Basic Research in Cardiology

, Volume 104, Issue 4, pp 377–389 | Cite as

Protection of peroxiredoxin II on oxidative stress-induced cardiomyocyte death and apoptosis

  • Wen Zhao
  • Guo-Chang Fan
  • Zhi-Guo Zhang
  • Arun Bandyopadhyay
  • Xiaoyang Zhou
  • Evangelia G. KraniasEmail author


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.


peroxiredoxin II cardiomyocytes protection H2O2 apoptosis 



This study was supported by NIH grants HL-26057, HL-64018, HL-77101 and the Leducq Foundation (to E.G.K), and by NIH grant HL-087861 (Dr. G. C. Fan).


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Copyright information

© Steinkopff Verlag Darmstadt 2008

Authors and Affiliations

  • Wen Zhao
    • 1
  • Guo-Chang Fan
    • 1
  • Zhi-Guo Zhang
    • 1
  • Arun Bandyopadhyay
    • 2
  • Xiaoyang Zhou
    • 3
  • Evangelia G. Kranias
    • 1
    • 4
    Email author
  1. 1.Dept. of Pharmacology and Cell BiophysicsUniversity of Cincinnati College of MedicineCincinnatiUSA
  2. 2.Indian Institute of Chemical BiologyKolkataIndia
  3. 3.Dept. of CardiologyRenmin Hospital of Wuhan UniversityWuhanPeople’s Republic of China
  4. 4.Foundation for Biomedical Research of the Academy of AthensAthensGreece

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