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学科主题: 临床医学
题名:
Hydrogen Sulfide Alleviates Myocardial Collagen Remodeling in Association with Inhibition of TGF-beta/Smad Signaling Pathway in Spontaneously Hypertensive Rats
作者: Sun, Lili1; Jin, Hongfang2,3; Sun, Lujing1; Chen, Siyao2; Huang, Yaqian2; Liu, Jia2; Li, Zhenzhen2; Zhao, Manman2; Sun, Yan2; Tang, Chaoshu4,5; Zhao, Bin1; Du, Junbao2
刊名: MOLECULAR MEDICINE
发表日期: 2014-07-01
DOI: 10.2119/molmed.2013.00096
卷: 20, 页:503-515
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Biochemistry & Molecular Biology ; Cell Biology ; Medicine, Research & Experimental
研究领域[WOS]: Biochemistry & Molecular Biology ; Cell Biology ; Research & Experimental Medicine
关键词[WOS]: GROWTH-FACTOR-BETA ; CARDIAC FIBROBLASTS ; EXTRACELLULAR-MATRIX ; FIBROSIS ; CELL ; PATHOGENESIS ; EXPRESSION ; PEPTIDE ; TIMP-1 ; MMP-13
英文摘要:

The study was designed to explore the role and possible mechanisms of hydrogen sulfide (H2S) in the regulation of myocardial collagen remodeling in spontaneously hypertensive rats (SHRs). We treated nine-week-old male SHRs and age-and sex-matched Wistar-Kyoto rats (WKYs) with NaHS (90 mu mol/kg(-1).day(-1)) for 9 wks. At 18 wks, plasma H2S, tail arterial pressure, morphology of the heart, myocardial ultrastructure and collagen volume fraction (CVF), myocardial expressions of collagen I and III protein and procollagen I and III mRNA, transforming growth factor-beta 1 (TGF-beta 1), TGF-beta type I receptor (T beta R-I), type II receptor (T beta R-II), p-Smad2 and 3, matrix metalloproteinase (MMP)-13 and tissue inhibitors of MMP (TIMP)-1 proteins were determined. TGF-beta 1-stimulated cultured cardiac fibroblasts (CFs) were used to further study the mechanisms. The results showed that compared with WKYs, SHRs showed a reduced plasma H2S, elevated tail artery pressure and increased myocardial collagen, TGF-beta 1, T beta R-II, p-Smad2 and p-Smad3 expressions. However, NaHS markedly decreased tail artery pressure and inhibited myocardial collagen, TGF-beta 1, T beta R-II, p-Smad2 and p-Smad3 protein expressions, but H2S had no effect on the expressions of MMP-13 and TIMP-1. Hydralazine reduced blood pressure but had no effect on myocardial collagen, MMP-13 and TIMP-1 expressions and TGF-beta 1/Smad signaling pathway. H2S prevented activation of the TGF-beta 1/Smad signaling pathway and abnormal collagen synthesis in CFs. In conclusion, the results suggested that H2S could prevent myocardial collagen remodeling in SHR. The mechanism might be associated with inhibition of collagen synthesis via TGF-beta 1/Smad signaling pathway.

语种: 英语
所属项目编号: 2012CB517806 ; 2013CB933801 ; 2011CB503904 ; 31130030 ; 81370154 ; 81100181 ; 81121061 ; 7122184 ; 7121014 ; 2014XXGB02
项目资助者: Major Basic Research Development Program of People&prime ; s Republic of China ; National Natural Science Foundation of China ; Beijing Natural Science Foundation ; Key Laboratory of Remodeling-related Cardiovascular Diseases, Ministry of Education
WOS记录号: WOS:000349473000001
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/50145
Appears in Collections:北京大学第一临床医学院_儿科_期刊论文

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作者单位: 1.Beijing Jishuitan Hosp, Dept Emergency Med, Beijing 100035, Peoples R China
2.Peking Univ, Hosp 1, Dept Pediat, Beijing 100871, Peoples R China
3.Capital Med Univ, Key Lab Remodeling Related Cardiovasc Dis, Beijing Inst Heart Lung & Blood Vessel Dis, Beijing Zhen Hosp,Minist Educ, Beijing, Peoples R China
4.Peking Univ, Hlth Sci Ctr, Dept Physiol & Pathophysiol, Beijing 100871, Peoples R China
5.Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing, Peoples R China

Recommended Citation:
Sun, Lili,Jin, Hongfang,Sun, Lujing,et al. Hydrogen Sulfide Alleviates Myocardial Collagen Remodeling in Association with Inhibition of TGF-beta/Smad Signaling Pathway in Spontaneously Hypertensive Rats[J]. MOLECULAR MEDICINE,2014,20:503-515.
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