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实验性短暂全脑及局灶性脑缺血再灌注后海马及半暗带中miR-126表达的动态变化

Dynamic Changes in miR-126 Expression in the Hippocampus and Penumbra Following Experimental Transient Global and Focal Cerebral Ischemia-Reperfusion.

作者信息

Xiao Zhang Hong, Wang Li, Gan Ping, He Jing, Yan Bing Chun, Ding Li Dong

机构信息

Department of Neurology, Taizhou Second People's Hospital, Taizhou, 225500, People's Republic of China.

Department of Neurology, Affiliated Hospital, Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, Yangzhou University, Yangzhou, 225001, People's Republic of China.

出版信息

Neurochem Res. 2020 May;45(5):1107-1119. doi: 10.1007/s11064-020-02986-4. Epub 2020 Feb 17.

Abstract

miR-126 which is considered one of the most important miRNAs for maintaining vascular integrity, plays an important role in neuroprotection after cerebral ischemia-reperfusion (I-R). Moreover, vascular endothelial growth factor A (VEGFA), sprouty-related EVH1 domain-containing protein 1 (SPRED1), and Raf-1 are also involved in physiological processes of vascular endothelial cells (ECs). This study investigated how miR-126 changes with reperfusion time in different brain tissues after global cerebral ischemia and focal cerebral ischemia and examined the underlying mechanism miR-126 involving VEGFA, SPRED1, and Raf-1 after I-R. The results indicated decreases in the levels of miR-126-3p and miR-126-5p expression in mice and gerbils after I-R, consistent with the results after oxygen and glucose deprivation and reperfusion (OGD/R) in PC12 cells. Glial cells were activated as neuronal damage gradually increased after I-R. Inhibition of miR-126-3p exacerbated the OGD/R-induced cell death and reduced cell viability. After miR-126-3p inhibition, the levels of SPRED1 and VEGFA expression were increased, and p-Raf-1 expression was decreased after OGD/R. Moreover, based on the intervention of miR-126-3p inhibition, we found that the expression of p-Raf-1 was significantly increased after the intervention of siSPRED1, while it was not statistically significant after intervention of siVEGFA. The reduction of miR-126 expression after global and focal cerebral ischemia exacerbated neuronal death, which was closely related to increasing the SPRED1 activation and inhibiting the Raf-1 expression.

摘要

miR-126被认为是维持血管完整性最重要的微小RNA之一,在脑缺血再灌注(I-R)后的神经保护中发挥重要作用。此外,血管内皮生长因子A(VEGFA)、含Sprouty相关EVH1结构域蛋白1(SPRED1)和Raf-1也参与血管内皮细胞(ECs)的生理过程。本研究调查了在全脑缺血和局灶性脑缺血后不同脑组织中miR-126如何随再灌注时间变化,并探讨了I-R后miR-126涉及VEGFA、SPRED1和Raf-1的潜在机制。结果表明,I-R后小鼠和沙鼠中miR-126-3p和miR-126-5p表达水平降低,这与PC12细胞氧糖剥夺和再灌注(OGD/R)后的结果一致。I-R后随着神经元损伤逐渐增加,胶质细胞被激活。抑制miR-126-3p会加剧OGD/R诱导的细胞死亡并降低细胞活力。抑制miR-126-3p后,OGD/R后SPRED1和VEGFA表达水平升高,p-Raf-1表达降低。此外,基于miR-126-3p抑制的干预,我们发现siSPRED1干预后p-Raf-1表达显著增加,而siVEGFA干预后无统计学意义。全脑和局灶性脑缺血后miR-126表达降低加剧了神经元死亡,这与SPRED1激活增加和Raf-1表达抑制密切相关。

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