PUM2 knockdown regulates the expression and alternative splicing of genes associated with myocardial fibrosis in H9C2 cells

Myocardial fibrosis (MF) represents a major pathological alteration observed in the progression of numerous heart conditions. The presence of excessive myocardial fibrosis is instrumental in the worsening of different heart diseases, which can ultimately lead to heart failure. It has been found that abnormal expression of Pumilio RNA-binding family member 2 (PUM2), an RNA-binding protein, is a contributing factor in the development of a variety of diseases. This study aims to investigate how PUM2 affects the expression and alternative splicing of genes associated with MF in H9C2 cells, thereby elucidating the role of PUM2 in this context. Overall design: Inhibition of PUM2 expression in H9C2 cardiomyocytes was achieved through siRNA transfection. Cell proliferation was assessed using the Cell Counting Kit-8 (CCK-8) assay, while apoptosis was detected via flow cytometry. RNA-seq was utilized to analyze the differential gene expression profiles and alternative splicing events in H9C2 cells regulated by PUM2. The sequencing results were confirmed through real-time quantitative polymerase chain reaction (RT-qPCR) experiments.