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The decrease of GluN2B and its phosphorylation at Tyr-1336 in extrasynaptic subunits is associated with neuroprotection induced by hypoxia preconditioning

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机构： [1]Department of Neurosurgery, Dongguan Qingxi Hospital, Dongguan, PR China [2]Inner Mongolia Key Laboratory of Hypoxic Translational Medicine, Baotou Medical College, Baotou, PR China [3]Beijing Key Laboratory of Hypoxic Conditioning Translational Medicine, Xuanwu Hospital, Capital Medical University, Beijing, PR China [4]Longgang Institute of Medical Imaging, Shantou University Medical College & The Third People’s Hospital of Longgang District, Shenzhen, PR China [5]Department of Oral and Maxillofacial Surgery, University of California San Francisco, San Francisco, USA [6]Department of Neurology, University of California San Francisco, San Francisco, CA, USA

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关键词： Hypoxic preconditioning Neuroprotection GluN2B Synapse

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Prior research has firmly established that the N-methyl-d-aspartate (NMDA) receptor subunit 2 B (GluN2B) and its phosphorylation contribute to ischemic/hypoxic brain injury. Hypoxic preconditioning (HPC) is an endogenous mechanism that protects the brain from both ischaemic and hypoxic damage. In this study, we explored the effects of HPC on GluN2B and its phosphorylation at two sites (tyrosine residues 1252 and 1336), catalysed by Fyn, in the hippocampus both in vivo and in vitro. Animal and cellular models of HPC were developed by subjecting mice and the mouse hippocampal neuronal cell line HT22 to repeated hypoxia. Levels of GluN2B and its phosphorylation at the tyrosine residues 1336 (pY1336 GluN2B) and 1252 (pY1252 GluN2B) were detected in HPC-treated hippocampi and HT22 cells using western blotting and immunofluorescence. The distributions of GluN2B, pY1336 GluN2B, and pY1252 GluN2B in the synaptic (TxP) and extrasynaptic components (TxS) were analysed by western blotting. Caspase-3 and spectrin, both markers of cellular injury, were further measured using western blotting. HPC downregulated GluN2B and pY1336 GluN2B levels in the hippocampus and HT22 cells. The changes in GluN2B and pY1336 GluN2B levels in the extrasynaptic components were similar to those in the hippocampus and HT22 cells, while the changes in the synaptic components showed the opposite trend which increased after HPC. The downregulation of GluN2B and pY1336 GluN2B may be associated with neuroprotection induced by HPC. Additionally, their localization at synaptic and extrasynaptic sites may play distinct roles in neuroprotection.Copyright © 2025 The Authors. Published by Elsevier Inc. All rights reserved.

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出版当年[2025]版：

大类 | 3 区医学

小类 | 3 区神经科学

最新[2025]版：

大类 | 3 区医学

小类 | 3 区神经科学

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出版当年[2023]版：

Q2 NEUROSCIENCES

最新[2024]版：

Q2 NEUROSCIENCES

影响因子： 3.7 最新[2024版] 3.6 最新五年平均 3.5 出版当年[2023版] 3.6 出版当年五年平均 3.8 出版前一年[2022版] 3.7 出版后一年[2024版]

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第一作者机构： [1]Department of Neurosurgery, Dongguan Qingxi Hospital, Dongguan, PR China

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通讯机构： [2]Inner Mongolia Key Laboratory of Hypoxic Translational Medicine, Baotou Medical College, Baotou, PR China [3]Beijing Key Laboratory of Hypoxic Conditioning Translational Medicine, Xuanwu Hospital, Capital Medical University, Beijing, PR China [4]Longgang Institute of Medical Imaging, Shantou University Medical College & The Third People’s Hospital of Longgang District, Shenzhen, PR China

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