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Protein S-nitrosylation: a role of nitric oxide signaling in cardiac ischemic preconditioning / 生理学报
Acta Physiologica Sinica ; (6): 544-552, 2007.
Article in English | WPRIM | ID: wpr-258623
Responsible library: WPRO
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.
Subject(s)
Full text: Available Index: WPRIM (Western Pacific) Main subject: Oxidation-Reduction / Physiology / Myocardial Reperfusion Injury / Reperfusion Injury / Signal Transduction / Protein S / Cyclic GMP / Ischemic Preconditioning / Heart / Metabolism Language: English Journal: Acta Physiologica Sinica Year: 2007 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Main subject: Oxidation-Reduction / Physiology / Myocardial Reperfusion Injury / Reperfusion Injury / Signal Transduction / Protein S / Cyclic GMP / Ischemic Preconditioning / Heart / Metabolism Language: English Journal: Acta Physiologica Sinica Year: 2007 Type: Article