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

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 brain-derived 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.

Automated summary

In this study, the expression and role of microRNA-195-3p and brain-derived neurotrophic factor (BDNF) in hypoxic-treated human umbilical vein endothelial cells (HUVECs) were investigated. It was found that microRNA-195-3p and BDNF levels were upregulated and apoptosis was increased under hypoxic conditions. Additionally, BDNF/P-ERK1/2 was shown to regulate the expression of mitochondrial apoptosis pathway proteins Bcl-2/BAX. The results suggest that therapeutic intervention targeting the microRNA-195-3p/BDNF/P-ERK1/2/Bcl-2/BAX axis could be a new treatment strategy for coronary heart disease (CHD).