Objectives: Coronary 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 brainderived neurotrophic factor (BDNF) in hypoxic-treated human umbilical vein endothelial cells (HUVECs).Measures: We induced hypoxia in HUVECs using the "anaerobic tank method."Results: We 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.Conclusions: Therapeutic 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.Abbreviations: 3ʹ-UTR = 3ʹ-untranslated region, BDNF = brain-derived neurotrophic factor, CHD = coronary heart disease, ECs = endothelial cells, HIF1A = hypoxia-inducible factor 1 subunit alpha, HUVECs = human umbilical vein endothelial cells, , mRNA = messenger RNA, NC = negative control.

Coronary heart disease is the most common heart disease and is the leading cause of cardiovascular death worldwide. Revascularization methods are considered effective against coronary heart disease However, the mechanism of molecular revascularization remains largely unknown. Endothelial cells are the primary cells that initiate angiogenesis and arteriogenesis and require a hypoxic environment for induction. In this study, we aimed to determine the expression and role of microRNA-195-3p in hypoxia-treated HUVEs (human umbilical vein endothelial cells). Herein, we induced hypoxia in human umbilical vein endothelial cells using the "Anaerobic tank method." Hypoxia injured human umbilical vein endothelial cells showed upregulation of microRNA-195-3p; decreased cell proliferation, migration, and autophagy; and increased apoptosis. Furthermore, the microRNA-195-3p inhibitor partially reversed the effects of hypoxia-induced injury of human umbilical vein endothelial cells. Therapeutic intervention using microRNA-195-3p inhibitor could maintain endothelial cell function under hypoxic conditions, improve cell activity, and be considered a new treatment strategy for coronary heart diseases.