ライフサイエンスコーパス: smooth muscle

1 gy-dynamic but not fully differentiated from smooth muscle.

2 of individual elastic lamellae and vascular smooth muscle.

3 erties and the resting membrane potential of smooth muscle.

4 on bradykinin-induced contraction, in airway smooth muscle.

5 iveness: the excessive contraction of airway smooth muscle.

6 c field stimulation (EFS) in bovine tracheal smooth muscle.

7 ation of RLC phosphorylation in tonic airway smooth muscle.

8 apidity of pCPI-17 inactivation in mammalian smooth muscles.

9 f striated muscles and attachment plaques of smooth muscles.

10 oth muscle actin, myosin heavy chain 11, and smooth muscle 22 alpha.

11 ion also reduced hepatic expression of alpha-smooth muscle actin (0.19 +/- 0.007-fold compared with c

12 Interestingly, LPS down-modulated alpha-smooth muscle actin (activated HSC marker) and collagen

13 The expression of alpha-smooth muscle actin (alpha-SMA) and Collagen I were redu

14 ssociated with increased expression of alpha-smooth muscle actin (alpha-SMA) and collagen in fibrotic

15 ted the induction of activation marker alpha-smooth muscle actin (alpha-SMA) in rat and mouse HSCs.

16 Alpha-smooth muscle actin (alpha-SMA) is a marker of activated

17 n of EMT resulted in the generation of alpha-smooth muscle actin (alpha-SMA)-positive myofibroblasts

18 osition, immune cell infiltration, and alpha-smooth muscle actin (alpha-SMA)-positive myofibroblasts.

19 ells were enriched in proximity to the alpha-smooth muscle actin (alpha-SMA+) area within mild fibros

20 population with elevated expression of alpha-smooth muscle actin (alphaSMA) located immediately adjac

21 Cells that co-express Thy-1 and alpha-smooth muscle actin (alphaSMA), a CAF marker, were locat

22 aracterized by increased expression of alpha-smooth muscle actin and collagen 1.

23 nd the increase in mesenchymal markers alpha-smooth muscle actin and fibroblast-specific protein 1.

24 oxaban deactivated HSC, with decreased alpha-smooth muscle actin and mRNA expression of other HSC act

25 In contrast, alpha-smooth muscle actin expression by infarct myofibroblasts

26 Exposure to mtDNA augments alpha-smooth muscle actin expression in NHLFs.

27 ed with cholangiocyte supernatants and alpha-smooth muscle actin levels were measured.

28 en fluorescent protein costaining with alpha-smooth muscle actin or collagen 1alpha in left ventricul

29 otoxic, and a more potent inhibitor of alpha-smooth muscle actin protein expression than CCG-203971.

30 MesoMT marker alpha-smooth muscle actin was reduced in 9ING41-treated mice.

31 pha 1, matrix metalloproteinase 2, and alpha-smooth muscle actin) markers.

32 er cells expressed increased levels of alpha-smooth muscle actin, a marker of CAF, compared with MSC

33 c flow contained reduced myosin heavy chain, smooth muscle actin, and desmin, and increased markers o

34 ted positively with CSE, myosin heavy chain, smooth muscle actin, and desmin, and negatively with cel

35 rrelated positively with myosin heavy chain, smooth muscle actin, and desmin.

36 on of the fibroblast markers vimentin, alpha-smooth muscle actin, and S100A4.

