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Protein {sl S}--nitrosylation: A role of nitric oxide signaling in cardiac ischemic preconditioning

Sun Junhui

Vascular Medicine Branch, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892

Abstract

Nitric oxide (NO) has been shown as an important signaling messenger involved in cardioprotection of ischemic preconditioning (IPC). To date, most studies suggest that NO might provide its protective effects by regulating the mitochondrial ATP-sensitive potassium (K_(ATP)) channel via the classic NO/cGMP-dependent pathway. However, there is emerging data suggesting that NO might also elicit its physiological role through protein S-nitrosylation. Protein S-nitrosylation, the covalent attachment of an NO moiety to sulfhydryl group(s) of cysteine residue(s) of proteins, is a reversible post-translational protein modification involved in redox-based cellular signaling. IPC has been found to increase S-nitrosothiol content and result in increased S-nitrosylation of proteins, which not only induces the structural and functional changes of modified proteins, but also prevents the target cysteine residue(s) from the further oxidative modification. In addition, S-nitrosothiols could elicit pharmacological preconditioning effect and protect against myocardial ischemia-reperfusion injury. Thus, protein S-nitrosylation is emerging as an important contributor to cardioprotection in IPC, providing protection from cellular oxidative and nitrosative stress,

Key words: S-nitrosylation;ischemic preconditioning;Nitric oxide;cardioprotection

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Citing This Article：

Sun Junhui. Protein {sl S}--nitrosylation: A role of nitric oxide signaling in cardiac ischemic preconditioning. Acta Physiol Sin 2007; 59 (5): 544-552 (in Chinese with English abstract).