ライフサイエンスコーパス: airway smooth muscle

1 way contractility is primarily determined by airway smooth muscle.

2 responsiveness: the excessive contraction of airway smooth muscle.

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

4 pe 17 cytokines cause hyperresponsiveness of airway smooth muscle.

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

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

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

8 ing signaling and growth inhibition in human airway smooth muscle.

9 drenergic receptor signaling and function in airway smooth muscle.

10 tion of GPCR signaling and function in human airway smooth muscle.

11 nhanced, methacholine-induced contraction of airway smooth muscle.

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

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

14 responsiveness: the excessive contraction of airway smooth muscle.

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

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

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

18 4 (RGS4), a cytoplasmic protein expressed in airway smooth muscle and bronchial epithelium that regul

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

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

21 Tensin1 expression was increased in the airway smooth muscle and lamina propria in COPD tissue,

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

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

24 In asthma, the contraction of the airway smooth muscle and the subsequent decrease in airf

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

26 transgelin-2 with specific agonists relaxes airway smooth muscles and reduces pulmonary resistance i

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

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

29 marked contraction and delayed relaxation of airway smooth muscle, and that this is mediated by the d

30 stem, alpha5-containing GABA(A) receptors in airway smooth muscles are considered as an emerging targ

31 However, it protects the airway smooth muscle (ASM) against a loss of smooth musc

32 insulin promotes beta-AR desensitization in airway smooth muscle (ASM) and compromises airway relaxa

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

34 olatile odorants on the contractile state of airway smooth muscle (ASM) and uncovered a complex mecha

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

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

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

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

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

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

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

42 Increased airway smooth muscle (ASM) cell mass and secretory funct

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

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

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

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

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

48 Airway smooth muscle (ASM) cells play important physiolo

49 n to have extraoral localizations, including airway smooth muscle (ASM) cells, in which TAS2R have be

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

71 NF), on airway contractility [ via increased airway smooth muscle (ASM) intracellular calcium [Ca(2+)

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

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

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

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

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

77 Altered airway smooth muscle (ASM) mass and extracellular matrix

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

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

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

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

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

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

84 Airway smooth muscle (ASM) progenitors map exclusively t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

100 signaling and immunomodulatory functions in airway smooth muscle (ASM).

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

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

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

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

105 ecruitment of mesenchymal progenitors to the airway smooth muscle bundle.

106 2 cysLT receptors (CysLTRs), which constrict airway smooth muscle, but elicits airflow obstruction an

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

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

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

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

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

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

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

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

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

116 that miR-145-5p was strongly associated with airway smooth muscle cell growth in vitro.

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

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

119 ldren with asthma and additionally increases airway smooth muscle cell proliferation.

120 ive and function-selective ERK inhibitors on airway smooth muscle cell proliferation.

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

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

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

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

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

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

127 same receptor to preferentially colonize at airway smooth muscle cells (ASMCs)-a rich source of coll

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

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

130 exerts a direct impact on the contraction of airway smooth muscle cells (ASMCs).

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

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

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

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

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

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

137 Tensin1 expression in cultured human airway smooth muscle cells (HASMCs) was evaluated using

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

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

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

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

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

143 0019), bronchial epithelial (P = 0.0002) and airway smooth muscle cells (P = 0.0352) of patients with

144 2-dependent gene expression in primary human airway smooth muscle cells and the human monocytic cell

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

146 o in adjacent mesenchymal tissues, including airway smooth muscle cells and their extracellular prote

147 of TRPA1 in human lung myofibroblasts, human airway smooth muscle cells but not lung mast cells.

148 hown to relax the myosin cytoskeleton of the airway smooth muscle cells by acting as a receptor for e

149 In contrast, loss of DGKzeta in airway smooth muscle cells decreased AHR but not airway

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

154 Airway smooth muscle cells grown from bronchial biopsies

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

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

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

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

159 fy autocrine prostaglandin E(2) signaling in airway smooth muscle cells that eventually triggered cAM

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

161 morphology, adhesion, and migration of human airway smooth muscle cells transfected with PKAc variant

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

163 hi isolated from human lung tissue and human airway smooth muscle cells were treated for 2 and 1 day(

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

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

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

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

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

169 (TAS2R14) is a GPCR also expressed on human airway smooth muscle cells, which signals to intracellul

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

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

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

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

174 n as a new Plk1-interacting protein in human airway smooth muscle cells.

175 th IL-13 and IL-4 in human bronchi and human airway smooth muscle cells.

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

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

178 Airway smooth muscle CFTR may represent a therapeutic ta

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

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

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

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

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

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

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

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

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

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

189 3-muscarinic acetylcholine receptor mediated airway smooth muscle contraction is poorly understood.

190 Airway smooth muscle contraction is typically the key me

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

192 er, these data indicate that IL-17A promotes airway smooth muscle contraction via direct recruitment

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

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

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

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

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

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

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

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

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

202 Airway smooth muscle-derived CCL2 mediates FC migration

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

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

205 o by inactivating Myocardin, which prevented airway smooth muscle differentiation.

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

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

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

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

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

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

212 Using human fetal airway smooth muscle (fASM) cells, we investigated basel

213 Airway smooth muscle from asthma patients can be disting

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

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

216 Airway smooth muscle from individuals with asthma exhibi

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

218 Airway smooth muscle function was determined with tissue

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

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

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

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

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

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

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

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

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

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

229 of immortalized cell lines and primary human airway smooth muscle (HASM) cells.

230 sserted both EP2 and EP4 expression in human airway smooth muscle (HASM), a recent study asserted EP4

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

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

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

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

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

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

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

238 Airway smooth muscle hypertrophy is one of the hallmarks

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

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

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

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

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

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

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

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

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

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

249 Airway smooth muscle is best known for its role as an ai

250 r demonstrate that during development, while airway smooth muscle is dispensable for epithelial branc

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

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

253 Furthermore, exposure to allergens enhanced airway smooth muscle layer and paxillin phosphorylation

254 enesis of allergen-induced thickening of the airway smooth muscle layer by affecting paxillin phospho

255 Allergic asthma is characterized by airway smooth muscle layer thickening, which is largely

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

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

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

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

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

261 lymphoid cells type 2 (ILCs), and increased airway smooth muscle mass via recruitment of mesenchymal

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

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

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

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

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

267 phorins 3E (Sema3E) in growth factor-induced airway smooth muscle proliferation and migration in vitr

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

269 their combined targeting optimally inhibits airway smooth muscle proliferation.

270 del, supported by in vitro data, posits that airway smooth muscle promotes lung branching through per

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

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

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

274 tes extracellular matrix deposition in human airway smooth muscle remodeling via NF-kappaB pathway.

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

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 mouse, mesenchymal cells differentiate into airway smooth muscle that wraps around epithelial branch

291 esses evoking airway hyperresponsiveness and airway smooth muscle thickening occur independent from i

292 22, enhanced contractile force generation of airway smooth muscle through an IL-17 receptor A (IL-17R

293 ructural changes within the airways, such as airway smooth muscle tissue hypertrophy.

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

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

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

297 Airway smooth muscle treated with activated mast cell su

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

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

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