ライフサイエンスコーパス: smooth muscle

1 n might initiate and spread in this myogenic smooth muscle.

2 tid, which was not myoepithelial or vascular smooth muscle.

3 een in glia, interstitial cells of Cajal, or smooth muscle.

4 ytokines cause hyperresponsiveness of airway smooth muscle.

5 g growth factor beta (TGF-beta) signaling in smooth muscle.

6 Here we have solved the structure of smooth muscle 10S myosin by cryo-electron microscopy wit

7 Immunostaining with alpha-smooth muscle actin (alpha SMA) revealed a significant r

8 ss fibers, exhibited greater levels of alpha-smooth muscle actin (alpha-SMA) expression, and exerted

9 itative proteomic comparison of mature alpha-smooth muscle actin (alpha-SMA)+ myofibroblasts (verifie

10 ding collagen Ialpha1 (colIalpha1) and alpha-smooth muscle actin (alpha-SMA), and cell migration/woun

11 lls, associated with overexpression of alpha-smooth muscle actin (alpha-SMA), and differential upregu

12 munohistochemical studies were performed for smooth muscle actin (alpha-SMA), pancytokeratin, and CK7

13 ions in the gene, ACTA2, which encodes alpha-smooth muscle actin (alpha-SMA).

14 s well as alcohol-induced TGFbeta1 and alpha-smooth muscle actin (SMA) protein expression in PLFs.

15 nthase 2, HAS2, and PDPN increased and alpha-smooth muscle actin alphaSMA mRNA decreased.

16 associated with reduced expression of alpha-smooth muscle actin and Sox2.

17 The amount of alpha-smooth muscle actin and tgf-beta were significantly less

18 s I and VI, and the profibrotic factor alpha-smooth muscle actin compared with placebo in subcutaneou

19 own of GalR1 in cholangiocytes reduced alpha-smooth muscle actin expression in LX-2 cells treated wit

20 uces collagen I, fibronectin, elastin, alpha-smooth muscle actin in human adult dermal (HDFs) and neo

21 e from neural/glial antigen 2 positive/alpha-smooth muscle actin negative to neural/glial antigen 2 p

22 ive to neural/glial antigen 2 positive/alpha-smooth muscle actin positive in some pericytes (PCs) on

23 concentration reduced the intensity of alpha-smooth muscle actin staining by 56% and periostin mRNA l

24 Similarly, alpha-smooth muscle actin(alpha-SMA) expression, aortic collag

25 s >60% of fibroblasts formed alphaSMA (alpha-smooth muscle actin) stress fibers and expressed myofibr

26 markers CNN-1 (calponin 1), alpha-SMA (alpha-smooth muscle actin), and SM22-alpha (smooth muscle prot

27 fibrotic markers f-actin, fibronectin, alpha smooth muscle actin, and collagen type 1 were equally di

28 fibrotic markers f-actin, fibronectin, alpha smooth muscle actin, and collagen type 1 were performed.

29 in, alpha(1) -antitrypsin, glypican-3, alpha-smooth muscle actin, and collagen type 1A2 markers were

30 n, hepatic expressions of collagen-1a, alpha-smooth muscle actin, and mononuclear cell infiltration (

31 expression of three fibrotic markers: alpha-smooth muscle actin, collagen 1, and fibronectin.

32 activation, increases in the levels of alpha-smooth muscle actin, connective tissue growth factor and

33 o express tumor-promoting factors, and alpha-smooth muscle actin, fibronection, and CTGF, markers of

34 and PECAM1 and increases in collagen, alpha-smooth muscle actin, TGFbeta receptor 1, and the transcr

35 stress to promote fibrosis in the absence of smooth muscle actin-expressing myofibroblasts, a key pro

36 s1(-/-)) mice and from mice expressing alpha-smooth muscle actin-green fluorescent protein that label

37 ted hepatic stellate cell; aHSCs) expressing smooth muscle alpha-actin (alphaSMA) and platelet-derive

38 ), a cytoplasmic protein expressed in airway smooth muscle and bronchial epithelium that regulates th

39 s and thrombocytes that induce expression of smooth muscle and collagen genes.

40 he variant were differentiated into vascular smooth muscle and endothelial cells that demonstrated ha

41 Actomyosin-based contractility in smooth muscle and nonmuscle cells is regulated by signal

42 also be localized in subepithelium, detrusor smooth muscles and afferent neurons.

43 lso located within vascular (endothelium and smooth muscle) and muscle (cardiac and skeletal) tissue.

44 ucosa tissue, full-thickness bladder but not smooth muscle, and sustained muscle contractions.

45 tion, a mechanism by which those channels in smooth muscle are thought to be targets of endothelium-d

46 lpha5-containing GABA(A) receptors in airway smooth muscles are considered as an emerging target for

47 However, it protects the airway smooth muscle (ASM) against a loss of smooth muscle myos

48 n promotes beta-AR desensitization in airway smooth muscle (ASM) and compromises airway relaxation re

49 odorants on the contractile state of airway smooth muscle (ASM) and uncovered a complex mechanism of

50 ns desmin and vimentin in obstructed bladder smooth muscle (BSM).

