Document Detail


Ischemic preconditioning attenuates mitochondrial localization of PTEN induced by ischemia-reperfusion.
MedLine Citation:
PMID:  21421815     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Lingyun Zu; Xiaoxu Zheng; Bing Wang; Nirmal Parajuli; Charles Steenbergen; Lewis C Becker; Zheqing P Cai
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-03-18
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  300     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2011 Jun 
Date Detail:
Created Date:  2011-06-02     Completed Date:  2011-08-23     Revised Date:  2014-03-19    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H2177-86     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / physiology
Hydrogen Peroxide / metabolism
Ischemic Preconditioning, Myocardial*
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Mitochondria, Heart / metabolism*
Models, Animal
Myocardial Reperfusion Injury / metabolism*,  pathology*
Myocardium / metabolism,  pathology
PTEN Phosphohydrolase / deficiency,  genetics,  metabolism*
Reactive Oxygen Species / metabolism
bcl-2-Associated X Protein / metabolism
Grant Support
ID/Acronym/Agency:
HL-65608/HL/NHLBI NIH HHS; HL-88071/HL/NHLBI NIH HHS; R01 HL039752/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Reactive Oxygen Species; 0/bcl-2-Associated X Protein; BBX060AN9V/Hydrogen Peroxide; EC 3.1.3.67/PTEN Phosphohydrolase
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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