IR@PKUHSC  > 北京大学第一临床医学院  > 老年病内科
学科主题临床医学
Hydrogen sulfide suppresses migration, proliferation and myofibroblast transdifferentiation of human lung fibroblasts
Fang, Li-Ping1; Lin, Qing1; Tang, Chao-Shu2; Liu, Xin-Min1
关键词Hydrogen Sulfide Migration Proliferation Transdifferentiation
刊名PULMONARY PHARMACOLOGY & THERAPEUTICS
2009-12-01
DOI10.1016/j.pupt.2009.07.003
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
WOS记录号WOS:000272072600015
Citation statistics
Cited Times:27[WOS]   [WOS Record]     [Related Records in WOS]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/51422
Collection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
Recommended Citation
GB/T 7714
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.
APA Fang, Li-Ping,Lin, Qing,Tang, Chao-Shu,&Liu, Xin-Min.(2009).Hydrogen sulfide suppresses migration, proliferation and myofibroblast transdifferentiation of human lung fibroblasts.PULMONARY PHARMACOLOGY & THERAPEUTICS,22(6),554-561.
MLA Fang, Li-Ping,et al."Hydrogen sulfide suppresses migration, proliferation and myofibroblast transdifferentiation of human lung fibroblasts".PULMONARY PHARMACOLOGY & THERAPEUTICS 22.6(2009):554-561.
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