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首页> 外文期刊>Brain research >The ERK5-MEF2C transcription factor pathway contributes to anti-apoptotic effect of cerebral ischemia preconditioning in the hippocampal CA1 region of rats.
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The ERK5-MEF2C transcription factor pathway contributes to anti-apoptotic effect of cerebral ischemia preconditioning in the hippocampal CA1 region of rats.

机译：ERK5-MEF2C转录因子途径有助于大鼠海马CA1区脑缺血预处理的抗凋亡作用。

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The purpose of the present study was to investigate the role of myocyte enhancer binding factor 2C (MEF2C), a common substrate of p38 kinase and extracellular signal-regulated kinase 5 (ERK5) in the hippocampal CA1 region following cerebral ischemia preconditioning (CIP) and without CIP. In animals that did not undergo preconditioning, MEF2C was significantly activated with an early peak at 30 min of reperfusion, which was followed by a pronounced decrease of MEF2C protein levels in the late phase of reperfusion (3-5 d). Co-immunoprecipitation studies failed to show an interaction between ERK5 and MEF2C, and ERK5-antisense oligonucleotide (ERK5-AS) had no effect on MEF2C activation, suggesting that the MEF2C activation is mediated by a kinase other than ERK5. Following preconditioning (3 min ischemia), MEF2C was strongly activated during the late stage of reperfusion (6 h-5 d). Co-immunoprecipitation studies showed that the interaction of ERK5 and MEF2C significantly increased at 3 d of reperfusion, and this increase was markedly inhibited by ERK5-AS. Inhibition of the ERK5-MEF2C pathway resulted in a significant increase in the number of TUNEL-positive apoptotic cells compared with CIP groups in the hippocampal CA1 region, and abolished the neuroprotective effect induced by CIP. Taken together, these results demonstrate that ERK5-MEF2C signaling is significantly enhanced in the hippocampus CA1 following CIP, and that ERK5-MEF2C signaling plays a critical role in the mediation of the anti-apoptotic and neuroprotective actions of ischemic preconditioning.
机译：本研究的目的是研究脑缺血预处理（CIP）后海马CA1区中p38激酶和细胞外信号调节激酶5（ERK5）的常见底物-肌细胞增强剂结合因子2C（MEF2C）的作用。没有CIP。在未进行预处理的动物中，MEF2C被显着激活，并在再灌注30分钟时出现一个高峰，随后在再灌注后期（3-5天）MEF2C蛋白水平显着下降。免疫共沉淀研究未能显示ERK5与MEF2C之间的相互作用，并且ERK5反义寡核苷酸（ERK5-AS）对MEF2C激活没有影响，这表明MEF2C激活是由ERK5以外的激酶介导的。预处理（3分钟局部缺血）后，MEF2C在再灌注后期（6 h-5 d）被强烈激活。免疫共沉淀研究表明，ERK5和MEF2C的相互作用在再灌注3 d时显着增加，而这种增加被ERK5-AS明显抑制。与海马CA1区的CIP组相比，ERK5-MEF2C途径的抑制导致TUNEL阳性凋亡细胞的数量显着增加，并消除了CIP诱导的神经保护作用。综上所述，这些结果表明，CIP后海马CA1中ERK5-MEF2C信号显着增强，并且ERK5-MEF2C信号在缺血预处理的抗凋亡和神经保护作用的调节中起关键作用。

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