Circ_0000566 contributes oxygen-glucose deprivation and reoxygenation (OGD/R)-induced human brain microvascular endothelial cell injury via regulating miR-18a-5p/ACVR2B axis.

Circular RNAs (circRNAs) exert regulatory roles in cerebrovascular disease. Human brain microvascular endothelial cells (HBMECs) participated in brain vascular dysfunction in ischemic stroke. Herein, the functions of circ_0000566 in oxygen-glucose deprivation and reoxygenation (OGD/R)-induced HBMECs were investigated. The expression of circ_0000566, miR-18a-5p, and Activin receptor type 2B (ACVR2B) was measured via quantitative real-time PCR (qRT-PCR). Cell Counting Kit-8 (CCK-8) and flow cytometry assays were utilized to detect cell viability and cell apoptosis. Western blot assay was employed to measure the levels of apoptotic-related proteins and ACVR2B. The secretion of IL-1ß, IL-6, and TNF-α was detected via corresponding kits. The relationship between miR-18a-5p and circ_0000566 or ACVR2B was examined via dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Circ_0000566 and ACVR2B were highly expressed, while miR-18a-5p was down-regulated in OGD/R-treated HBMECs. OGD/R treatment promoted HBMECs apoptosis and inflammation and suppressed cell viability, which could be attenuated by silencing of circ_0000566. Circ_0000566 acted as a miR-18a-5p sponge to contribute to OGD/R-induced HBMECs injury. ACVR2B served as a direct target of miR-18a-5p, and ACVR2B overexpression might abolish the inhibitory role of miR-18a-5p on OGD/R-treated HBMEC injury. Circ_0000566 sponged miR-18a-5p to regulate OGD/R-induced HBMECs injury via regulating ACVR2B expression.