miR‐34a‐5p was involved in chronic intermittent hypoxia‐induced autophagy of human coronary artery endothelial cells via Bcl‐2/beclin 1 signal transduction pathway

Autophagy refers to the genetically regulated process to regulate the survival and death of cells, which is conserved in evolution. Typically, autophagy exerts a vital part under physiopathological conditions. Whether autophagy can be resulted from chronic intermittent hypoxia (CIH), a prominent characteristic of obstructive sleep apnea‐hypopnea syndrome (OSAHS), remains to be investigated. Furthermore, microRNAs (miRNAs) can serve as the regulating factors in a variety of benign and malignant diseases; nonetheless, it remains to be fully illustrated about the way by which miRNAs modulate autophagy. According to our results, for human coronary artery endothelial cells (HCAECs), CIH increased the expression of autophagy‐associated proteins, which depended on the concentration and time; besides, it could promote autophagic vacuole (AV) formation. In addition, CIH could activate beclin 1, which was dependent on dose and time. In HCAECs, microRNA‐34a‐5p (miR‐34a‐5p) was overexpressed after exposed to CIH, and its target protein B‐cell lymphoma 2 (Bcl‐2) was downregulated. Moreover, inhibiting miR‐34a‐5p increased Bcl‐2 and p62 expression, while downregulating beclin 1, Vps34, Atg5, and LC3 levels, implying the role of miR‐34a‐5p in CIH‐induced autophagy. Moreover, exogenous upregulation of Bcl‐2 could block miR‐34a‐5p influence on CIH‐induced autophagy through suppressing beclin 1 expression. Additionally, beclin 1 could enhance the autophagy induced by CIH. In conclusion, overexpression of miR‐34a‐5p activated beclin 1 through Bcl‐2 inhibition in CIH and participated in CIH‐induced autophagy. CIH induces injury of human coronary artery endothelial cells (HCAECs) via upregulating the autophagy. Beclin 1 upregulation is involved in CIH‐induced HCAECs autophagy. miR‐34a‐5p upregulation contributes to CIH‐induced HCAECs autophagy via Bcl‐2/beclin 1 pathway.