37 ers against decapentaplegic homolog 4, alpha-smooth muscle actin, CD31, phospho-vascular endothelial

38 pression of fibronectin-1, collagen I, alpha-smooth muscle actin, connective tissue growth factor (CT

39 n levels of fibronectin-1, collagen I, alpha-smooth muscle actin, CTGF, and PAI-1, but decreased Smad

40 ion of selective VSMCs markers such as alpha smooth muscle actin, myosin heavy chain 11, and smooth m

41 fibroblasts, shown by up-regulation of alpha-smooth muscle actin, pro-collagen 1, and F-actin express

42 sis (IPF) involves the accumulation of alpha-smooth muscle actin-expressing myofibroblasts arising fr

43 wth factors and cytokines, decrease of alpha-smooth muscle actin-positive ASFs, and finally in a sign

44 tor receptor-alpha-positive cells, and alpha-smooth muscle actin-positive blood vessels were assayed

45 ctor receptor-alpha-positive cells, 4) alpha-smooth muscle actin-positive blood vessels, and 5) of ke

46 a 1.35-fold increase in proliferative alpha-smooth muscle actin-positive cells in the lungs of ITSN-

47 Smooth-muscle actin expression by stellate cells and CD3

48 e myofibroblastic markers vimentin and alpha-smooth-muscle actin in developing kidneys.

49 t in lung myofibroblast collagen-1 and alpha-smooth-muscle actin synthesis.

50 t to identify the mechanism by which loss of smooth muscle alpha-actin causes aortic disease.

51 l effects of infarct scar maturation, causes smooth muscle alpha-actin fiber formation, up-regulation

52 These findings reveal that disruption of smooth muscle alpha-actin filaments in smooth muscle cel

53 Furthermore, disruption of smooth muscle alpha-actin filaments in wild-type smooth

54 LAM is characterized by neoplastic growth of smooth muscle-alpha-actin-positive cells that destroy lu

55 We found that the smooth muscle alphasm-actin isoform was the dominantly e

56 ed blood vessels of all caliber and putative smooth muscle and astroglial basement membrane compartme

57 nced atherosclerotic plaques with diminished smooth muscle and collagen content.

58 mote migration and proliferation of vascular smooth muscle and endothelial cells via P1 and P2Y recep

59 t this locus in primary cultures of vascular smooth muscle and endothelial cells.

60 nd in specialized contractile cells, such as smooth muscle and myoepithelial cells.

61 MP) as well as adjacent urethra comprised of smooth muscle and peri-urethral mesenchyme.

62 reases STOC activity in contractile vascular smooth muscle and show that a critical step is the activ

63 43 and miR-145 expression is enriched in the smooth muscle and trabecular meshwork in the eye.

64 d epithelioid cells (LAM cells) that express smooth-muscle and melanocyte-lineage markers, harbor mTO

65 and subsequent differentiation into coronary smooth muscle, and restores Wt1 activity upon MI.

66 A role for smooth muscle ARHGEF1 in asthmatic airway hyper-responsi

67 eosinophils, lung Il13 levels, collagen, and smooth muscle, as well as a significant depletion of gob

68 stent airflow obstruction had greater airway smooth muscle (Asm) area with decreased periostin and tr

69 mechanism along the cholinergic nerve-airway smooth muscle (ASM) axis that underlies prolonged airway

70 on, mucus hypersecretion and abnormal airway smooth muscle (ASM) contraction.

71 is commonly associated with increased airway smooth muscle (ASM) mass.

72 f human LTCCs during SN DA-like and arterial smooth muscle (aSM)-like activity patterns using whole-c

73 tin to impair tension transmission in airway smooth muscle (ASM).

74 Perivascular access to smooth muscle basement membrane compartments also exhibi

75 ooth muscle cells (ASMCs) were isolated from smooth muscle bundles in airway of rats.

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

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

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

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

80 Smooth muscle cell (SMC) differentiation is essential fo

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

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

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

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

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

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

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

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

89 Smooth muscle cell contraction significantly increased t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

122 1.5 protein expression were decreased in PAH smooth muscle cells (primary culture).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

178 DRP1 inhibition in human smooth muscle cells undergoing osteogenic differentiatio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

199 rentially expressed in vascular and visceral smooth muscle cells.

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

201 crostructure including elastin, collagen and smooth muscle cells.

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

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

204 ignificantly alter the phenotype of vascular smooth muscle cells.

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

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

207 of intraluminal pressure in cerebral artery smooth muscle cells.

