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IR@PKUHSC  > 北京大学第三临床医学院  > 心血管内科  > 期刊论文
学科主题: 临床医学
题名:
Ischemic preconditioning attenuates mitochondrial localization of PTEN induced by ischemia-reperfusion
作者: Zu, Lingyun1,2; Zheng, Xiaoxu1; Wang, Bing3; Parajuli, Nirmal1; Steenbergen, Charles4; Becker, Lewis C.1; Cai, Zheqing P.1
关键词: Bax ; reperfusion injury ; apoptosis ; phosphatase and tensin homologs deleted on chromosome 10
刊名: AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
发表日期: 2011-06-01
DOI: 10.1152/ajpheart.01138.2010
卷: 300, 期:6, 页:H2177-H2186
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Cardiac & Cardiovascular Systems ; Physiology ; Peripheral Vascular Disease
研究领域[WOS]: Cardiovascular System & Cardiology ; Physiology
关键词[WOS]: SIGNAL-REGULATED KINASE ; PERMEABILITY TRANSITION ; INTACT HEARTS ; NITRIC-OXIDE ; ISCHEMIA/REPERFUSION INJURY ; INDUCED CARDIOPROTECTION ; DIFFERENTIAL ACTIVATION ; PROSURVIVAL KINASES ; OXIDATIVE STRESS ; PROTEIN-KINASES
英文摘要:

Zu L, Zheng X, Wang B, Parajuli N, Steenbergen C, Becker LC, Cai ZP. Ischemic preconditioning attenuates mitochondrial localization of PTEN induced by ischemia-reperfusion. Am J Physiol Heart Circ Physiol 300: H2177-H2186, 2011. First published March 18, 2011; doi: 10.1152/ajpheart.01138.2010.-Although the induction of myocyte apoptosis by ischemia-reperfusion (I/R) is attenuated by ischemic preconditioning (IPC), the underlying mechanism is not fully understood. Phosphatase and tensin homologs deleted on chromosome 10 (PTEN) promotes apoptosis through Akt-dependent and -independent mechanisms. We tested the hypothesis that IPC attenuates the mitochondrial localization of PTEN in the myocardium induced by I/R. Isolated hearts from wild-type mice were exposed to IPC or normal perfusion followed by 30 min of ischemia and reperfusion. IPC attenuated myocardial infarct size and apoptosis after I/R. Heart fractionation showed that mitochondrial PTEN and Bax protein levels and the physical association between them were increased by 30 min of I/R and that IPC attenuated all of these effects of I/R. Muscle-specific PTEN knockout decreased mitochondrial Bax protein levels in the reperfused myocardium and increased cell survival. To determine whether PTEN relocalization to mitochondria was influenced by I/R-induced production of ROS, hearts were perfused with N-acetylcysteine (NAC) to scavenge ROS or H(2)O(2) to mimic I/R-induced ROS. Mitochondrial PTEN protein levels were decreased by NAC and increased by H(2)O(2). PTEN protein overexpression was generated in mouse hearts by adenoviral gene transfer. PTEN overexpression increased mitochondrial PTEN and Bax protein levels and ROS production, whereas muscle-specific PTEN knockout produced the opposite effects. In conclusion, myocardial I/R causes PTEN localization to the mitochondria, related to the generation of ROS; IPC attenuates the mitochondrial localization of PTEN after I/R, potentially inhibiting the translocation of Bax to the mitochondria and resulting in improved cell viability.

语种: 英语
所属项目编号: HL-65608 ; HL-88071
项目资助者: National Heart, Lung, and Blood Institute
WOS记录号: WOS:000291209300024
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/55367
Appears in Collections:北京大学第三临床医学院_心血管内科_期刊论文

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作者单位: 1.Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD USA
2.Johns Hopkins Univ, Sch Med, Dept Med, Div Cardiol, Baltimore, MD 21205 USA
3.Peking Univ, Hosp 3, Dept Cardiol, Beijing 100871, Peoples R China
4.Johns Hopkins Univ, Sch Med, Dept Anesthesiol, Baltimore, MD USA

Recommended Citation:
Zu, Lingyun,Zheng, Xiaoxu,Wang, Bing,et al. Ischemic preconditioning attenuates mitochondrial localization of PTEN induced by ischemia-reperfusion[J]. AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY,2011,300(6):H2177-H2186.
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