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Int. J. Mol. Sci. 2016, 17(7), 1100; doi:10.3390/ijms17071100

Neuroprotective Effects of Inhibiting Fyn S-Nitrosylation on Cerebral Ischemia/Reperfusion-Induced Damage to CA1 Hippocampal Neurons

1,2,†
,
1,3,†
,
1
,
1,‡
and
1,*
1
Research Center for Biochemistry and Molecular Biology, and Jiangsu Key Laboratory of Brain Disease Bioinformation, Xuzhou Medical University, Xuzhou 221002, China
2
Jiangsu Key Laboratory of Anesthesia and Analgesia Application Technology, Xuzhou 221002, China
3
Department of Laboratory Medicine, Affiliated Municipal Hospital of Xuzhou Medical University, Xuzhou 221002, China
These authors contributed equally to this work.
This author has passed away.
*
Author to whom correspondence should be addressed.
Academic Editor: Katalin Prokai-Tatrai
Received: 1 May 2016 / Revised: 10 June 2016 / Accepted: 4 July 2016 / Published: 12 July 2016
(This article belongs to the Special Issue Neuroprotective Strategies 2016)
View Full-Text   |   Download PDF [3253 KB, uploaded 12 July 2016]   |  

Abstract

Nitric oxide (NO) can regulate signaling pathways via S-nitrosylation. Fyn can be post-translationally modified in many biological processes. In the present study, using a rat four-vessel-occlusion ischemic model, we aimed to assess whether Fyn could be S-nitrosylated and to evaluate the effects of Fyn S-nitrosylation on brain damage. In vitro, Fyn could be S-nitrosylated by S-nitrosoglutathione (GSNO, an exogenous NO donor), and in vivo, endogenous NO synthesized by NO synthases (NOS) could enhance Fyn S-nitrosylation. Application of GSNO, 7-nitroindazole (7-NI, an inhibitor of neuronal NOS) and hydrogen maleate (MK-801, the N-methyl-d-aspartate receptor (NMDAR) antagonist) could decrease the S-nitrosylation and phosphorylation of Fyn induced by cerebral ischemia/reperfusion (I/R). Cresyl violet staining validated that these compounds exerted neuroprotective effects against the cerebral I/R-induced damage to hippocampal CA1 neurons. Taken together, in this study, we demonstrated that Fyn can be S-nitrosylated both in vitro and in vivo and that inhibiting S-nitrosylation can exert neuroprotective effects against cerebral I/R injury, potentially via NMDAR-mediated mechanisms. These findings may lead to a new field of inquiry to investigate the underlying pathogenesis of stroke and the development of novel treatment strategies. View Full-Text
Keywords: cerebral ischemia and reperfusion; Fyn; S-nitrosylation; phosphorylation; neuroprotection cerebral ischemia and reperfusion; Fyn; S-nitrosylation; phosphorylation; neuroprotection
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Hao, L.; Wei, X.; Guo, P.; Zhang, G.; Qi, S. Neuroprotective Effects of Inhibiting Fyn S-Nitrosylation on Cerebral Ischemia/Reperfusion-Induced Damage to CA1 Hippocampal Neurons. Int. J. Mol. Sci. 2016, 17, 1100.

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