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

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

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

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

212 1.3% of vessels with recruitment of vascular smooth muscle cells; VSMCs) in the presence of enhanced

213 Smooth-muscle cells from mouse tracheas were assayed in

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

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

216 pithelial ion transport and fluid secretion, smooth muscle constriction, neuronal excitability, and c

217 Tracheal smooth muscle contains significant amounts of myosin bin

218 minant mutations in actin gamma 2 (ACTG2), a smooth muscle contractile gene.

219 tro approach for studying characteristics of smooth muscle contractility even though this experimenta

220 ss, but how they interact to regulate airway smooth muscle contractility is not fully understood.

221 enzyme expression, endothelial dysfunction, smooth muscle contractility, and vascular remodeling.

222 hose vascular effects include stimulation of smooth muscle contractility, migration, and proliferatio

223 matrix and, to our knowledge, novel model of smooth muscle contractility.

224 eletal dense bodies, and impaired intestinal smooth muscle contractility.

225 a vital mechanism for the control of airway smooth muscle contraction and thus are a critical factor

226 congenital disorder characterized by loss of smooth muscle contraction in the bladder and intestine.

227 ABSTRACT: Airway smooth muscle contraction is typically the key mechanism

228 latory light chain (RLC) phosphorylation for smooth muscle contraction with subsequent dephosphorylat

229 oded by TMEM16A control neuronal signalling, smooth muscle contraction, airway and exocrine gland sec

230 n, transforming growth factor-beta, vascular smooth muscle contraction, and the hedgehog and Wnt sign

231 ching morphogenesis, the frequency of airway smooth muscle contraction, and the rate of developmental

232 , and identified distinct pathways linked to smooth muscle contraction, inflammatory cytokines, immun

233 re preceded by long-duration waves of airway smooth muscle contraction.

234 trix was prepared from decellularized airway smooth muscle cultures.

235 and suggest its role in establishing normal smooth muscle cytoskeletal-contractile coupling.

236 In contrast, microanastomosis leads to early smooth muscle death and subsequent colonization of the v

237 fic demethylase and promote adipogenesis and smooth muscle development.

238 t CD146 is transiently expressed in vascular smooth muscle development.

239 lso found that TSPAN2 is highly expressed in smooth muscle-enriched tissues and down-regulated in in

240 by promoting monocyte firm adhesion, whereas smooth muscle EphA2 expression may regulate the progress

241 a) channels are key determinants of vascular smooth muscle excitability.

242 nic hedgehog expression, leading to aberrant smooth muscle formation and defective contraction of the

243 airment in BKCa channel function in vascular smooth muscle from diabetic patients through unique mech

244 similar alterations occur in native vascular smooth muscle from humans with type 2 diabetes is unclea

245 tudy, we evaluated BKCa function in vascular smooth muscle from small resistance adipose arteries of

246 Endothelial and smooth muscle function were diminished in uterine (and t

247 a histone acetyltransferase and a driver of smooth muscle gene expression.

248 istically with SRF and myocardin to regulate smooth muscle gene expression.

249 nscription co-factor CRP2 was a regulator of smooth muscle gene expression.

250 , GATA6 and CRP2 required CSRP2BP for robust smooth muscle gene promoter activity.

251 CSRP2BP synergistically activated smooth muscle gene promoters in an SRF-dependent manner.

252 lar matrix, which enhanced subsequent airway smooth muscle growth by 1.5-fold (P < 0.05), which was d

253 ransiently increasing MMP activation, airway smooth muscle growth, and airway responsiveness.

254 sthma, mast cells are associated with airway smooth muscle growth, MMP-1 levels are associated with b

255 KATP channels in vascular smooth muscle have a well-defined role in regulating vas

256 e thickening, subepithelial fibrosis, airway smooth muscle hyperplasia and increased angiogenesis.

257 Selective expression of TSPAN2 in vascular smooth muscle is independently regulated by TGF-beta1/SM

258 RATIONALE: Mutations in ACTA2, encoding the smooth muscle isoform of alpha-actin, cause thoracic aor

259 nslocation and Rho-kinase activity in airway smooth muscle largely via ARHGEF1, but independently of

260 creased thickness, p = 0.005) and within the smooth muscle layer (p = 0.004).

