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学科主题临床医学
Hydrogen sulfide attenuates epithelial-mesenchymal transition of human alveolar epithelial cells
Fang, Li-Ping1; Lin, Qing1; Tang, Chao-Shu2; Liu, Xin-Min1
关键词Hydrogen Sulfide Alveolar Epithelial Cell Transforming Growth Factor-beta Smad2/3
刊名PHARMACOLOGICAL RESEARCH
2010-04-01
DOI10.1016/j.phrs.2009.10.008
61期:4页:298-305
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Pharmacology & Pharmacy
资助者National Natural Sciences Foundation of the People&prime ; s Republic of China ; National Natural Sciences Foundation of the People&prime ; s Republic of China
研究领域[WOS]Pharmacology & Pharmacy
关键词[WOS]IDIOPATHIC PULMONARY FIBROSIS ; TGF-BETA ; RAT LUNG ; NITRIC-OXIDE ; MYOFIBROBLASTS ; TRANSDIFFERENTIATION ; PATHOGENESIS ; MECHANISMS ; TGF-BETA-1 ; DISEASE
英文摘要

We previously reported that the endogenous cystathionine gamma-lyase (CSE)/hydrogen sulfide (H(2)S) pathway is implicated in the pathogenesis of bleomycin-induced pulmonary fibrosis in rats, but the exact cellular mechanisms are not well characterized. Epithelial-mesenchymal transition (EMT), induced by transforming growth factor beta 1 (TGF-beta 1) in alveolar epithelial cells, plays an important role in the pathogenesis of pulmonary fibrosis. We studied whether H(2)S could attenuate EMT in cultured alveolar epithelial cells and TGF-beta 1 treatment suppressed CSE expression in A549 cells. Inhibition of endogenous CSE by DL-propargylglycine led to spontaneous EMT, as manifested by decreased E-cadherin level, increased vimentin expression and fibroblast-like morphologic features. Exogenous H(2)S applied to TGF-beta 1-treated A549 cells decreased vimentin expression, increased E-cadherin level and retained epithelial morphologic features. In addition, preincubation with H(2)S decreased Smad2/3 phosphorylation in A549 cells stimulated by TGF-beta 1, and H(2)S-inhibited alveolar EMT was mimicked by treatment with SB505124, a Smad2/3 inhibitor, but not pinacidil, an ATP-sensitive K(+) channel (K(ATP)) opener. H(2)S serves a critical role in preserving an epithelial phenotype and in attenuating EMT in alveolar epithelial cells, mediated, at least in part, by decreased Smad2/3 phosphorylation and not dependent on K(ATP) channel opening. (C) 2009 Elsevier Ltd. All rights reserved.

语种英语
所属项目编号30572072
资助者National Natural Sciences Foundation of the People&prime ; s Republic of China ; National Natural Sciences Foundation of the People&prime ; s Republic of China
WOS记录号WOS:000276581300005
引用统计
被引频次:18[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/55470
专题北京大学第一临床医学院_老年病内科
作者单位1.Peking Univ, Hosp 1, Dept Geriatr, Beijing 100871, Peoples R China
2.Peking Univ, Hosp 1, Inst Cardiovasc Dis, Beijing 100871, Peoples R China
推荐引用方式
GB/T 7714
Fang, Li-Ping,Lin, Qing,Tang, Chao-Shu,et al. Hydrogen sulfide attenuates epithelial-mesenchymal transition of human alveolar epithelial cells[J]. PHARMACOLOGICAL RESEARCH,2010,61(4):298-305.
APA Fang, Li-Ping,Lin, Qing,Tang, Chao-Shu,&Liu, Xin-Min.(2010).Hydrogen sulfide attenuates epithelial-mesenchymal transition of human alveolar epithelial cells.PHARMACOLOGICAL RESEARCH,61(4),298-305.
MLA Fang, Li-Ping,et al."Hydrogen sulfide attenuates epithelial-mesenchymal transition of human alveolar epithelial cells".PHARMACOLOGICAL RESEARCH 61.4(2010):298-305.
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