MicroRNAs (miRNAs) have emerged as critical regulators of neuronal survival during cerebral ischemia/reperfusion injury. Accumulating evidence has shown that miR-211 plays a crucial role in regulating apoptosis and survival in various cell types. However, whether miR-211 is involved in regulating neuronal survival during cerebral ischemia/reperfusion injury remains unknown. In this study, we aimed to explore the biological role of miR-211 in regulating neuronal injury induced by oxygen-glucose deprivation/reoxygenation (OGD/R) and transient cerebral ischemia/reperfusion (I/R) injury in vitro and in vivo. We found that miR-211 expression was significantly downregulated in PC12 cells in response to OGD/R and in the penumbra of mouse in response to MCAO. Overexpression of miR-211 alleviated OGD/R-induced PC12 cell apoptosis, whereas miR-211 inhibition facilitated OGD/R-induced PC12 cell apoptosis in vitro. Moreover, overexpression of miR-211 reduced infarct volumes, neurologic score, and neuronal apoptosis in vivo, whereas miR-211 inhibition increased infarct volumes, neurologic score and neuronal apoptosis in vivo. Notably, our results identified P53-up-regulated modulator of apoptosis (PUMA) as a target gene of miR-211. Our findings suggested that miR-211 may protect against MCAO injury by targeting PUMA in rats, which paves a potential new way for the therapy of cerebral I/R injury.

中文翻译：

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MiR-211通过抑制细胞凋亡来保护脑缺血/再灌注损伤。

MicroRNA（miRNA）已成为脑缺血/再灌注损伤期间神经元存活的关键调节剂。越来越多的证据表明，miR-211在调节各种细胞类型的凋亡和存活中起着至关重要的作用。但是，miR-211是否参与调节脑缺血/再灌注损伤期间的神经元存活。在这项研究中，我们旨在探讨miR-211在调节体内和体外由氧葡萄糖剥夺/复氧（OGD / R）和短暂性脑缺血/再灌注（I / R）损伤引起的神经元损伤中的生物学作用。我们发现在响应OGD / R的PC12细胞中以及在响应MCAO的小鼠半影中miR-211表达明显下调。miR-211的过表达减轻了OGD / R诱导的PC12细胞凋亡，而miR-211抑制促进了OGD / R诱导的PC12细胞体外凋亡。此外，miR-211的过表达减少了体内的梗塞体积，神经系统评分和神经元凋亡，而miR-211抑制作用则增加了体内的梗塞体积，神经系统评分和神经元凋亡。值得注意的是，我们的研究结果确定了P53上调的凋亡调节剂（PUMA）是miR-211的靶基因。我们的发现表明，miR-211可以通过靶向大鼠PUMA来预防MCAO损伤，这为治疗脑I / R损伤铺平了一条潜在的新途径。我们的结果确定了P53上调的凋亡调节剂（PUMA）是miR-211的靶基因。我们的发现表明，miR-211可以通过靶向大鼠PUMA来预防MCAO损伤，这为治疗脑I / R损伤铺平了一条潜在的新途径。我们的结果确定了P53上调的凋亡调节剂（PUMA）是miR-211的靶基因。我们的发现表明，miR-211可以通过靶向大鼠PUMA来预防MCAO损伤，这为治疗脑I / R损伤铺平了一条潜在的新途径。