The expression of SIRT3 signaling in hypoxia-induced endothelial injury
CHEN Chun-juan1
LIN Mei-ling2
WANG Wei1
YU Wei3
1.Department of Cardiology, Second Affiliated Hospital of Shantou University Medical College, Shantou 515041, China2.Department of Cardiology, Second Affiliated Hospital of Shantou University Medical College, Shantou 515041, China;Department of Cardiology, First Affiliated Hospital of Shantou University Medical College, Shantou 515041, China3.Department of Cardiology, Second Affiliated Hospital of Shantou University Medical College, Shantou 515041, China;Department of Internal Medicine, Xiang'an Hospital of Xiamen University, Xiamen 361102, China
摘要:Background Oxidative injury to the endothelial cells plays an important role in development of atherosclero-sis.Investigation of the mechanisms of oxidative endothelial injury is of great importance.Our previous report has demonstrated that Sirtuin 3(SIRT3)protect cardiomyocytes from oxidative stress-mediated cell death via acti-vating the nuclear factor kappa-B(NF-κB)signaling pathway.However,the role and exact mechanisms of SIRT3 signaling in endothelial hypoxia injury are largely unknown.The present study aimed to investigate the expres-sion of SIRT3,hypoxia-inducible factor 1α(HIF-1α),and NF-KB/TNF-α(tumor necrosis factor-α)in human um-bilical vein endothelial cells(HUVECs)treated by hypoxia.Methods Hypoxia model was established by anox-ic tank and randomly divided into 3 groups:control group,lh hypoxia group,and 3h hypoxia group.3-(4,5-dime-trylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)detected the cell viability under hypoxia condition,and the intracellular reactive oxygen species(ROS)generation was determined by 2',7'-Dichlorodihydrofluorescein diacetate(DCFH-DA).The expression of mRNA and protein of the SIRT3 signaling were detected by real-time quantitative polymerase chain reaction(qPCR)and western blot analysis,respectively.Results Hypoxia treat-ment time-dependently decreased the cell viability,especially in the first hour.ROS production significantly in-creased in the first hour of hypoxia compared with those in the second and the third hour.Hypoxic stimuli signifi-cantly elevated SIRT3 mRNA and protein expression.Furthermore,real-time qPCR results showed that elevated SIRT3 significantly increased the mRNA expression of HIF-1α and NF-KB/TNF-α in lh hypoxia group.Western blot results also showed that elevated SIRT3 significantly increased the protein expression of NF-κB in the lh hy-poxia group.Conclusions The present study indicated that hypoxic stimuli promoted the expression of SIRT3,HIF-1α,and NF-KB/TNF-α,and suggested that SIRT3 signaling pathway may participate in the physiological process of acute ischemic hypoxia stress in human endothelial cells.
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论文发表日期:2020-12-30
在线出版日期:2025-08-15(本平台首次上网日期,不代表文献的发表时间)
页数:8( 277-284 )
英文信息展开
岭南心血管病杂志(英文版)

岭南心血管病杂志(英文版)

ISSN:1009-8933
年,卷(期):2020,21(4)
所属栏目:BASIC RESEARCH