ライフサイエンスコーパス: airway smooth muscle

1 ause of airway obstruction is contraction of airway smooth muscle.

2 airway epithelium, vascular endothelium, and airway smooth muscle.

3 per-responsiveness through direct effects on airway smooth muscle.

4 r regulation of RLC phosphorylation in tonic airway smooth muscle.

5 drenergic receptor signaling and function in airway smooth muscle.

6 TGFbeta regulation of gene transcription in airway smooth muscle.

7 determine the roles of TLRs in activation of airway smooth muscle.

8 ell as on bradykinin-induced contraction, in airway smooth muscle.

9 responsiveness: the excessive contraction of airway smooth muscle.

10 way contractility is primarily determined by airway smooth muscle.

11 responsiveness: the excessive contraction of airway smooth muscle.

12 tify the subcellular localization of CFTR in airway smooth muscle.

13 For instance, in asthma, activation of airway smooth muscle abruptly changes the airway size an

14 role for airway epithelial Syk in modulating airway smooth muscle activity.

15 esults reveal stereotyped differentiation of airway smooth muscle adjacent to nascent epithelial buds

16 Moreover, RyR1 and/or RyR3 in mouse airway smooth muscle also appear to mediate bronchoconst

17 ilia, mast cell hyperplasia, IgE production, airway smooth muscle alterations, and airways hyperreact

18 Together, these roles make airway smooth muscle an attractive target for asthma the

19 ted the hypothesis that CFTR is expressed in airway smooth muscle and directly affects airway smooth

20 iNO preserves structure and function of airway smooth muscle and enhances alveolar development i

21 s PIP5K1gamma is the major source of PIP2 in airway smooth muscle and its activity is regulated by hi

22 PS, may be achieved by cooperativity between airway smooth muscle and leukocytes involved in immune s

23 prevailing hypothesis focuses on contracting airway smooth muscle and posits a nonlinear dynamic inte

24 to the sarcoplasmic reticulum compartment of airway smooth muscle and regulates airway smooth muscle

25 icated in the control of oxidative stress in airway smooth muscle and their role in contractility.

26 confirmed the presence of CHRNA5/3 in lung, airway smooth muscle, and bronchial epithelial cells.

27 LC phosphorylation during the contraction of airway smooth muscle, and that it regulates contraction

28 Multiple and paradoxical effects of airway smooth muscle (ASM) 7-transmembrane-spanning rece

29 l in regulating bronchomotor tone in asthma, airway smooth muscle (ASM) also modulates airway inflamm

30 We found expression of TAS2Rs on human airway smooth muscle (ASM) and considered these to be av

31 irway remodeling, which are characterized by airway smooth muscle (ASM) and pulmonary arterial vascul

32 h persistent airflow obstruction had greater airway smooth muscle (Asm) area with decreased periostin

33 Immunostained sections were assessed for airway smooth muscle (ASM) area, subepithelial basement

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

35 hown that a lack of eosinophils in asthmatic airway smooth muscle (ASM) bundles in contrast to the la

36 in vivo evidence of GC-resistant pathways in airway smooth muscle (ASM) bundles that can be modeled i

37 pathogenesis through their relocation to the airway smooth muscle (ASM) bundles.

38 ct of epidermal growth factor (EGF) on human airway smooth muscle (ASM) by promoting sustained late-p

39 the existence of GC-insensitive pathways in airway smooth muscle (ASM) caused by a defect in GC rece

40 n-coupled bitter taste receptors (TAS2Rs) in airway smooth muscle (ASM) causes a stronger bronchodila

41 ating the bronchial submucosa and disrupting airway smooth muscle (ASM) cell-extracellular matrix (EC

42 Contact between airway smooth muscle (ASM) cells and activated CD4(+) T

43 educe mean contractile force when applied to airway smooth muscle (ASM) cells and tissue strips.

44 of IL-1beta and TNF-alpha on cultured human airway smooth muscle (ASM) cells are tightly regulated b

45 Airway smooth muscle (ASM) cells can act as effector cel

46 Given earlier evidence demonstrating that airway smooth muscle (ASM) cells express MHC class II mo

47 (HS) and chondroitin sulfate (CS) by murine airway smooth muscle (ASM) cells in the presence of radi

48 Increased proliferation of airway smooth muscle (ASM) cells leading to hyperplasia

49 e also indicates that, in part, migration of airway smooth muscle (ASM) cells may contribute to airwa

50 Airway smooth muscle (ASM) cells play important physiolo

51 In immortalized human airway smooth muscle (ASM) cells, Sul-121 dose-dependent

52 in vitro model of bacterial exacerbation in airway smooth muscle (ASM) cells, we show that activatio

53 ced proliferation and wound healing in human airway smooth muscle (ASM) cells.

