title: Cerebral ischemia-reperfusion induces GAPDH S-nitrosylation and nuclear translocation.
abstract: 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.
authors: Jiangsu Province Key Laboratory of Brain Disease Bioinformation and Research Center of Biochemistry and Molecular Biology, Xuzhou Medical College, Xuzhou 221002, Jiangsu, China.
authors: Chong
authors: C
authors: Li
authors: Jun-Jun
authors: JJ
authors: Feng
authors: Yong-Ping
authors: YP
authors: Wu
authors: Guang-Yi
authors: GY
authors: Zhang
mesh_terms: D021581:Active Transport, Cell Nucleus / Q000187:drug effects; D000704:Analysis of Variance; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D002545:Brain Ischemia / Q000378:metabolism*; D056547:CA1 Region, Hippocampal / Q000187:drug effects; D002467:Cell Nucleus / Q000201:enzymology; D016291:Dizocilpine Maleate / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000737:chemistry / Q000378:metabolism*; D006801:Humans; D007191:Indazoles / Q000494:pharmacology; D008297:Male; D008995:Monoamine Oxidase / Q000378:metabolism; D018696:Neuroprotective Agents / Q000494:pharmacology*; D009569:Nitric Oxide / Q000378:metabolism; D052248:Nitric Oxide Synthase Type I / Q000037:antagonists & inhibitors / Q000378:metabolism; D009603:Nitroso Compounds / Q000737:chemistry; D009687:Nuclear Proteins / Q000378:metabolism; D017966:Pyramidal Cells / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors; D015427:Reperfusion Injury / Q000378:metabolism*; D012642:Selegiline / Q000494:pharmacology; D044767:Ubiquitin-Protein Ligases / Q000378:metabolism; D014805:Vitamin B 12 / Q000031:analogs & derivatives / Q000737:chemistry; D000098563:Seven in Absentia Proteins
chemical_list: D004791:Enzyme Inhibitors; D007191:Indazoles; D018696:Neuroprotective Agents; D009603:Nitroso Compounds; D009687:Nuclear Proteins; D016194:Receptors, N-Methyl-D-Aspartate; C113298:nitrosylcobalamin; D012642:Selegiline; D009569:Nitric Oxide; D016291:Dizocilpine Maleate; D052248:Nitric Oxide Synthase Type I; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases; D008995:Monoamine Oxidase; D044767:Ubiquitin-Protein Ligases; D000098563:Seven in Absentia Proteins; D014805:Vitamin B 12; C080122:7-nitroindazole