Long non-coding RNA SNHG16 inhibits the oxygen-glucose deprivation and reoxygenation-induced apoptosis in human brain microvascular endothelial cells by regulating miR-15a-5p/bcl-2

MicroRNA (miR) 15a-5p can promote ischemia/reperfusion (I/R)-induced apoptosis of cerebral vascular endothelial cells, which is inhibited by long non-coding RNAs (lncRNAs). The present study investigated the potential of lncRNAs targeting miR-15a-5p to regulate oxygen-glucose deprivation and reoxygenation (OGD-R)-induced apoptosis of human brain microvascular endothelial cells (hBMECs). hBMECs were transfected with or without miR-15a-5p or its mutant, together with p-small nucleolar RNA host gene 16 (SNHG16) or its mutant. Following OGD-R, proliferation, apoptosis and miR-15a-5p, SNHG16 and Bcl-2 expression levels were determined using MTT, flow cytometry, reverse transcription-quantitative PCR or western blotting. The potential interaction of SNHG16 with miR-15a-5p was analyzed by pull-down, luciferase and immunoprecipitation assays. OGD-R induced apoptosis of hBMECs and increased miR-15a-5p expression levels in a time-dependent manner. miR-15a-5p overexpression decreased the proliferation of hBMECs and promoted apoptosis by decreasing Bcl-2 expression levels. SNHG16 was pulled-down by miR-15a-5p and anti-Ago2. miR-15a-5p overexpression significantly decreased SNHG16-regulated luciferase activity and hBMEC survival by increasing apoptosis. SNHG16 overexpression decreased miR-15a-5p expression levels in hBMECs. SNHG16 gradually decreased following OGD-R and its overexpression decreased miR-15a-5p expression levels and promoted the proliferation of hBMECs by decreasing apoptosis. SNHG16 enhanced Bcl-2 expression levels in hBMECs, which was abrogated by miR-15a-5p. Bioinformatics suggest that SNHG16 may antagonize the binding of miR-15a-5p to the 3′UTR of Bcl-2 mRNA. These findings suggest that SNHG16 may protect hBMECs from OGD-R-induced apoptosis by antagonizing the miR-15a-5p/bcl-2 axis. Thus, targeting SNHG16-based mechanisms may provide novel therapeutic strategies for treatment of ischemic stroke.