261 ion of extracellular matrix (ECM) and larger smooth muscle mass are correlated with increased airway

262 ated features of airway remodeling including smooth muscle mass, extracellular matrix deposition and

263 Our findings suggest that airway smooth muscle/mast cell interactions contribute to asthm

264 selective genetic deletion of melanopsin in smooth muscle mostly removed the light-induced, but not

265 showed that the interaction between CBFbeta-smooth muscle myosin heavy chain (SMMHC; encoded by CBFB

266 Smooth muscle myosin light chain kinase (smMLCK) is a me

267 KEY POINTS: Smooth muscle myosin regulatory light chain (RLC) is pho

268 Vascular smooth muscle NOX4, the common denominator of ischemia w

269 with highest expression in the purely phasic smooth muscle of anococcygeus (ASM) vs. the truly tonic

270 le of anococcygeus (ASM) vs. the truly tonic smooth muscle of IAS.

271 and provide a functional innervation of the smooth muscle of the bowel wall.

272 renal progenitors and were distinct from the smooth muscle or epithelial lineages.

273 compartment that began to express markers of smooth muscle precursors and adventitial fibrocytes, res

274 ifferentiation and proliferation of ureteric smooth muscle progenitor cells during murine kidney-uret

275 A distinct population of CD146(+) smooth muscle progenitor cells emerges during embryonic

276 on to advanced atherosclerosis by regulating smooth muscle proliferation and extracellular matrix dep

277 ast cell numbers were associated with airway smooth muscle proliferation and MMP-1 protein associated

278 hetic phenotype, and EphA2 depletion reduces smooth muscle proliferation, mitogenic signaling, and ex

279 tion of the endothelium coordinates vascular smooth muscle relaxation along resistance arteries durin

280 y activated by cAMP (Epac), induces vascular smooth muscle relaxation by increasing the activity of r

281 regulator of O2-dependent NO degradation in smooth muscle remains elusive.

282 ignalling pathway, thereby regulating airway smooth muscle remodelling in asthma.

283 sing calpain knockout mice attenuated airway smooth muscle remodelling in mouse asthma models.

284 proliferation of ASMCs and attenuated airway smooth muscle remodelling in mouse asthma models.

285 However, the role of calpain in airway smooth muscle remodelling remains unknown.

286 onotherapy equally reverse peripheral airway smooth muscle remodelling.

287 bular maturation, and the differentiation of smooth muscle, renin, and mesangial cells were impaired.

288 KEY POINTS: Non-muscle (NM) and smooth muscle (SM) myosin II are both expressed in smoot

289 of non-muscle (NM) isoforms of myosin II in smooth muscle (SM) tissues and their possible role in co

290 ization of freshly dispersed ICC and colonic smooth muscles, suggesting that this conductance is acti

291 mmalian cells, including epithelia, vascular smooth muscle tissue, electrically excitable cells, and

292 Contractile stimulation of tracheal smooth muscle tissues stimulates phosphorylation of the

293 muscle (SM) myosin II are both expressed in smooth muscle tissues, however the role of NM myosin in

294 vasoactive compounds that regulate vascular smooth muscle tone.

295 otype, EphA2 shows enhanced expression after smooth muscle transition to a synthetic phenotype, and E

296 Airway smooth muscle treated with activated mast cell supernata

297 antly influencing the phenotypic tonicity in smooth muscle via ROCK2: a lack of tone in ASM may be as

298 E: Decreasing Ca(2+) sensitivity of vascular smooth muscle (VSM) allows for vasodilation without lowe

299 crease phosphorylation of myosin in vascular smooth muscle (VSM) cells, causing persistent constricti

300 ay inflammation, mucus, fibrosis, and airway smooth muscle were no different in Ormdl3(Delta2-3/Delta