54 Chemokine receptors (CCRs) are expressed on airway smooth muscle (ASM) cells.

55 sly expressed G s-coupled receptors in human airway smooth muscle (ASM) cells.

56 protein-coupled receptors (C3aR and C5aR) in airway smooth muscle (ASM) cells.

57 ion of COX-2 protein and PGE2 secretion from airway smooth muscle (ASM) cells.

58 inflammation in ozone-exposed mice and human airway smooth muscle (ASM) cells.

59 d desensitization as a means of manipulating airway smooth muscle (ASM) contractile state, we assesse

60 Increased airway smooth muscle (ASM) contractility and the develop

61 ll and molecular biology of inflammation and airway smooth muscle (ASM) contractility have identified

62 Airway smooth muscle (ASM) contraction is an important c

63 Receptor-mediated airway smooth muscle (ASM) contraction via G(alphaq), an

64 ary for ACh-induced actin polymerization and airway smooth muscle (ASM) contraction, but the mechanis

65 lammation, mucus hypersecretion and abnormal airway smooth muscle (ASM) contraction.

66 result primarily from inflammation-triggered airway smooth muscle (ASM) contraction.

67 othesized that the transcriptomic profile of airway smooth muscle (ASM) distinguishes atopic asthma f

68 Since airway smooth muscle (ASM) expresses Ca(v)1.2 and all th

69 Altered airway smooth muscle (ASM) function and enrichment of th

70 or crosstalk between mAChRs and beta2ARs in airway smooth muscle (ASM) helps determine the contracti

71 f allergic asthma and is caused primarily by airway smooth muscle (ASM) hypercontractility.

72 Airway smooth muscle (ASM) hyperplasia is a feature of a

73 Mucous cell hyperplasia and airway smooth muscle (ASM) hyperresponsiveness are hallm

74 factor receptor staining), mucin expression, airway smooth muscle (ASM) hypertrophy and inflammatory

75 ge in early life led to a 2-fold increase in airway smooth muscle (ASM) innervation (P<0.05) and pers

76 Increased airway smooth muscle (ASM) is a feature of established a

77 Phenotypic modulation of airway smooth muscle (ASM) is an important feature of ai

78 Dysfunctional neural control of airway smooth muscle (ASM) is involved in inflammatory d

79 osition of extracellular matrix (ECM) in the airway smooth muscle (ASM) layer as observed in asthma m

80 r can be exploited to alter, the increase in airway smooth muscle (ASM) mass and cellular remodeling

81 The increase in airway smooth muscle (ASM) mass is an essential componen

82 Airway smooth muscle (ASM) mass is increased in asthma,

83 uding asthma, are characterized by increased airway smooth muscle (ASM) mass that is due in part to g

84 ugh it is commonly associated with increased airway smooth muscle (ASM) mass.

85 Beta2AR desensitization in airway smooth muscle (ASM) mediated by airway inflammati

86 (Epac), not PKA, mediates the relaxation of airway smooth muscle (ASM) observed with beta-agonist tr

87 Airway smooth muscle (ASM) plays a key role in airway hy

88 Airway smooth muscle (ASM) progenitors map exclusively t

89 Airway smooth muscle (ASM) proliferation and migration a

90 t to beta2AR physiological function, such as airway smooth muscle (ASM) relaxation leading to broncho

91 Effects of loss of RGS2 on mouse airway smooth muscle (ASM) remodeling, contraction, intr

92 Pulmonary function is largely determined by airway smooth muscle (ASM) tone and contractility.

93 o be expressed on extraoral cells, including airway smooth muscle (ASM) where they evoke relaxation.

94 In many tissues, such as airway smooth muscle (ASM), complex, unexpected, or para

95 g abnormalities in structural cells, such as airway smooth muscle (ASM), contribute to the asthmatic

96 reticular basement membrane (RBM) thickness, airway smooth muscle (ASM), mucus gland area, vascularit

97 educed IL-13-induced release of eotaxin from airway smooth muscle (ASM), similar to effects of these

98 Mast cell localization within the airway smooth muscle (ASM)-bundle plays an important rol

99 Inhaled beta-agonists are effective airway smooth muscle (ASM)-relaxing agents that help rev

100 corticoids may also alter gene expression of airway smooth muscle (ASM).

