NDLI: Nuclear Factor E2-Related Factor 2-Dependent Myocardiac Cytoprotection Against Oxidative and Electrophilic Stress

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Nuclear Factor E2-Related Factor 2-Dependent Myocardiac Cytoprotection Against Oxidative and Electrophilic Stress

Content Provider	Springer Nature Link
Author	Zhu, Hong Jia, Zhenquan Misra, Bhaba R. Zhang, Li Cao, Zhuoxiao Yamamoto, Masayuki Trush, Michael A. Misra, Hara P. Li, Yunbo
Copyright Year	2008
Abstract	Nuclear factor E2-related factor 2 (Nrf2) is a critical regulator of cytoprotective gene expression. However, the role of this transcription factor in myocardiac cytoprotection against oxidative and electrophilic stress remains unknown. This study was undertaken to investigate if Nrf2 signaling could control the constitutive and inducible expression of antioxidants and phase 2 enzymes in primary cardiomyocytes as well as the susceptibility of these cells to oxidative and electrophilic injury. The basal expression of a series of antioxidants and phase 2 enzymes was significantly lower in cardiomyocytes from Nrf2$^{−/−}$ mice than those from wild-type littermates. Incubation of wild-type cardiomyocytes with 3H-1,2-dithiole-3-thione (D3T) led to significant induction of various antioxidants and phase 2 enzymes, including catalase, glutathione, glutathione peroxidase (GPx), glutathione reductase, glutathione S-transferase, NAD(P)H:quinone oxidoreductase 1, and heme oxygenase-1. The inducibility of the above cellular defenses except GPx by D3T was abolished in Nrf2$^{−/−}$ cardiomyocytes. As compared to wild-type cells, Nrf2$^{−/−}$ cardiomyocytes were much more susceptible to cell injury induced by H$_{2}$O$_{2}$, peroxynitrite, and 4-hydroxy-2-nonenal. Treatment of wild-type cardiomyocytes with D3T, which upregulated the cellular defenses, resulted in increased resistance to the above oxidant- and electrophile-induced cell injury, whereas D3T treatment of Nrf2$^{−/−}$ cardiomyocytes provided no cytoprotection. This study demonstrates that Nrf2 is an important factor in controlling both constitutive and inducible expression of a wide spectrum of antioxidants and phase 2 enzymes in cardiomyocytes and is responsible for protecting these cells against oxidative and electrophilic stress. These findings also implicate Nrf2 as an important signaling molecule for myocardiac cytoprotection.
Starting Page	71
Ending Page	85
Page Count	15
File Format	PDF
ISSN	15307905
Journal	Cardiovascular Toxicology
Volume Number	8
Issue Number	2
e-ISSN	15590259
Language	English
Publisher	Humana Press Inc
Publisher Date	2008-05-08
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Nrf2 Cardiomyocytes Antioxidants Phase 2 enzymes Oxidative stress Electrophilic stress Cardiology Pharmacology/Toxicology
Content Type	Text
Resource Type	Article
Subject	Molecular Biology Toxicology Cardiology and Cardiovascular Medicine

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