GSE209940
RBM25 affects the immune and inflammatory progress by binding to and modulating alternative splicing levels of associated genes in rat H9C2 cells [ABL2020-10020-ABF_RBM25_OE]
Alternative splicing (AS) enables genes to be translated into a vast diversity of proteins while aberrant AS predisposes cells to abnormal biological processes. As is closely associated with AS, RNA binding proteins (RBPs) are gradually gaining attention. RBM 25 was reported to participate in the cardiac pathophysiological process via AS regulation. Nonetheless, gaps still existed in whether RBM 25 functions in heart failure by its splicing factor role. H9C2 cells with excessively expressed RBM25 were used to filtrate different expression genes (DEGs) and analyze for RBM25-regulated AS by RNA-seq. Next, iRIP-seq was performed to examine its binding targets. For genes screened, further RT-qPCR-based validation was conducted. RBM25 overexpression caused expressive alteration in 80 genes mainly involved in the inflammatory response and virus response. Notably, RBM25 partially modulated AS of differential genes enriched in the apoptotic process and bound to genes clustered at inflammation response. Further, qRT-PCR verified Slc38a9, IL-17RC, Csf1, and Coro6 as targets of RBM25 being bound to and AS-regulated. Herein, our work demonstrated that by exerting its binding capability, RBM25 may serve as a regulator of related RNA expressive levels and AS process to confer negative impacts on cardiac inflammation in cardiomyocytes. Our study provided preliminary evidence regarding the understanding of RBM25 in heart failure complicated by inflammation. Overall design: H9C2 cells with excessively expressed RBM25 were used to filtrate different expression genes (DEGs) and analyze for RBM25-regulated AS by RNA-seq. Next, iRIP-seq was performed to examine its binding targets.