101 assium (BK) channels are highly expressed in airway smooth muscle (ASM).

102 tors due primarily to their ability to relax airway smooth muscle (ASM).

103 mpartmentalized beta(2)AR signaling in human airway smooth muscle (ASM).

104 well as NT receptors are expressed in human airway smooth muscle (ASM).

105 ibronectin to impair tension transmission in airway smooth muscle (ASM).

106 of multiple GPCRs endogenously expressed in airway smooth muscle (ASM).

107 regard, TSLP appears to also be expressed in airway smooth muscle (ASM); however, its role is unknown

108 tension generation during the contraction of airway smooth muscle (ASM); however, the role of VASP in

109 Beta-agonist-promoted desensitization of airway smooth muscle beta-2-adrenergic receptors, mediat

110 ine receptor expression by mast cells in the airway smooth muscle bundle in bronchial biopsies from s

111 2 cysLT receptors (CysLTRs), which constrict airway smooth muscle, but elicits airflow obstruction an

112 h proinflammatory cytokines in primary human airway smooth muscle, but no important functional respon

113 Here, we show that in airway smooth muscle, Ca2+ sparks under physiological co

114 romote a synergistic increase in the rate of airway smooth muscle cell (ASM) proliferation.

115 a negative correlation desmin expression in airway smooth muscle cell (ASMC) and airway hyperrespons

116 endent, NF-kappaB-dependent allergen-induced airway smooth muscle cell (ASMC) hyperproliferation and

117 Airway smooth muscle cell (ASMC) migration is an importa

118 Airway smooth muscle cell (ASMC) migration is one of the

119 CXCL1, CXCL2, and CXCL3) production promoted airway smooth muscle cell (ASMC) migration, and conseque

120 al organs and systems including vascular and airway smooth muscle cell (SMC) contraction.

121 By doing so, it can modulate airway smooth muscle cell contraction and leucocyte migr

122 rosine kinase inhibition directly attenuates airway smooth muscle cell contraction independent of its

123 In asthma, mast cells infiltrate the airway smooth muscle cell layer and secrete proinflammat

124 These data indicate that established airway smooth muscle cell layer thickening and subepithe

125 ften follow viral infections with subsequent airway smooth muscle cell proliferation and the formatio

126 Here, we answer these two questions, using airway smooth muscle cells (ASMC) as a specific example.

127 relative CS insensitivity has been shown in airway smooth muscle cells (ASMC) from patients with SA.

128 Activated CD4 T cells connect to airway smooth muscle cells (ASMCs) in vitro via lymphocy

129 corticosteroid insensitivity was present in airway smooth muscle cells (ASMCs) of patients with seve

130 cular, recent studies have suggested that in airway smooth muscle cells (ASMCs) provoked by spasmogen

131 Airway smooth muscle cells (ASMCs) were isolated from sm

132 o be important in regulating healthy primary airway smooth muscle cells (ASMCs), whereas changed expr

133 asthma is driven by excessive contraction of airway smooth muscle cells (ASMCs).

134 o pathway and inhibiting Fgf10 expression in airway smooth muscle cells (ASMCs).

135 asthma is driven by excessive contraction of airway smooth muscle cells (ASMCs).

136 the frequency of Ca(2+) oscillations within airway smooth muscle cells (ASMCs).

137 ion, we developed coculture systems of human airway smooth muscle cells (HASM) with primary human mas

138 smooth muscle cells (MASM) and primary human airway smooth muscle cells (HASM).

139 of human lung mast cells (HLMCs) with human airway smooth muscle cells (HASMCs) are partially depend

140 Muscle cells, including human airway smooth muscle cells (HASMCs) express ankyrin repe

141 In cultured human airway smooth muscle cells (hASMCs), TGF-beta pre-treatm

142 Here we address this question using human airway smooth muscle cells (hASMCs).

143 ify miR-26a as a hypertrophic miRNA of human airway smooth muscle cells (HASMCs).

