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学科主题: 临床医学
题名:
Hydrogen sulfide suppresses migration, proliferation and myofibroblast transdifferentiation of human lung fibroblasts
作者: Fang, Li-Ping1; Lin, Qing1; Tang, Chao-Shu2; Liu, Xin-Min1
关键词: Hydrogen sulfide ; Migration ; Proliferation ; Transdifferentiation
刊名: PULMONARY PHARMACOLOGY & THERAPEUTICS
发表日期: 2009-12-01
DOI: 10.1016/j.pupt.2009.07.003
卷: 22, 期:6, 页:554-561
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Pharmacology & Pharmacy ; Respiratory System
研究领域[WOS]: Pharmacology & Pharmacy ; Respiratory System
关键词[WOS]: TRANSFORMING-GROWTH-FACTOR ; HEPATIC STELLATE CELLS ; PULMONARY-FIBROSIS ; CARBON-MONOXIDE ; NITRIC-OXIDE ; GENE-EXPRESSION ; BLOOD-FLOW ; BLEOMYCIN ; PATHWAY ; H2S
英文摘要:

We previously reported that hydrogen sulfide (H(2)S) was implicated in the pathogenesis of bleomycin-induced pulmonary fibrosis in rat, but the cellular mechanisms underlying the role it played were not well characterized. The present study was undertaken to investigate the role of the exogenous H(2)S in human lung fibroblast (MRC5) migration, proliferation and myofibroblast transdifferentiation induced by fetal bovine serum (FBS) and growth factors in vitro, to elucidate the mechanisms by which H(2)S inhibits pathogenesis of pulmonary fibrosis. We found that H(2)S incubation significantly decreased the MRC5 cell migration distance stimulated by FBS and basic fibroblast growth factor (bFGF), inhibited MRC5 cell proliferation induced by FBS and platelet-derived growth factor-BB (PDGF-BB), and also inhibited transforming growth factor-beta 1 (TGF-beta 1) induced MRC5 cell transdifferentiation into myofibroblasts. Moreover, preincubation with H(2)S decreased extracellular signal-regulated kinase (ERK1/2) phosphorylation in MRC5 cells induced by FBS, PDGF-BB, TGF-beta 1, and bFGF. However, the inhibition effects of H(2)S on MRC5 cell migration, proliferation and myofibroblast transdifferentiation were not attenuated by glibenclamide, an ATP-sensitive K(+) channel (K(ATP)) blocker. Thus, H(2)S directly suppressed fibroblast migration, proliferation and phenotype transform stimulated by FBS and growth factors in vitro, which suggests that it could be an important mechanism of H(2)S-suppressed pulmonary fibrosis. These effects of H(2)S on pulmonary fibroblasts were, at least in part, mediated by decreased ERK phosphorylation and were not dependent on K(ATP) channel opening. (c) 2009 Elsevier Ltd. All rights reserved.

语种: 英语
项目资助者: National Natural Sciences Foundation of the People&prime ; s Republic of China
WOS记录号: WOS:000272072600015
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/51422
Appears in Collections:北京大学第一临床医学院_老年病内科_期刊论文

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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

Recommended Citation:
Fang, Li-Ping,Lin, Qing,Tang, Chao-Shu,et al. Hydrogen sulfide suppresses migration, proliferation and myofibroblast transdifferentiation of human lung fibroblasts[J]. PULMONARY PHARMACOLOGY & THERAPEUTICS,2009,22(6):554-561.
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