Protection of peroxiredoxin II on oxidative stress-induced cardiomyocyte death and apoptosis.
Protection of peroxiredoxin II on oxidative stress-induced cardiomyocyte death and apoptosis.
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DOI：
10.1007/s00395-008-0764-6
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发表时间：
2009-07
影响因子：
9.5
通讯作者：
Kranias EG
中科院分区：
文献类型：
--
作者：
Zhao W;Fan GC;Zhang ZG;Bandyopadhyay A;Zhou X;Kranias EG
Peroxiredoxin II, a cytosolic isoform of the antioxidant enzyme family, has been implicated in cancer-associated cell death and apoptosis, but its functional role in the heart remains to be elucidated. Interestingly, the expression levels of peroxiredoxin II were decreased in mouse hearts upon ischemia-reperfusion, while they were elevated in two genetically modified hyperdynamic hearts with phospholamban ablation or protein phosphatase 1 inhibitor 1 overexpression. To delineate the functional significance of altered peroxiredoxin II expression, adenoviruses encoding sense or antisense peroxiredoxin II were generated; cardiomyocytes were infected, and then subjected to H2O2 treatment to mimic oxidative stress-induced cell death and apoptosis. H2O2 stimulation resulted in a significant decrease of endogenous peroxiredoxin II expression, along with reduced cell viability in control cells. However, overexpression of peroxiredoxin II significantly protected from H2O2-induced apoptosis and necrosis, while downregulation of this enzyme promoted the detrimental effects of oxidative stress in cardiomyocytes. The beneficial effects of peroxiredoxin II were associated with increased Bcl-2 expression, decreased expression of Bax and attenuated activity of caspases 3, 9 and 12. Furthermore, there were no significant alterations in the expression levels of the other five isoforms of peroxiredoxin, as well as active catalase or glutathione peroxidase-1 after ischemia-reperfusion or H2O2 treatment. These findings suggest that peroxiredoxin II may be a unique antioxidant in the cardiac system and may represent a potential target for cardiac protection from oxidative stress-induced injury.
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DOI：
10.1152/ajpheart.2001.281.6.h2612
发表时间：
2001-12-01
影响因子：
4.8
作者：
Bao, JL;Sato, K;Post, MJ
通讯作者：
Post, MJ
影响因子：
5
作者：
Cullingford, TE;Wait, R;Sugden, PH
通讯作者：
Sugden, PH
影响因子：
9.5
作者：
Liu, Yanping;Yang, Xi-Ming;Downey, James M.
通讯作者：
Downey, James M.
影响因子：
20.1
作者：
Fan, GC;Chu, GX;Kranias, EG
通讯作者：
Kranias, EG
影响因子：
9.5
作者：
Dost, Turhan;Cohen, Michael V.;Downey, James M.
通讯作者：
Downey, James M.