144 tion of hyaluronan "cables" in primary mouse airway smooth muscle cells (MASM) and primary human airw

145 In this study, we show that murine airway smooth muscle cells (MASM) treated with polyinosi

146 0019), bronchial epithelial (P = 0.0002) and airway smooth muscle cells (P = 0.0352) of patients with

147 essed in stimulated, cultured, primary human airway smooth muscle cells and an antigen-driven rat mod

148 2-dependent gene expression in primary human airway smooth muscle cells and the human monocytic cell

149 In addition, TMEM16A is expressed in airway smooth muscle cells and the smooth muscle cells o

150 Functional studies in primary human airway smooth muscle cells demonstrate that Gs-biased pe

151 Airway smooth muscle cells from healthy and severe asthm

152 his study, we defined the mechanism in human airway smooth muscle cells from nonasthmatic and asthmat

153 ines in supernatants from stimulated ex vivo airway smooth muscle cells from subjects with and withou

154 Airway smooth muscle cells generated pro-MMP-1, which wa

155 Airway smooth muscle cells grown from bronchial biopsies

156 Asthmatic human airway smooth muscle cells hypersecrete VEGF, but the me

157 or expression was significantly increased in airway smooth muscle cells in allergen-treated mice comp

158 ed cAMP accumulation (0-30 minutes) in human airway smooth muscle cells in the presence and absence o

159 kewise, knockdown of IQGAP1 in primary human airway smooth muscle cells increased RhoA activity.

160 beta(2)-adrenergic receptors (beta(2)ARs) in airway smooth muscle cells results in uncoupling of beta

161 Incubation of S1P with airway smooth muscle cells significantly increased contr

162 the most effective bronchodilators and relax airway smooth muscle cells through increased cAMP concen

163 Methods: Airway smooth muscle cells were cultured with TLR agonis

164 oline challenge, and bronchoscopy, and their airway smooth muscle cells were grown in culture.

165 GC occurred in human lung slices or in human airway smooth muscle cells when given chronic NO exposur

166 The molecular mechanisms responsible for airway smooth muscle cells' (aSMCs) contraction and prol

167 cells, human bronchus fibroblasts and human airway smooth muscle cells).

168 methyl-beta-cyclodextrin indicating that, in airway smooth muscle cells, activation of these pathways

169 alpha, a smooth muscle-specific promoter, in airway smooth muscle cells, and we demonstrate that this

170 Taken together, our results suggest that in airway smooth muscle cells, spatial compartmentalization

171 Notably, in human airway smooth muscle cells, the physiological target of

172 In airway smooth muscle cells, these Ca(2+) oscillations ar

173 In monocytic THP-1 and primary airway smooth muscle cells, Wnt4 induced inflammation an

174 ced interleukin (IL)-8 release from cultured airway smooth muscle cells.

175 kade of M3 muscarinic receptors expressed on airway smooth muscle cells.

176 ase expression was found in human and murine airway smooth muscle cells.

177 is and calcium flux in both murine and human airway smooth muscle cells.

178 ions of the plasma membrane in primary human airway smooth muscle cells.

179 ing the function of other cell types such as airway smooth muscle cells.

180 sHA rapidly activated RhoA, ERK, and Akt in airway smooth-muscle cells, but only in the presence of

181 Airway smooth muscle CFTR may represent a therapeutic ta

182 nsiveness, but how they interact to regulate airway smooth muscle contractility is not fully understo

183 RhoA, a regulator of airway smooth muscle contractility, was activated in air

184 Here, we determined that IQGAP1 modulates airway smooth muscle contractility.

185 way physiology as a consequence of increased airway smooth muscle contractility.

186 in airway smooth muscle and directly affects airway smooth muscle contractility.

187 , Drosophila) gene (PDE4D) is a regulator of airway smooth-muscle contractility, and PDE4 inhibitors

188 ium are a vital mechanism for the control of airway smooth muscle contraction and thus are a critical

189 ium are a vital mechanism for the control of airway smooth muscle contraction and thus are a critical

190 n alpha9beta1 appears to serve as a brake on airway smooth muscle contraction by recruiting SSAT, whi

191 In analyses of airway smooth muscle contraction ex vivo, PKC inhibition

192 eta1 increased in vitro airway narrowing and airway smooth muscle contraction in murine and human air

193 3-muscarinic acetylcholine receptor mediated airway smooth muscle contraction is poorly understood.

194 ABSTRACT: Airway smooth muscle contraction is typically the key me

195 Airway smooth muscle contraction is typically the key me

196 The role of Pak in airway smooth muscle contraction was evaluated by inhibi

197 conformation and function of vinculin during airway smooth muscle contraction was evaluated.

198 ay branching morphogenesis, the frequency of airway smooth muscle contraction, and the rate of develo

199 and RhoA, inactivating RhoA and suppressing airway smooth muscle contraction.

