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增加颞肌中 microRNA-126-5p 的表达可以促进两血管阻塞加脑膜脑肌血管融通术大鼠慢性缺血大脑中的血管生成。

Increasing the expression of microRNA-126-5p in the temporal muscle can promote angiogenesis in the chronically ischemic brains of rats subjected to two-vessel occlusion plus encephalo-myo-synangiosis.

机构信息

Department of Neurosurgery, Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510630, Guangdong, PR China.

Department of Rehabilitation, Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510630, Guangdong, PR China.

出版信息

Aging (Albany NY). 2020 Jul 9;12(13):13234-13254. doi: 10.18632/aging.103431.

DOI:10.18632/aging.103431
PMID:32644942
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7377842/
Abstract

BACKGROUND: miR-126-5p plays an important role in promoting endothelial cell (EC) proliferation. We thus explored whether miR-126-5p can promote EC proliferation and angiogenesis in chronically ischemic brains (CIBs). RESULTS: Improved revascularization in moyamoya patients was correlated with upregulated miR-126-5p expression in the TM and DM. In vitro experiments showed that miR-126-5p promoted EC proliferation through the PI3K/Akt pathway. CIBs from the agomir group exhibited significantly higher p-Akt, VEGF, CD31 and eNOS expression compared with the control CIBs. The ICBP and the RCF were significantly better in the agomir compared with the control group. CONCLUSION: Increasing miR-126-5p expression in the TM can promote EC proliferation and angiogenesis in CIBs of 2VO+EMS rats through the PI3K/Akt pathway. METHODS: We assessed the correlation between revascularization and miR-126-5p expression in the temporal muscle (TM) and dura mater (DM) of moyamoya patients. The effect of miR-126-5p on EC proliferation and downstream signaling pathways was explored in vitro. We established an animal model of two-vessel occlusion plus encephalo-myo-synangiosis (2VO+EMS), transfected the TM with miR-126-5p agomir/antagomir, compared the expression of miR-126-5p and relevant downstream cytokines in brain tissue among different groups, and investigated the improvement in cerebral blood perfusion (ICBP) and the recovery of cognitive function (RCF).

摘要

背景：miR-126-5p 在促进内皮细胞（EC）增殖方面发挥着重要作用。因此，我们探讨了 miR-126-5p 是否可以促进慢性缺血性脑（CIB）中的 EC 增殖和血管生成。

结果：烟雾病患者的再血管化改善与 TM 和 DM 中 miR-126-5p 表达上调相关。体外实验表明，miR-126-5p 通过 PI3K/Akt 通路促进 EC 增殖。与对照组相比，激动组的 CIB 中 p-Akt、VEGF、CD31 和 eNOS 的表达明显更高。激动组的 ICBP 和 RCF 明显优于对照组。

结论：在 2VO+EMS 大鼠中，增加 TM 中的 miR-126-5p 表达可通过 PI3K/Akt 通路促进 CIB 中的 EC 增殖和血管生成。

方法：我们评估了再血管化与烟雾病患者颞肌（TM）和硬脑膜（DM）中 miR-126-5p 表达之间的相关性。在体外研究了 miR-126-5p 对 EC 增殖和下游信号通路的影响。我们建立了两血管闭塞加脑肌血管吻合术（2VO+EMS）的动物模型，将 TM 转染 miR-126-5p 激动剂/拮抗剂，比较不同组间脑组织中 miR-126-5p 及相关下游细胞因子的表达，并研究脑血灌注（ICBP）的改善和认知功能（RCF）的恢复。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e0aa/7377842/1a0b820aaf07/aging-12-103431-g015.jpg
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本文引用的文献

[1]
Hydrogen Sulfide Protects Against High Glucose-Induced Human Umbilical Vein Endothelial Cell Injury Through Activating PI3K/Akt/eNOS Pathway.

Drug Des Devel Ther. 2020-2-14

[2]
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