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Downregulation of Endogenous Hydrogen Sulfide Pathway Is Involved in Mitochondrion-Related Endothelial Cell Apoptosis Induced by High Salt
المؤلفون المشاركون
Junbao, D.
Zong, Yanfang
Huang, Yaqian
Chen, Siyao
Zhu, Mingzhu
Chen, Qinghua
Feng, Shasha
Sun, Yan
Zhang, Qingyou
Tang, Chaoshu
Jin, Hongfang
المصدر
Oxidative Medicine and Cellular Longevity
العدد
المجلد 2015، العدد 2015 (31 ديسمبر/كانون الأول 2015)، ص ص. 1-11، 11ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2015-05-11
دولة النشر
مصر
عدد الصفحات
11
التخصصات الرئيسية
الملخص 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.
نمط استشهاد جمعية علماء النفس الأمريكية (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
نمط استشهاد الجمعية الأمريكية للغات الحديثة (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
نمط استشهاد الجمعية الطبية الأمريكية (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
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1075758
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
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