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首页> 外文期刊>Brain research >Regulation on Beclin-1 expression by mTOR in CoCl2-induced HT22 cell ischemia-reperfusion injury
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Regulation on Beclin-1 expression by mTOR in CoCl2-induced HT22 cell ischemia-reperfusion injury

机译：mTOR对CoCl2诱导的HT22细胞缺血再灌注损伤中Beclin-1表达的调节

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It has been reported that cerebral ischemia/reperfusion (I/R) injury can activate autophagy. However, the role of autophagy in cerebral I/R injury remains controversy. Two major proteins, mTOR and Beclin-1, govern the formation of autophagosomes to regulate autophagy activity. However, the cross-talking between Beclin-1 and mTOR in cerebral MR injury remains elusive. In this study, global cerebral I/R injury animal model and focal cerebral I/R injury animal model were induced to test the variation of Beclin-1 level in vivo. To further confirm the variation of Beclin-1 level and investigate the cross-talking between Beclin-1 and mammalian target of rapamycin (mTOR) in YR injury, we used cobalt chloride (CoC12) to develop an I/R injury cell model in HT22 cell line. Our data showed that the levels of Beclin-1 and phosphorylated mammalian target of rapamycin (p-mTOR) were clearly induced by I/R injury in vitro. And the time course studies suggested that the Beclin-1 and mTOR may have coordinated regulation in ischemia stages but not in reperfusion stages. Moreover, inhibitor of mTOR could prevent Beclin-1 decreasing, but this prevention may play opposite roles in different stages of I/R injury. We conclude that this study represents a major advance in our understanding of the cross-talking of two key proteins, Beclin-1 and mTOR, in autophagy and the role of autophagy in cerebral MR injury. (C) 2015 Elsevier B.V. All rights reserved.
机译：据报道，脑缺血/再灌注（I / R）损伤可激活自噬。然而，自噬在脑I / R损伤中的作用仍存在争议。两种主要蛋白质，mTOR和Beclin-1，控制自噬小体的形成以调节自噬活性。但是，Beclin-1和mTOR在脑MR损伤中的相互影响仍然难以捉摸。在这项研究中，诱导整体脑I / R损伤动物模型和局灶性脑I / R损伤动物模型来测试Beclin-1水平在体内的变化。为了进一步证实Beclin-1水平的变化并研究Beclin-1与哺乳动物雷帕霉素靶标（mTOR）在YR损伤中的相互作用，我们使用氯化钴（CoC12）建立了HT22中的I / R损伤细胞模型细胞系。我们的数据表明Beclin-1和雷帕霉素（p-mTOR）的磷酸化哺乳动物靶标的水平明显受到体外I / R损伤的诱导。时程研究表明，Beclin-1和mTOR在缺血阶段可能具有协同调节作用，而在再灌注阶段则没有。此外，mTOR抑制剂可以阻止Beclin-1的下降，但这种预防在I / R损伤的不同阶段可能起相反的作用。我们得出的结论是，这项研究代表了我们对自噬和自噬在脑MR损伤中两种关键蛋白Beclin-1和mTOR的相互作用的理解方面的重大进展。 （C）2015 Elsevier B.V.保留所有权利。

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