S-nitrosylation of PTEN Invovled in Ischemic Brain Injury in Rat Hippocampal CA1 Region
The tumor suppressor PTEN (phosphatase and tensin homolog deleted on chromosome 10) is not only a protein, but also a lipid phosphatase that can negatively regulate the serine/threonine kinase Akt. It has been reported that PTEN can be regulated by means of phosphorylation. However, whether PTEN can be regulated by another post-translational protein modification (S-nitrosylation) was not fully elucidated. In this study, we investigated the S-nitrosylation of PTEN during transient cerebral ischemia/reperfusion in rat hippocampus. Transient brain ischemia was induced by the four-vessel occlusion in Sprague–Dawley rats. Our data show that S-nitrosylation of PTEN was increased significantly after 12 h of reperfusion compared with sham control. Pretreatment with the inhibitor of nNOS (7-NI) and the inhibitor of iNOS could inhibit PTEN’s activity and decrease S-nitrosylation of PTEN. Taken together, these results indicate that nitric oxide could regulate PTEN’s activity via S-nitrosylation during transient global ischemia in rat hippocampus.
KeywordsCerebral ischemia S-nitrosylation PTEN
This article was supported by a grant from the Project of the National Natural Science Foundation of China (No. 30800309). President Special Grant of Xuzhou Medical College 08KJZ02 and Natural Science Research Funds of Jiangsu Province (No. BK2006035 and BK2006536).
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