PRMT1 alleviates isoprenaline-induced myocardial hypertrophy by methylating SRSF1

• DOI: 10.3724/abbs.2024175
• Publication Date: 2024-09-29T08:03:43Z
• Authors: Zi Yan; Wenhui Zhao; Naixin Zhao; Yufeng Liu; Bowen Yang; Li Wang; Jingyi Liu; Deping Wang; Jin Wang; Xiangying Jiao; Jimin Cao; Jianguo Li
• Keywords: Isoprenaline; Myocardial hypertrophy

Myocardial hypertrophy (MH) is an important factor contributing to severe cardiovascular disease. Previous studies have demonstrated that specific deletion of the protein arginine methyltransferase 1 (PRMT1) leads MH, but exact mechanism remains unclear. Serine/arginine-rich splicing (SRSF1) affects development and progression disease by selectively downstream signaling proteins. The present study designed determine whether PRMT1 involved in MH regulating SRSF1 and, if so, explore underlying mechanisms. Adult male mice H9C2 cardiomyocytes are treated with isoprenaline (ISO) establish models. expression levels significantly decreased ISO-induced models, inhibiting worsens whereas overexpression ameliorates MH. serves as target PRMT1, its markedly elevated Moreover, increases mRNA expressions CaMKIIδ A B, decreases C altering selective CaMKIIδ, further participates In addition, there interaction between SRSF1, whereby reduces phosphorylation level via methylation, thus functional activity eventually improving Our demonstrates relieves methylating which expected provide a new theoretical basis for pathogenic potential drug targets reducing associated