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Cerebral Ischemia–Reperfusion Induces GAPDH S-Nitrosylation and Nuclear Translocation

Chong Li1‡, Jun-Jun Feng1‡, Yong-Ping Wu2, and Guang-Yi Zhang1*

1Jiangsu Province Key Laboratory of Brain Disease Bioinformation and Research Center of Biochemistry and Molecular Biology, Xuzhou Medical College, 84 West Huai-hai Road, Xuzhou 221002, Jiangsu, China; fax: +86-516-8574-8486; E-mail: gyzhang@xzmc.edu.cn

2Jiangsu Province Key Laboratory of Anesthesiology, Xuzhou Medical College, Xuzhou, Jiangsu, China

These authors contributed equally to this work.

* To whom correspondence should be addressed.

Received December 2, 2011; Revision received March 10, 2012
Glyceraldehyde-3-phosphate dehydrogenase (GAPDH), a glycolytic enzyme, plays an important role in glycolysis. It was reported that GAPDH undergoes S-nitrosylation, which facilitated its binding to Siah1 and resulted in nuclear translocation and cell apoptosis. The results of this study show that GAPDH S-nitrosylation, Siah1 binding, translocation to nucleus, and concomitant neuron death occur during the early stages of reperfusion in the rat four-vessel occlusion ischemic model. N-Methyl-D-aspartate receptor antagonist MK801, neuronal nitric oxide synthase inhibitor 7-nitroindazole, or monoamine oxidase-B inhibitor (R)-(–)-deprenyl hydrochloride could inhibit GAPDH S-nitrosylation and translocation and exert neuroprotective effects.
KEY WORDS: GAPDH, S-nitrosylation, Siah1, deprenyl hydrochloride, cerebral ischemia

DOI: 10.1134/S0006297912060156