[The splicing factor HNRNPH1 regulates Circ-MYOCD back-splicing to modulate the course of cardiac hypertrophy].

• DOI: 10.12122/j.issn.1673-4254.2025.03.16
• Publication Date: 2025-03-20
• Authors: Rui Cai; Zhuo Huang; Wenxia He; Tianhong Ai; Xiaowei Song; Shuting Hu
• Keywords: Splicing factor

To explore the mechanism of Circ-MYOCD back-splicing and its regulatory role in myocardial hypertrophy. Sanger sequencing RNase R assays were performed to verify circularity stability Circ-MYOCD, whose subcellular distribution was determined by nuclear-cytoplasmic fractionation. Bioinformatics analysis mass spectrometry from pull-down conducted predict RNA-binding proteins (RBPs) interacting with Circ-MYOCD. In rat cardiomyocytes H9C2 cells, effects HNRNPH1 HNRNPL knockdown overexpression on evaluated. a cell model angiotensin II (Ang II)-induced hypertrophy, expression detected, progression hypertrophy assessed, effect analyzed. confirmed that junction primers could amplify correct sequence. fractionation showed stable predominantly localized cytoplasm. assay identified as RBPs significantly enhanced while inhibited back-splicing; obviously increased expressions markers ANP BNP, produced opposite effect. Ang II-induced which exhibited significant increase expression, decreased MYOCD lowered both BNP expressions. regulates influence