51 ent of mesenchymal progenitors to the airway smooth muscle bundle.

52 polarization decreases pericyte and vascular smooth muscle [Ca(2+)](i) levels, thereby relaxing the c

53 nized and fragmented elastic fibers, reduced smooth muscle calponin expression, and increased macroph

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

78 Smooth muscle cell migration is essential for many diver

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

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

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

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

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

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

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

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

87 Smooth muscle cell-specific overexpression of Smad7 comp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

156 Vascular smooth muscle cells going from a proliferative and motil

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

193 diomyocytes compared to neurons and vascular smooth muscle cells.

194 imary human airway epithelial progenitor and smooth muscle cells.

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

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

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

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

199 tor ROCKi significantly relax human ureteral smooth muscle cells.

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

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

202 racheal mesoderm containing chondrocytes and smooth muscle cells.

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

204 to longitudinal proliferation of arteriolar smooth muscle cells.

205 3 and IL-4 in human bronchi and human airway smooth muscle cells.

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

207 unter to the expectation that the absence of smooth muscle constriction would lead to a more relaxed

208 regression and niche relocation through the smooth muscle contractile machinery that generates centr

209 the first time, that effects of compromised smooth muscle contractility are more important in terms

210 grity, aberrant collagen remodeling, reduced smooth muscle contractility, and dysfunctional mechanose

211 st that directly inhibits calcium influx and smooth muscle contractility, leading to voiding dysfunct

212 h have each been implicated as regulators of smooth muscle contractility, though they display differe

213 l negative feedback mechanism that regulates smooth muscle contractility.

214 a(1A)-adrenoreceptor, a GPCR that stimulates smooth muscle contraction in response to binding noradre

215 light chain, which is essential for vascular smooth muscle contraction.

216 mbryo and is regulated by adrenergic uterine smooth muscle contractions.

217 l mesenchymal specification to cartilage and smooth muscle, coupling epithelial identity with mesench

218 In smooth muscle, cytoglobin (Cygb) functions as a potent n

219 expression along with reduced expression of smooth muscle differentiation markers in the carotids.

220 rplasia, diseases linked to loss of vascular smooth muscle differentiation.

221 activating Myocardin, which prevented airway smooth muscle differentiation.

222 ated with the life-threatening multisystemic smooth muscle dysfunction syndrome (MSMDS) due to mutati

223 irway hyperresponsiveness as an indicator of smooth muscle dysfunction, and treating them appropriate

224 agonist Bay k8644 abrogates ketamine-induced smooth muscle dysfunction.

225 In tracheal smooth muscle ex vivo, in organ baths, isometric contrac

226 causing tissue depolarization and increased smooth muscle excitability.

227 Using human fetal airway smooth muscle (fASM) cells, we investigated baseline exp

228 restores body umbrella shape, causing radial smooth muscle fibers to converge around 'hubs' which ser

229 myosin heavy chain (smMHC) and several other smooth muscle gene transcripts, indicating these cells a

230 rtalized cell lines and primary human airway smooth muscle (HASM) cells.

231 (-/-) mice rendered both bladder and urethra smooth muscle hypercontractile.

232 As rapamycin can attenuate bladder smooth muscle hypertrophy and dysfunction during the gen

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

234 Although both smooth-muscle-induced physical forces and mesenchymal ce

235 Airway smooth muscle is best known for its role as an airway co

236 channel localizes to vascular endothelium or smooth muscle is controversial and the distribution and

237 strate that during development, while airway smooth muscle is dispensable for epithelial branching, i

238 ajor constituent alpha-terpinene on tracheal smooth muscle isolated from rats.

239 adapted to an ischemic environment to drive smooth muscle layer expansion, which may reveal new targ

240 xcitability and contractility of the uterine smooth muscle layer, the myometrium, increase drasticall

241 senchyme to produce rhythmically contracting smooth muscle layers.

242 e of EECM-BMEC-like cells with hiPSC-derived smooth muscle-like cells or their conditioned medium fur

243 t and cardiovascular system, blood, kidneys, smooth muscle lineage and limb skeleton in the developin

244 2B subunits are expressed in mouse lymphatic smooth muscle (LSM) and form functional K(ATP) channels

245 yperpolarized both mouse and human lymphatic smooth muscle (LSM).

246 ated support cells that include fibroblasts, smooth muscle, macrophages and other immune cells.

247 or DR3 restricted increases in peribronchial smooth muscle mass and accumulation of lung collagen, pr

248 pathogenesis is unclear, although increased smooth muscle mass is present.

