Inhibiting miR-186 expression alleviates mitochondrial damage in hypoxic human umbilical vein endothelial cells.
10.12122/j.issn.1673-4254.2019.08.04
- Author:
Haifan YANG
1
;
Jiangang XIE
2
;
Jinming ZHANG
1
;
Yuan CHANG
1
;
Jing HAN
1
Author Information
1. Key Laboratory of Modern Teaching Technology of Ministry of Education, Shaanxi Normal University, Xi'an 710062, China.
2. Department of Emergency Medicine, Xijing Hospital, Air Force Medical University, Xi'an 710032, China.
- Publication Type:Journal Article
- Keywords:
hypoxia-inducible factor-1α;
miR-186;
mitochondrial damage;
vascular endothelial cells
- MeSH:
Cell Hypoxia;
Human Umbilical Vein Endothelial Cells;
Humans;
Hypoxia;
Hypoxia-Inducible Factor 1, alpha Subunit;
MicroRNAs;
Mitochondria;
Umbilical Veins
- From:
Journal of Southern Medical University
2019;39(8):898-903
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the effect of miR-186 inhibition on the expression of hypoxia-inducible factor-1α (HIF-α) and mitochondrial function in hypoxic vascular endothelial cells.
METHODS:Human umbilical vein endothelial cells (HUVECs) cultured in routine or hypoxic conditions for 6 h were examined for the expression of miR-186. A miR-186 inhibitor was transfected in the HUVECs, and the cells were subsequently cultured in hypoxic condition for 6 h to observe the changes in the mitochondrial structure under an electron microscope. The changes in the mRNA and protein expressions of HIF-1α in response to miR-186 interference were tested using real-time fluorescent quantitative PCR and Western blotting.
RESULTS:The expression of miR-18 was mildly increased in HUVECs after hypoxic exposure for 6 h (=0.0188). Interference of miR-186 expression obviously promoted the mRNA and protein expressions of HIF-1α in HUVECs. In hypoxic conditions, miR-186 interference significantly reduced mitochondrial damage in HUVECs as observed under electron microscope (=0.0297).
CONCLUSIONS:Inhibition of miR-186 protects vascular endothelial cells against hypoxic injuries by promoting HIF-α expression to lessen mitochondrial damage, suggesting the possibility of targeted miR-186 interference for treatment of hemorrhagic shock.
