Objective To investigate whether microRNA-20a-5p (miR-20a-5p) regulates the proliferation and apoptosis of human brain microvascular endothelial cells by down-regulating the BMPR2 gene. Methods MiR-20a-5p mimics, BMPR2 small interfering RNA (si-BMPR2) or overexpression plasmid (pcDNA-BMPR2) were transfected into immortalized human brain microvascular endothelial cells (hCMEC / D3). qRT-PCR was used to determine the expression of miR-20a-5p. Western Blot detected the expression of BMPR2, CyclinD1, Cleaved-caspase-3, p-PI3K, p-AKT protein, thiazole blue (MTT) to assay cell proliferation, and flow cytometry to detect cell apoptosis. Bioinformatics prediction and luciferase reporter gene detection analyzed the relationship between miR-20a-5p and BMPR2. Co-transfected miR-20a-5p mimics and pcDNA-BMPR2, using the above method to evaluate their effects on cell proliferation, apoptosis and PI3K/AKT signaling pathway. Results Overexpression of miR-20a-5p significantly increased hCMEC/D3 cell activity, CyclinD1, p-PI3K, and p-AKT protein expression, and greatly decreased the apoptosis rate and Cleared-caspase-3 protein expression (P＜0.05). Low expression of BMPR2 obviously enhanced hCMEC/D3 cell activity, CyclinD1 protein expression level, dramatically reduced the apoptosis rate and the level of Cleaved-caspase 3 protein expression(P＜0.05), while high expression of BMPR2 showed the opposite effects. miR-20a-5p targets BMPR2 and regulates the expression of BMPR2 protein. Overexpression of BMPR2 can reverse the effects of miR-20a-5p on promoting hCMEC / D3 proliferation, PI3K/AKT signaling pathway activity and inhibiting apoptosis. Conclusion miR-20a-5p activates PI3K/AKT signaling pathway by targeting BMPR2, promotes the proliferation of human brain microvascular endothelial cells, and inhibits apoptosis.