200 es, this interaction inhibited IP3-dependent airway smooth muscle contraction.

201 tylcholine release from nerve terminals, and airway smooth muscle contraction.

202 chain of myosin (MLC20) phosphorylation and airway smooth muscle contraction.

203 , and are preceded by long-duration waves of airway smooth muscle contraction.

204 ylation of myosin light chain, which induces airway smooth muscle contraction.

205 uman lung mast cell migration was induced by airway smooth muscle cultures predominantly through acti

206 ular matrix was prepared from decellularized airway smooth muscle cultures.

207 Airway smooth muscle-derived CCL2 mediates FC migration

208 al regulator of the earliest aspects of lung airway smooth muscle development.

209 es that promote the earliest aspects of lung airway smooth muscle development.

210 is required for normal tension generation in airway smooth muscle during contractile stimulation and

211 itical role for localized differentiation of airway smooth muscle during epithelial bifurcation in th

212 oupling the airway to cross-bridge models of airway smooth muscle dynamics and force generation.

213 ysteresis loops are highly dependent on both airway smooth muscle dynamics, and the length-tension re

214 rnative pathway that involves activating the airway smooth muscle enzyme, soluble guanylate cyclase (

215 Increases in airway smooth muscle, extracellular matrix, and vascular

216 saicin-induced reflex-mediated relaxation of airway smooth muscle following vagotomy is mediated by s

217 Airway smooth muscle from asthma patients can be disting

218 ARHGEF1 expression was also enhanced in airway smooth muscle from asthmatic patients and ovalbum

219 he asthmatic environment as in vitro primary airway smooth muscle from individuals with asthma compar

220 Airway smooth muscle from individuals with asthma exhibi

221 Loss of CFTR alters porcine airway smooth muscle function and may contribute to the

222 Airway smooth muscle function was determined with tissue

223 ncluding airways inflammation, alteration in airway smooth muscle function, and airway remodeling.

224 fects of T(H)17 cytokines on mouse and human airway smooth muscle function.

225 onstriction and airway remodeling, including airway smooth muscle growth and inflammation.

226 racellular matrix, which enhanced subsequent airway smooth muscle growth by 1.5-fold (P < 0.05), whic

227 of disease; however, the ability to prevent airway smooth muscle growth was lost after the progressi

228 ty by transiently increasing MMP activation, airway smooth muscle growth, and airway responsiveness.

229 h in turn increased epithelial viral burden, airway smooth muscle growth, and type 2 inflammation.

230 In asthma, mast cells are associated with airway smooth muscle growth, MMP-1 levels are associated

231 ed intracellular signaling and primary human airway smooth muscle growth, whereas only FR900359 effec

232 abundant microRNA expressed in primary human airway smooth muscle (HASM) cells, accounting for > 20%

233 In human airway smooth muscle (HASM) cells, the expression and fu

234 ce that prolonged exposure of cultured human airway smooth muscle (HuASM) cells to beta(2)-agonists d

235 atment of asthma by preventing IL-13-induced airway smooth muscle hyper-responsiveness.

236 promotion of oxidative stress and consequent airway smooth muscle hypercontractility.

237 membrane thickening, subepithelial fibrosis, airway smooth muscle hyperplasia and increased angiogene

238 airway obstruction, subepithelial fibrosis, airway smooth muscle hyperplasia, and pathophysiological

239 out of Plk1 attenuated airway resistance and airway smooth muscle hyperreactivity in a murine model o

240 yperresponsiveness, which largely stems from airway smooth muscle hyperreactivity.

241 translational control pathway contributes to airway smooth muscle hypertrophy in vitro and in vivo.

242 Airway smooth muscle hypertrophy is one of the hallmarks

243 thase kinase-3beta (GSK-3beta) inhibition in airway smooth muscle hypertrophy, a structural change fo

244 (damage) include bronchial wall thickening, airway smooth muscle hypertrophy, bronchiectasis and emp

245 hat eIF2B is required for GSK-3beta-mediated airway smooth muscle hypertrophy.

