LncRNA MIAT activates vascular endothelial growth factor A through RAD21 to promote nerve injury repair in acute spinal cord injury

The main pathological feature of acute spinal cord injury (ASCI) is neuronal apoptosis and Long non-coding RNA (lncRNA) myocardial infarction-related transcript (MIAT) is involved in the regulation of neuronal apoptosis. This study aimed to investigate the role and potential mechanism of LncRNA MIAT in neuronal apoptosis induced by ASCI. After Lenti-MIAT lentivirus was microinjected into ASCI rats, Basso, Beattie and Bresnahan Score, Hematoxylin-eosin staining, TUNEL staining, immunohistochemical, immunofluorescence, quantitative real-time PCR and Western blot were used to observe the effect of LncRNA MIAT on the nerve function of ASCI rats. MTT and flow cytometry assays were used to identify the in vitro function of LncRNA MIAT. RNA immunoprecipitation, RNA pull-down, Cycloheximide chase and Chromatin immunoprecipitation combined with qPCR experiments were used to study the mechanism. The overexpression of LncRNA MIAT was conducive to the recovery of motor function in ASCI rats and repressed neuronal cell apoptosis and increased neuronal cell viability. Furthermore, the overexpression of LncRNA MIAT in PC12 cells upregulated RAD21 expression by repressing RAD21 protein degradation and further promoted VEGFA transcription to inhibit neuronal cell apoptosis, ultimately improved ASCI. Our data indicated that the overexpression of LncRNA MIAT activated VEGFA through RAD21 to inhibit neuronal cell apoptosis in ASCI. •Protective effect of LncRNA MIAT on nerves in ASCI rats.•LncRNA MIAT binds to RAD21 protein and regulates its expression.•RAD21 regulates the transcription of VEGFA in PC12 cells.•LncRNA MIAT promotes the survival and regeneration of injured neurons through the RAD21/VEGFA signaling pathway.