The PPARγ Agonist Protects Cardiomyocytes from Oxidative Stress and Apoptosis <i>via</i> Thioredoxin Overexpression

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  • KIM Yeon-Jung
    Department of Internal Medicine, College of Medicine, Chungbuk National University
  • PARK Keon-Jea
    Department of Internal Medicine, College of Medicine, Chungbuk National University
  • SONG Joong-Ki
    Department of Internal Medicine, College of Medicine, Chungbuk National University
  • SHIM Tae-Jin
    Department of Veterinary Medicine, College of Veterinary Medicine, Chungbuk National University
  • ISLAM Kazi N
    Center for Translational Medicine, Temple University School of Medicine
  • BAE Jang-Whan
    Department of Internal Medicine, College of Medicine, Chungbuk National University
  • KIM Sang-Min
    Department of Internal Medicine, College of Medicine, Chungbuk National University
  • LEE Sang-Yeub
    Department of Internal Medicine, College of Medicine, Chungbuk National University
  • HWANG Kyung-Kuk
    Department of Internal Medicine, College of Medicine, Chungbuk National University
  • KIM Dong-Woon
    Department of Internal Medicine, College of Medicine, Chungbuk National University
  • CHO Myeong-Chan
    Department of Internal Medicine, College of Medicine, Chungbuk National University
  • RYU Keun Ho
    Database and Bioinformatics Laboratory, Chungbuk National University

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  • The PPARγ Agonist Protects Cardiomyocytes from Oxidative Stress and Apoptosis via Thioredoxin Overexpression
  • The PPARgamma agonist protects cardiomyocytes from oxidative stress and apoptosis via thioredoxin overexpression

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Oxidative stress has been implicated in the pathogenesis of various cardiovascular diseases, including ischemic heart disease and heart failure. The peroxisome proliferator-activated receptor gamma (PPARγ) agonist improves insulin sensitivity and limits tissue inflammation and cellular apoptosis, but there are few data on the relationship between the PPARγ agonist, rosiglitazone (RSG), and the thioredoxin (TRx) system in oxidatively stressed cardiomyocytes (CMCs). Here we provide evidence that the PPARγ agonist RSG protects rat CMCs from hydrogen peroxide (H2O2)-induced apoptosis by TRx overexpression. The expression levels of pAkt/Akt, pErk/Erk, survivin, Bcl-2/Bax-α, and manganese-superoxide dismutase were increased by RSG pretreatment in H2O2-injured rat CMCs. On the contrary, the expression levels of caspase-3 and p53 were decreased by RSG pretreatment. These effects of RSG were reversed by chemical inhibitors of TRx and the PPARγ antagonist. This suggests that RSG protects rCMCs from H2O2-induced oxidative stress through TRx overexpression and a PPARγ-dependent mechanism.

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