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学科主题临床医学
Downregulation of Endogenous Hydrogen Sulfide Pathway Is Involved in Mitochondrion-Related Endothelial Cell Apoptosis Induced by High Salt
Zong, Yanfang1; Huang, Yaqian1; Chen, Siyao1; Zhu, Mingzhu1; Chen, Qinghua1; Feng, Shasha1; Sun, Yan1; Zhang, Qingyou1; Tang, Chaoshu2,3; Du, Junbao1,2; Jin, Hongfang1
刊名OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
2015
DOI10.1155/2015/754670
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Cell Biology
研究领域[WOS]Cell Biology
关键词[WOS]CYSTATHIONINE GAMMA-LYASE ; OXIDATIVE STRESS ; SENSITIVE HYPERTENSION ; BLOOD-PRESSURE ; SODIUM-INTAKE ; RATS ; ALDOSTERONE ; ANGIOTENSIN ; INHIBITION ; ACTIVATION
英文摘要

Background. The study aimed to investigate whether endogenous H2S pathway was involved in high-salt-stimulated mitochondria-related vascular endothelial cell (VEC) apoptosis. Methods. Cultured human umbilical vein endothelial cells (HUVECs) were used in the study. H2S content in the supernatant was detected. Western blot was used to detect expression of cystathionine gamma-lyase (CSE), cleaved-caspase-3, and mitochondrial and cytosolic cytochrome c (cytc). Fluorescent probes were used to quantitatively detect superoxide anion generation and measure the in situ superoxide anion generation in HUVEC. Mitochondrial membrane pore opening, mitochondrial membrane potential, and caspase-9 activities were measured. The cell apoptosis was detected by cell death ELISA and TdT-mediated dUTP nick end labeling (TUNEL) methods. Results. High-salt treatment downregulated the endogenous VEC H2S/CSE pathway, in association with increased generation of oxygen free radicals, decreased mitochondrial membrane potential, enhanced the opening of mitochondrial membrane permeability transition pore and leakage of mitochondrial cytc, activated cytoplasmic caspase-9 and caspase-3 and subsequently induced VEC apoptosis. However, supplementation of H2S donor markedly inhibited VEC oxidative stress and mitochondria-related VEC apoptosis induced by high salt. Conclusion. H2S/CSE pathway is an important endogenous defensive system in endothelial cells antagonizing high-salt insult. The protective mechanisms for VEC damage might involve inhibiting oxidative stress and protecting mitochondrial injury.

语种英语
WOS记录号WOS:000355870600001
项目编号2012CB517806 ; 2013CB933801 ; 2011CB503904 ; 31130030 ; 81370154 ; 81121061 ; 20130001120047 ; NCET-11-0005 ; 2014XXGB02
资助机构Major Basic Research Development Program of China ; National Natural Science Foundation of China ; Ministry of Education, China ; Open Project of Key Laboratory of Remodeling-Related Cardiovascular Diseases, Ministry of Education
引用统计
被引频次:8[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/400002259/57346
专题北京大学第一临床医学院_儿科
作者单位1.Peking Univ, Hosp 1, Dept Pediat, Beijing 100034, Peoples R China
2.Minist Educ, Key Lab Mol Cardiol, Beijing 100191, Peoples R China
3.Peking Univ, Hlth Sci Ctr, Dept Physiol & Pathophysiol, Beijing 100191, Peoples R China
推荐引用方式
GB/T 7714
Zong, Yanfang,Huang, Yaqian,Chen, Siyao,et al. Downregulation of Endogenous Hydrogen Sulfide Pathway Is Involved in Mitochondrion-Related Endothelial Cell Apoptosis Induced by High Salt[J]. OXIDATIVE MEDICINE AND CELLULAR LONGEVITY,2015.
APA Zong, Yanfang.,Huang, Yaqian.,Chen, Siyao.,Zhu, Mingzhu.,Chen, Qinghua.,...&Jin, Hongfang.(2015).Downregulation of Endogenous Hydrogen Sulfide Pathway Is Involved in Mitochondrion-Related Endothelial Cell Apoptosis Induced by High Salt.OXIDATIVE MEDICINE AND CELLULAR LONGEVITY.
MLA Zong, Yanfang,et al."Downregulation of Endogenous Hydrogen Sulfide Pathway Is Involved in Mitochondrion-Related Endothelial Cell Apoptosis Induced by High Salt".OXIDATIVE MEDICINE AND CELLULAR LONGEVITY (2015).
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