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MicroRNA miR-505-5p Promotes Oxygen-Glucose Deprivation/Reoxygenation-Induced Neuronal Injury via Negative Regulation of CREG1 in Cultured Neuron-Like Cells
Neurophysiology ( IF 0.5 ) Pub Date : 2019-11-01 , DOI: 10.1007/s11062-020-09835-8
Y. Gao , G. Nan , L. Chi

Cerebral ischemia/reperfusion (I/R) injury is associated with various cardiovascular and cerebrovascular diseases with high disability, morbidity, and mortality rates. MicroRNAs (miRNAs) are related to the pathogenesis of the above diseases. MiR-505-5p, a kind of such miRNAs, was found to be highly expressed in cerebral I/R injuries, but the mechanism of action of this miRNA in cerebral I/R injury was unclear. In our study, up-regulation of miR-505-5p was detected in cultured oxygen-glucose deprivation/reoxygenation (OGD/R)-subjected PC12 and HEC293 cells. Silencing of miR-505-5p in OGD/R-affected neuron-like cells not only decreased the OGD/R-injury (according to cell viability, SOD increase, and LDH and MDA decreases), but also reduced apoptosis (decreasing the cleaved caspase-3 and PARP protein levels). Interestingly, expression of CREG1 (Cellular Repressor of E1Astimulated Genes 1) was low in OGD/R-subjected neurons; it was verified as a possible target gene of miR-505-5p. CREG1 knockdown can reverse the effect of miR-505-5p silencing in OGD/R-induced neural injury. Taken together, the data obtained provide a new target for cerebral I/R injury treatment.

中文翻译:

MicroRNA miR-505-5p 通过培养神经元样细胞中 CREG1 的负调节促进氧-葡萄糖剥夺/再氧合诱导的神经元损伤

脑缺血/再灌注 (I/R) 损伤与各种心脑血管疾病相关,致残率、发病率和死亡率都很高。MicroRNAs(miRNAs)与上述疾病的发病机制有关。MiR-505-5p,一种这样的miRNA,被发现在脑I/R损伤中高表达,但该miRNA在脑I/R损伤中的作用机制尚不清楚。在我们的研究中,在培养的氧-葡萄糖剥夺/再氧合 (OGD/R) 的 PC12 和 HEC293 细胞中检测到 miR-505-5p 的上调。OGD/R 影响的神经元样细胞中 miR-505-5p 的沉默不仅减少了 OGD/R 损伤(根据细胞活力、SOD 增加和 LDH 和 MDA 减少),而且减少细胞凋亡(减少裂解caspase-3 和 PARP 蛋白水平)。有趣的是,CREG1(E1Astimulated Genes 1 的细胞抑制因子)在 OGD/R 受试神经元中的表达较低;它被证实为 miR-505-5p 的可能靶基因。CREG1 敲低可以逆转 miR-505-5p 沉默在 OGD/R 诱导的神经损伤中的作用。综上所述,所获得的数据为脑 I/R 损伤的治疗提供了新的靶点。
更新日期:2019-11-01
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