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miR-130a-5p 通过调控 FAS 促进内皮细胞损伤的进展。

MiR-130a-5p contributed to the progression of endothelial cell injury by regulating FAS.

机构信息

The First Clinical College of Jinan University, Guangzhou, and Surgical Oncology Department, the Second Affiliated Hospital of Bengbu Medical College, Bengbu.

Vascular Surgery Department, the First Affiliated Hospital of Bengbu Medical College, Bengbu.

出版信息

Eur J Histochem. 2022 May 31;66(2):3342. doi: 10.4081/ejh.2022.3342.

DOI:10.4081/ejh.2022.3342
PMID:35638591
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9201574/
Abstract

MicroRNAs (miRNAs) play critical roles in the development of vascular diseases. However, the effects of miR-130a-5p and its functional targets on atherosclerosis (AS) are still largely unknown. In this regard, our aim is to explore the potentially important role of miR-130a-5p and its target gene during the progression of endothelial cell injury. We first found oxidized low-density lipoprotein (ox-LDL) induced FAS and cell apoptosis in HUVECs. Subsequently, miR-130a-5p expression was verified to be downregulated after ox-LDL treatment and negatively correlated with FAS, and FAS was identified as substantially upregulated in the ox-LDL-treated HUVEC cells. After that, the knockdown of FAS and overexpression of miR-130a-5p together were observed to aggregate ox-LDL-induced reduction of cell viability and apoptosis, cell cycle progression, cell proliferation, cell migration and invasion. In conclusion, we detected that miR-130a-5p contributed to the progression of endothelial cell injury by regulating of FAS, which may provide a new and promising therapeutic target for AS.

摘要

微小 RNA(miRNAs)在血管疾病的发展中发挥着关键作用。然而,miR-130a-5p 及其功能靶基因对动脉粥样硬化(AS)的影响在很大程度上仍然未知。在这方面,我们的目的是探讨 miR-130a-5p 及其靶基因在血管内皮细胞损伤进展过程中的潜在重要作用。我们首先发现氧化低密度脂蛋白(ox-LDL)诱导 HUVEC 中的 FAS 和细胞凋亡。随后,证实 ox-LDL 处理后 miR-130a-5p 的表达下调,与 FAS 呈负相关,并且在 ox-LDL 处理的 HUVEC 细胞中 FAS 明显上调。之后,观察到 FAS 的敲低和 miR-130a-5p 的过表达共同聚集 ox-LDL 诱导的细胞活力和凋亡减少、细胞周期进程、细胞增殖、细胞迁移和侵袭。总之,我们通过调节 FAS 检测到 miR-130a-5p 促进内皮细胞损伤的进展,这可能为 AS 提供一个新的有前途的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8090/9201574/de2fc6b59d5c/ejh-66-2-3342-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8090/9201574/04949d8d5504/ejh-66-2-3342-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8090/9201574/68dd0a066910/ejh-66-2-3342-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8090/9201574/0dee43d22f83/ejh-66-2-3342-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8090/9201574/923735035a01/ejh-66-2-3342-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8090/9201574/c101aa83bfa5/ejh-66-2-3342-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8090/9201574/de2fc6b59d5c/ejh-66-2-3342-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8090/9201574/04949d8d5504/ejh-66-2-3342-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8090/9201574/68dd0a066910/ejh-66-2-3342-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8090/9201574/0dee43d22f83/ejh-66-2-3342-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8090/9201574/923735035a01/ejh-66-2-3342-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8090/9201574/c101aa83bfa5/ejh-66-2-3342-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8090/9201574/de2fc6b59d5c/ejh-66-2-3342-g006.jpg

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