Author:
Zhu Hezhong,Liang Hui,Gao Zhen,Zhang Xiaoqiao,He Qian,He Chaoyong,Cai Chao,Chen Jiajuan
Abstract
Abstract
Background
In light of the abnormal expression of microRNA (miR-483-5p) in patients with atherosclerosis (AS), its role in vascular endothelial cell injury was explored. And the mechanisms related to autophagy were also elucidated.
Methods
Human umbilical vein endothelial cells (HUVECs) were given 100 mg/L ox-LDL to induce endothelial injury. Cell transfection was done to regulate miR-483-5p levels. Cell viability and apoptosis were detected. qRT-PCR was employed for the mRNA levels’ detection.
Results
Autophagic flux impairment of HUVECs was detected after ox-LDL treatment, along with the upregulation of miR-483-5p. Ox-LDL inhibited cell viability and promoted cell apoptosis, but these influences were changed by miR-483-5p downregulation. MiR-483-5p downregulation decreased the mRNA levels of IL-1β, IL-6, ICAM-1 and VCAM-1. 3-MA, the autophagy inhibitor, reversed the beneficial role of miR-483-5p downregulation in ox-LDL-induced HUVECs’ injury. TIMP2 acts as a target gene of miR-483-5p, and was downregulated in HUVEC models.
Conclusion
MiR-483-5p downregulation alleviated ox-LDL-induced endothelial injury via activating autophagy, this might be related to TIMP2.
Publisher
Springer Science and Business Media LLC
Subject
Cardiology and Cardiovascular Medicine
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