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微小RNA-125b的上调导致内皮祖细胞对炎症损伤产生抗性。

Upregulation of MicroRNA-125b Leads to the Resistance to Inflammatory Injury in Endothelial Progenitor Cells.

作者信息

Yang Ke, Liu Xing, Lin Wanwen, Zhang Yuanyuan, Peng Chaoquan

机构信息

Department of Cardiology, The Third Affiliated Hospital, Sun Yat-sen University, Tian-he Road, Guangzhou 510630, China.

出版信息

Cardiol Res Pract. 2020 Sep 14;2020:6210847. doi: 10.1155/2020/6210847. eCollection 2020.

DOI:10.1155/2020/6210847
PMID:33005452
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7509550/
Abstract

OBJECTIVES

MicroRNA-125b (miR-125b) has been recognized as one of the key regulators of the inflammatory responses in cardiovascular diseases recently. This study sought to dissect the role of miR-125b in modulating the function of endothelial progenitor cells (EPCs) in the inflammatory environment of ischemic hearts.

METHODS

EPCs were cultured and transfected with miR-125b mimic and negative control mimic. Cell migration and adhesion assays were performed after tumor necrosis factor- (TNF-) treatment to determine EPC function. Cell apoptosis was analyzed by flow cytometry. The activation of the NF-B pathway was measured by western blotting. EPC-mediated neovascularization in vivo was studied by using a myocardial infarction model.

RESULTS

miR-125b-overexpressed EPCs displayed improved cell migration, adhesion abilities, and reduced cell apoptosis compared with those of the NC group after TNF- treatment. miR-125b overexpression in EPCs ameliorated TNF--induced activation of the NF-B pathway. Mice transplanted with miR-125b-overexpressed EPCs showed improved cardiac function recovery and capillary vessel density than the ones transplanted with NC EPCs.

CONCLUSIONS

miR-125b protects EPCs against TNF--induced inflammation and cell apoptosis by attenuating the activation of NF-B pathway and consequently improves the cardiac function recovery and EPC-mediated neovascularization in the ischemic hearts.

摘要

目的

微小RNA-125b（miR-125b）最近已被公认为心血管疾病炎症反应的关键调节因子之一。本研究旨在剖析miR-125b在缺血性心脏炎症环境中调节内皮祖细胞（EPCs）功能的作用。

方法

培养EPCs并分别用miR-125b模拟物和阴性对照模拟物进行转染。在肿瘤坏死因子-α（TNF-α）处理后进行细胞迁移和黏附试验以确定EPCs的功能。通过流式细胞术分析细胞凋亡。采用蛋白质印迹法检测核因子-κB（NF-κB）通路的激活情况。利用心肌梗死模型研究EPCs在体内介导的新生血管形成。

结果

与阴性对照（NC）组相比，TNF-α处理后，过表达miR-125b的EPCs表现出改善的细胞迁移、黏附能力以及减少的细胞凋亡。EPCs中miR-125b过表达减轻了TNF-α诱导的NF-κB通路激活。与移植NC EPCs的小鼠相比，移植过表达miR-125b的EPCs的小鼠心脏功能恢复和毛细血管密度得到改善。

结论

miR-125b通过减弱NF-κB通路的激活保护EPCs免受TNF-α诱导的炎症和细胞凋亡，从而改善缺血性心脏的心脏功能恢复和EPCs介导的新生血管形成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1b1/7509550/fb39a354e9d3/CRP2020-6210847.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1b1/7509550/c0d8a8e56454/CRP2020-6210847.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1b1/7509550/4fca2846da57/CRP2020-6210847.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1b1/7509550/fb39a354e9d3/CRP2020-6210847.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1b1/7509550/c0d8a8e56454/CRP2020-6210847.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1b1/7509550/4fca2846da57/CRP2020-6210847.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1b1/7509550/fb39a354e9d3/CRP2020-6210847.003.jpg

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