Up-Regulating MEF2D Alleviates Hypoxia-Induced Injury in Cultured Rat Cortical Neurons

Background: Stroke is a severe disease and the associated molecular mechanisms for its pathogenesis have not been fully understood. Myocyte enhancer factor 2 (MEF2) is a family of transcription factors that promote the expression of more than 100 proteins responsible for development and surviving of neurons in central nervous system. Recently, it is reported in animal studies that MEF2D dysfunction plays an important role in neurodegenerative diseases. However, the role of MEF2D in stroke is unknown. The objective of the present study was to provide data for changes and role of MEF2 following hypoxic neuronal injury. Methods: The hypoxic injury was induced by oxygen-glucose deprivation (OGD) in primary cultured rat cortical neurons. The levels and activity of MEF2D mRNA and protein were measured by real-time reverse transcription polymerase chain reaction (RT-PCR) and western blot. Additionally, MEF2D overexpression by lentivirus was used to up-regulate the level of MEF2D. The effect of MEF2D up-regulation on neuron hypoxic tolerance was evaluated by assaying of cell viability and extracellular lactate dehydrogenase (LDH) release as well as cell apoptosis analysis.Results: Compared with control group, the level of MEF2D protein and the activity of MEF2D were decreased after OGD challenge. Up-regulating the level of MEF2D could increase the cell viability, decrease the LDH release and inhibit the activation of apoptotic protein caspase-3.Conclusion: MEF2D is involved in the pathophysiological process of hypoxic injury in rat primary cortical neurons. Up-regulation of MEF2D could alleviate the hypoxia-induced injury and increase neuronal tolerance against hypoxia.  Citation: Li-Kai Shi, Min Cai, Zhi-Xin Wu, Si-Si Sun, Zong-Ping Fang, Ting Gu, et al. Up-regulating MEF2D alleviates hypoxia-induced injury in cultured rat cortical neurons. J Anesth Perioper Med 2015; 2: 175-82. doi: 10.24015/JAPM.2015.0024This is an open-access article, published by Evidence Based Communications (EBC). This work is licensed under the Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium or format for any lawful purpose. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.