• Medicine · Nov 2022

    miR-195-3p/BDNF axis regulates hypoxic injury by targeting P-ERK1/2 expression.

    • Wenjing Zhang, Bingshi Liu, Yanfang Wang, Lixian Sun Phd, Chao Liu, Haoran Zhang, Wei Qin, Jingyi Liu, Leng Han, and Weichao Shan.
    • Department of Cardiology, Affiliated Hospital of Chengde Medical University, Chengde, China.
    • Medicine (Baltimore). 2022 Nov 18; 101 (46): e31586e31586.

    ObjectivesCoronary heart disease (CHD) is the most common heart disease and the leading cause of cardiovascular deaths worldwide. Decreased endothelial cell (EC) proliferation, increased apoptosis, inflammation, and vascular dysfunction are considered vital factors in CHD. In this study, we aimed to determine the expression and role of microRNA-195-3p and brain-derived neurotrophic factor (BDNF) in hypoxic-treated human umbilical vein endothelial cells (HUVECs).MeasuresWe induced hypoxia in HUVECs using the "anaerobic tank method."ResultsWe found that the levels of microRNA-195-3p and BDNF were upregulated and apoptosis was increased. Furthermore, we found that BDNF/P-ERK1/2 regulated the expression of the mitochondrial apoptosis pathway proteins Bcl-2/BAX, which was downregulated under hypoxic conditions. Finally, the microRNA-195-3p inhibitor downregulated BDNF and P-ERK1/2, upregulated the Bcl-2/BAX axis, and partially reversed the effects of hypoxic-induced injury in HUVECs.ConclusionsTherapeutic intervention using the microRNA-195-3p/BDNF/P-ERK1/2/Bcl-2/BAX axis could maintain EC function under hypoxic conditions, improve cell activity, and serve as a new treatment strategy for CHDs.Copyright © 2022 the Author(s). Published by Wolters Kluwer Health, Inc.

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