Long non-coding RNA RMST promotes oxygen-glucose deprivation-induced injury in brain microvascular endothelial cells by regulating miR-204-5p/VCAM1 axis

Aims Many long non-coding RNAs (lncRNAs) have been suggested to play critical roles in the pathogenesis of ischemic stroke, including lncRNA rhabdomyosarcoma 2-associated transcript (RMST). We aimed to elucidate the role and molecular mechanism of RMST in ischemic stroke. Materials and methods The in vitro ischemic stroke model was established by treating brain microvascular endothelial cells with oxygen-glucose deprivation (OGD). The expression of RMST, miR-204-5p and vascular cell adhesion molecule 1 (VCAM1) were determined by quantitative real-time polymerase chain reaction (qRT-PCR). The interaction between miR-204-5p and RMST or VCAM1 was confirmed using dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Cell viability, migration and apoptosis were assessed by Cell Counting Kit-8 (CCK-8), wound healing assay and flow cytometry, respectively. Lactic dehydrogenase (LDH) leakage rate was determined by LDH activity assay kit. The protein level of VCAM1 was analyzed by western blot (WB) assay. Key findings RMST was upregulated in OGD-treated HBMEC and bEnd.3 cells. MiR-204-5p was a direct target of RMST, and miR-204-5p inhibition abated the inhibitory effect of RMST knockdown on OGD-induced injury via inhibiting cell viability and migration and promoting apoptosis in HBMEC and bEnd.3 cells. Moreover, VCAM1 was identified as a direct target of miR-204-5p, and VCAM1 alleviated the effect of miR-204-5p on reduction of OGD-induced injury in HBMEC and bEnd.3 cells. In addition, RMST regulated VCAM1 expression via sponging miR-204-5p. Significance RMST knockdown attenuated OGD-induced injury of HBMEC and bEnd.3 cells via regulating miR-204-5p/VCAM1 axis, indicating a possible therapeutic strategy for future ischemic stroke therapy.