combined with a smooth muscle cell (SMC) epigenetic lineage mark, we report tha

226 measured primary human aortic single smooth muscle cell (SMC) forces using nanonet force microscopy

227 tablished expandable cell lines under smooth muscle cell (SMC) growth conditions that retained a pati

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

229 Vascular smooth muscle cell (SMC) proliferation and endothelial cell (EC

230 f hyperglycemic ApoE(-/-) mice; also, smooth muscle cell (SMC), macrophage and leukocyte abundance wa

231 ell (BmxCreER(T2)-driven)-specific or smooth muscle cell (SMC, SmmhcCreER(T2)- or TaglnCre-driven)-sp

232 voltage-dependent Ca(2+) channels in smooth muscle cells (SMC) provide the Ca(2+) that triggers cont

233 mulated proliferation of human venous smooth muscle cells (SMC) was measured by a DNA-binding assay,

234 cells in HMGA2-uterine leiomyoma were smooth muscle cells (SMC) with HMGA2 overexpression.

235 annels was observed in ICC but not in smooth muscle cells (SMC).

236 Vascular smooth muscle cells (SMCs) and endothelial cells (ECs) are in c

237 ibited proliferation and migration of smooth muscle cells (SMCs) and promoted the tube formation from

238 NC) only differentiates into vascular smooth muscle cells (SMCs) around those aortic arches destined

239 Vascular smooth muscle cells (SMCs) can resist and repair artery damage,

240 GTPase-activating protein ARHGAP42 in smooth muscle cells (SMCs) controls blood pressure by inhibitin

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

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

243 differentiation into fibroblasts and smooth muscle cells (SMCs) is also described.

244 In mice, MR deficiency in smooth muscle cells (SMCs) protected against kidney IR injury.

245 Our MFS-hiPSC-derived smooth muscle cells (SMCs) recapitulated the pathology seen in

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

247 arrays on the phenotypically distinct smooth muscle cells (SMCs) within the rat anorectrum, we identi

248 rated TLR7 expression in macrophages, smooth muscle cells (SMCs), and endothelial cells from mouse at

249 ential layers of elastic lamellae and smooth muscle cells (SMCs), and many arterial diseases are char

250 ion of 5-HTT induced proliferation of smooth muscle cells (SMCs); however, this phenotype could be re

251 argeted mice with a cardiomyocyte- or smooth muscle cell-specific deletion of the BK (CMBK or SMBK kn

252 myoD is required for formation of a specific muscle cell subset: the longitudinal fibres, oriented al

253 (+) cells comprise a subpopulation of smooth muscle cells surrounding airway epithelia and promote ai

254 for muscle growth, myofiber maturation, and muscle cell survival and that alterations in its activit

255 ration site) signaling and regulating smooth muscle cell survival, as well as differentiation in adva

256 s through inhibition of APC, ensuring smooth muscle cell survival.

257 higher level of Ifn-beta gene expression in muscle cells than did CE(NiP) infection, consistent with

258 uman primary vascular endothelial and smooth muscle cells that endogenously express RXFP1, ML290 incr

259 stablishes the long-lived lineages of smooth muscle cells that make up the wall of the adult aorta.

260 In airway smooth muscle cells, these Ca(2+) oscillations are caused by cy

261 promotes EZH2 degradation in differentiating muscle cells through phosphorylation of threonine 372.

262 Exposure of human coronary artery smooth muscle cells to cigarette smoke extract led to induction

263 ich reflects the intrinsic ability of smooth muscle cells to contract in response to increases in int

264 he popliteal fossa of mice and removed their muscle cells to isolate intact LEC tubes (LECTs).

265 vation, promotes glucose uptake into fat and muscle cells to lower postprandial blood glucose, an enf

266 etal muscle during ageing and the ability of muscle cells to respond to increased ROS becomes defecti

267 x10(+) stem cells differentiated into smooth muscle cells to stabilize functional microvessels.

268 that dyW-/- muscles fail to generate enough muscle cells to sustain fetal myofiber growth.

269 without transdifferentiation to multiple non-muscle cell types and tested dystrophin restoration in m

270 ro (macrophages, endothelial cells, skeletal muscle cells under normal and hypoxia serum starvation c

271 DRP1 inhibition in human smooth muscle cells undergoing osteogenic differentiation atten

272 xperiments were performed with aortic smooth muscle cells using inhibitor screening, small interferin

273 Vascular smooth muscle cell (VSMC) activation in response to injury play

274 Vascular smooth muscle cell (VSMC) apoptosis precipitates AAA formation,

275 hophysiologic stimulation of vascular smooth muscle cell (VSMC) migration and proliferation.

276 um ([Ca(2+)]cyt) dynamics in vascular smooth muscle cells (VSMC).

277 a potent HIF-1 activator in vascular smooth muscle cells (VSMC).

278 erivascular cells, including vascular smooth muscle cells (vSMCs) and pericytes, are involved in new

279 xpressed in the cytoplasm of vascular smooth muscle cells (VSMCs) and tubular epithelial cells, with

280 proliferative and migratory vascular smooth muscle cells (VSMCs) are quite intricate with many chann

281 endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) converted 17-HDHA to SPMs, includin

282 J) along the borders between vascular smooth muscle cells (VSMCs) in the pressurized rat superior cer

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

284 Specific ablation of Plk1 in vascular smooth muscle cells (VSMCs) led to reduced arterial elasticity,

285 oliferation and migration of vascular smooth muscle cells (VSMCs) or endothelial cell (ECs) promote o

286 roRNAs are key regulators of vascular smooth muscle cells (VSMCs) phenotypic switch, one of the main

287 ABSTRACT: In vascular smooth muscle cells (VSMCs), stimulation of canonical transient

288 In vascular smooth muscle cells (VSMCs), stimulation of SOCs composed of ca

289 e that it may also stimulate vascular smooth muscle cells (VSMCs), thereby contributing to vasoregula

290 ll-cell adhesion molecule in vascular smooth muscle cells (VSMCs).

291 lammatory gene expression in vascular smooth muscle cells (VSMCs).

292 vessels with recruitment of vascular smooth muscle cells; VSMCs) in the presence of enhanced flow.

293 e, and bronchoscopy, and their airway smooth muscle cells were grown in culture.

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

295 The structure and function of muscle cells, which contain hundreds of nuclei, have bee

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

297 arterioles were aberrantly covered by smooth muscle cells, with increased interprocess spacing and ha

298 on in a small subset of mouse iris sphincter muscle cells, with the light-induced contractile signal

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

300 entiating AngII signaling in vascular smooth muscle cells without an increase in the exogenous levels