246 Genome-wide microarray of primary airway smooth muscle identified increased messenger RNA

247 TLR7 was expressed on airway nerves, but not airway smooth muscle, implicating airway nerves as the s

248 ine receptor on human lung mast cells in the airway smooth muscle in asthma and was expressed by 100%

249 te whether the burden of oxidative stress in airway smooth muscle in asthma is heightened and mediate

250 10 was expressed preferentially by asthmatic airway smooth muscle in bronchial biopsies and ex vivo c

251 We examined the oxidative stress burden of airway smooth muscle in bronchial biopsies and primary c

252 ially relevant was the mast cell increase in airway smooth muscle in CLE, which related significantly

253 ound that the oxidative stress burden in the airway smooth muscle in individuals with asthma is heigh

254 m for regulating the function of vinculin in airway smooth muscle in response to contractile stimulat

255 hypothesized that mast cells migrate toward airway smooth muscle in response to smooth muscle-derive

256 Exaggerated contraction of airway smooth muscle is the major cause of symptoms in a

257 hoA translocation and Rho-kinase activity in airway smooth muscle largely via ARHGEF1, but independen

258 Here, we showed that integrin alpha9beta1 on airway smooth muscle localizes the polyamine catabolizin

259 mooth muscle contractility, was activated in airway smooth muscle lysates from Iqgap1-/- mice.

260 ated gene-6) to the culture medium of murine airway smooth muscle (MASM) cells, would enhance leukocy

261 OVA-treated mice, concomitant with increased airway smooth muscle mass and peribronchial collagen dep

262 hasone, reversed the established increase in airway smooth muscle mass and subepithelial collagen dep

263 proposed mechanisms underlying the increased airway smooth muscle mass seen in airway remodeling of p

264 hial thermoplasty, a new technique to reduce airway smooth muscle mass, improves symptoms and reduces

265 Our findings suggest that airway smooth muscle/mast cell interactions contribute t

266 pathetic nerve-mediated reflex relaxation of airway smooth muscle measured in situ in the guinea-pig

267 oduction and contribution to the increase in airway smooth muscle migration.

268 man asthma such as increased mitochondria in airway smooth muscle, platelet activation and subepithel

269 Airway smooth muscle plays a multifaceted role in the pa

270 g in vivo evidence supports the concept that airway smooth muscle produces various immunomodulatory f

271 Mast cell numbers were associated with airway smooth muscle proliferation and MMP-1 protein ass

272 uding cardiomyocytes, pulmonary vascular and airway smooth muscle, proximal vascular endothelium, and

273 gene ablation augments beta-agonist-mediated airway smooth muscle relaxation, while augmenting beta-a

274 AR2) results in relief from bronchospasm via airway smooth muscle relaxation.

275 fluticasone monotherapy decreased peripheral airway smooth muscle remodelling after 12 weeks (p = 0.0

276 2/Akt signalling pathway, thereby regulating airway smooth muscle remodelling in asthma.

277 mobility group box-1 (HMGB1) which triggered airway smooth muscle remodelling in early-life.

278 lpain using calpain knockout mice attenuated airway smooth muscle remodelling in mouse asthma models.

279 d cell proliferation of ASMCs and attenuated airway smooth muscle remodelling in mouse asthma models.

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

281 asone monotherapy equally reverse peripheral airway smooth muscle remodelling.

282 In the trachea and bronchi of the mouse, airway smooth muscle (SM) and cartilage are localized to

283 deficiency in utero correlates with abnormal airway smooth muscle (SM) function in postnatal life.

284 In cultures of human airway smooth muscle, small interfering RNA-mediated kno

285 gonists used to combat hypercontractility in airway smooth muscle stimulate beta2AR-dependent cAMP pr

286 In airway smooth muscle, stimulus-induced contraction requi

287 Human airway smooth muscle strips were contracted with methach

288 ls of airway remodeling, including increased airway smooth muscle, subepithelial fibrosis, and mucus.

289 In airway smooth muscle, tension development caused by a co

290 22, enhanced contractile force generation of airway smooth muscle through an IL-17 receptor A (IL-17R

291 The contractile activation of airway smooth muscle tissues stimulates actin polymeriza

292 2) receptor activation with urocortin III on airway smooth muscle tone in vitro and in an acute model

293 Muscarinic receptors regulate airway smooth muscle tone, and asthmatics exhibit increa

294 an store-operated channels in the control of airway smooth muscle tone.

295 rtment of airway smooth muscle and regulates airway smooth muscle tone.

296 Airway smooth muscle treated with activated mast cell su

297 Reticular basement membrane thickness and airway smooth muscle were increased in patients with STR

298 of airway inflammation, mucus, fibrosis, and airway smooth muscle were no different in Ormdl3(Delta2-

299 n-dependent signaling mediates relaxation of airway smooth muscle, whereas beta-arrestin-dependent si

300 Coincubation of airway smooth muscle with peripheral blood mononuclear c