ArticleExperimental and therapeutic medicine2026
PUM2 knockdown regulates the expression and alternative splicing of genes associated with myocardial fibrosis in H9C2 cells.
Article in Experimental and therapeutic medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Myocardial fibrosis (MF) represents a major pathological alteration observed in the progression of numerous heart conditions. The presence of excessive MF is key in the progression of numerous heart diseases, which may lead to heart failure. 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. The present study aimed to investigate how PUM2 affected the expression and alternative splicing of genes associated with MF in H9C2 cells, thus evaluating the role of PUM2 in this context. Inhibition of PUM2 expression in H9C2 cardiomyocytes was achieved through small interfering RNA transfection. Cell viability was assessed using a Cell Counting Kit-8 assay, while apoptosis was detected through flow cytometry. RNA-sequencing (RNA-seq) was utilized to analyze the differential gene expression profiles and alternative splicing events (ASEs) in H9C2 cells regulated by PUM2. Sequencing results were confirmed through reverse transcription-quantitative PCR. The results showed that a reduction in PUM2 levels inhibited cell viability without affecting apoptosis. RNA-seq analysis revealed notable changes in the expression of various genes associated with MF, including adrenomedullin, NDRG family member 4, phospholipid phosphatase 3, integrin subunit α 8, regulator of G protein signaling 2, cadherin 11, integrin subunit α 11 and transforming growth factor β-induced, following PUM2 knockdown. In addition, PUM2 regulated ASEs in genes associated with fibrosis progression, such as tropomyosin 1 and actinin α1. The present study revealed that PUM2 had a regulatory effect on alternative splicing and gene expression associated with MF, suggesting PUM2 as a promising molecular target for MF therapy.
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