249 id cells type 2 (ILCs), and increased airway smooth muscle mass via recruitment of mesenchymal progen

250 , TPPP3/PRG4+ chondrogenic cells, and ITGA7+ smooth muscle-mesenchymal cells.

251 However, the role and mechanism of Abi1 in smooth muscle migration are largely unknown.

252 ption factors, and inactivation of Cav1.2 in smooth muscle mimics the ketamine cystitis phenotype.

253 polymerization in vitro of nonphosphorylated smooth muscle myosin filaments by the addition of MgATP

254 PDGFRalpha(+) cells in the PKJ co-expressed smooth muscle myosin heavy chain (smMHC) and several oth

255 layers of murine renal pelvis do not express smooth muscle myosin heavy chain (smMHC) but are in clos

256 airway smooth muscle (ASM) against a loss of smooth muscle myosin heavy chain (SMMHC) expression.

257 Nonphosphorylated smooth muscle myosin polymerizes in the presence of ATP

258 yo-electron microscopy structure of shutdown smooth muscle myosin with a resolution of 6 angstrom in

259 olymerization in vitro in both the presence (smooth muscle myosin) and absence of ATP, skeletal, card

260 nomers assemble into bipolar and side-polar (smooth muscle myosin) filaments.

261 4 h, the myosins form thick bipolar and, for smooth muscle myosin, side-polar filaments.

262 ) and absence of ATP, skeletal, cardiac, and smooth muscle myosins form tail-folded monomers without

263 Although it has long been recognized that smooth muscle Na/K ATPase modulates vascular tone and bl

264 odorant) G protein-coupled receptors on the smooth muscle of human bronchi suggests unappreciated th

265 ation, revealing extensive expression in the smooth muscle of resistance arterioles supplying skeleta

266 g revealed specific localization of TRPV1 to smooth muscle of terminal arterioles in the heart, adipo

267 Smooth muscles of the lower esophageal sphincter (LES) a

268 ver, in plasma and lung endothelium, but not smooth muscle or adventitia, miR-210 was observed in kno

269 erstanding of the roles of these channels in smooth muscle physiology and disease, particularly in co

270 pported by in vitro data, posits that airway smooth muscle promotes lung branching through peristalsi

271 (alpha-smooth muscle actin), and SM22-alpha (smooth muscle protein 22alpha) and an increase in synthe

272 animals die at 3 months of age because of a smooth muscle-related gastrointestinal phenotype.

273 Smoothelin-like 2 (SMTNL2), a member of the smooth-muscle-related Smoothelin protein family, in apic

274 cal administration of vasodilators and other smooth muscle relaxants.

275 tracellular Ca(2+) ([Ca(2+)](i)) and causing smooth muscle relaxation.

276 C processes and indicating the importance of smooth muscle response to vascular stress and phenotypic

277 responses to capsaicin revealing a vascular smooth muscle-restricted signalling mechanism.

278 gain-of-function KATP mutations in vascular smooth muscle resulted in cardiac remodeling.

279 cellular electrode measurements in lymphatic smooth muscle revealed only subtle, but not significant,

280 s widely expressed in many tissues including smooth muscle (SM), although its role in the regulation

281 00A4 is expressed in many tissues, including smooth muscle (SM), but its physiologic function is unkn

282 plex crosstalk between endothelial (ECs) and smooth muscle (SMCs) cells.

283 In contrast, smooth-muscle specific deletion of the L-type VGCC, Ca(v

284 In the present study, smooth muscle-specific acid ceramidase (Ac) gene knockou

285 Smooth muscle-specific expression of a Kir6.1 gain-of-fu

286 Smooth muscle-specific expression of Kir6.1 gain-of-func

287 rlap of these QTLs and their relationship to smooth muscle-specific genes and transcription factors.

288 ation genes (proteins) to the human vascular smooth muscle-specific protein-protein interactome (218

289 and lung inflammation in germline and airway smooth muscle-specific Rgs4(-/-) mice and in mice treate

290 To examine this possibility, we developed a smooth muscle-specific TRPC3 knockout (TRPC3smcKO) mouse

291 The periodic cartilage and smooth muscle structures in mammalian trachea are derive

292 NO produced by neurons diffuses into the smooth muscle surrounding cerebral arterioles, driving v

293 s, our study identifies the dermal sheath as smooth muscle that drives follicle regression for reunit

294 -type VGCCs are expressed in mouse lymphatic smooth muscle, they do not play a significant role in mo

295 rmediates and drug targets for regulation of smooth muscle tone.

296 Genetic ablation of smooth muscle TRPC3 channels shortened the duration of S

297 protein] receptor) is expressed in vascular smooth muscle (VSM) and increased VSM PTH1R signaling mi

298 d Kir6.1 subunits, respectively, of vascular smooth muscle (VSM) KATP channels.

299 Human myenteric ganglia and adjacent smooth muscle were isolated by laser-capture microdissec

300 a-pig urothelium, suburothelium, and bladder smooth muscle, with urothelial predominance.