Downregulation of Endogenous Hydrogen Sulfide Pathway Is Involved in Mitochondrion-Related Endothelial Cell Apoptosis Induced by High Salt
Joint Authors
Junbao, D.
Zong, Yanfang
Huang, Yaqian
Chen, Siyao
Zhu, Mingzhu
Chen, Qinghua
Feng, Shasha
Sun, Yan
Zhang, Qingyou
Tang, Chaoshu
Jin, Hongfang
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2015, Issue 2015 (31 Dec. 2015), pp.1-11, 11 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2015-05-11
Country of Publication
Egypt
No. of Pages
11
Main Subjects
Abstract EN
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.
American Psychological Association (APA)
Zong, Yanfang& Huang, Yaqian& Chen, Siyao& Zhu, Mingzhu& Chen, Qinghua& Feng, Shasha…[et al.]. 2015. Downregulation of Endogenous Hydrogen Sulfide Pathway Is Involved in Mitochondrion-Related Endothelial Cell Apoptosis Induced by High Salt. Oxidative Medicine and Cellular Longevity،Vol. 2015, no. 2015, pp.1-11.
https://search.emarefa.net/detail/BIM-1075758
Modern Language Association (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 No. 2015 (2015), pp.1-11.
https://search.emarefa.net/detail/BIM-1075758
American Medical Association (AMA)
Zong, Yanfang& Huang, Yaqian& Chen, Siyao& Zhu, Mingzhu& Chen, Qinghua& Feng, Shasha…[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. Vol. 2015, no. 2015, pp.1-11.
https://search.emarefa.net/detail/BIM-1075758
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1075758