MBNL1 regulates isoproterenol-induced myocardial remodelling in vitro and in vivo.

Abstract

Myocardial remodelling is a common phenomenon in cardiovascular diseases, which threaten human health and the quality of life. Due to the lack of effective early diagnosis and treatment methods, the molecular mechanism of myocardial remodelling should be explored in depth. In this study, we observed the high expression of MBNL1 in cardiac tissue and peripheral blood of an isoproterenol (ISO)-induced cardiac hypertrophy mouse model. MBNL1 promoted ISO-induced cardiac hypertrophy and fibrosis by stabilizing Myocardin mRNA in vivo and in vitro. Meanwhile, an increase in MBNL1 may induce the apoptosis of cardiomyocytes treated with ISO via TNF-α signalling. Interestingly, MBNL1 can be activated by p300 in cardiomyocytes treated with ISO. At last, Myocardin can reverse activate the expression of MBNL1. These results suggest that MBNL1 may be a potential target for the early diagnosis and clinical treatment of myocardial remodelling.

• Authors: Yao Xu, Chen Liang, Ying Luo, Tongcun Zhang
• Journal: Journal of cellular and molecular medicine (J Cell Mol Med) Vol. 25 Issue 2 Pg. 1100-1115 (01 2021) ISSN: 1582-4934 [Electronic] England
• PMID: 33295096 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: © 2020 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.

Chemical References

• 3' Untranslated Regions
• DNA-Binding Proteins
• Mbnl1 protein, mouse
• Nuclear Proteins
• RNA, Messenger
• RNA-Binding Proteins
• Trans-Activators
• Tumor Necrosis Factor-alpha
• myocardin
• E1A-Associated p300 Protein
• Ep300 protein, mouse
• Isoproterenol

Topics

• 3' Untranslated Regions (genetics)
• Animals
• Animals, Newborn
• Apoptosis
• Base Sequence
• Cardiomegaly (genetics, metabolism, pathology, physiopathology)
• DNA-Binding Proteins (genetics, metabolism)
• Disease Models, Animal
• E1A-Associated p300 Protein (metabolism)
• Fibrosis
• Gene Expression Regulation
• Isoproterenol
• MAP Kinase Signaling System
• Mice, Inbred C57BL
• Myocardium (metabolism)
• Myocytes, Cardiac (metabolism, pathology)
• Nuclear Proteins (genetics, metabolism)
• Protein Binding
• RNA, Messenger (genetics, metabolism)
• RNA-Binding Proteins (genetics, metabolism)
• Trans-Activators (genetics, metabolism)
• Transcription, Genetic
• Tumor Necrosis Factor-alpha (metabolism)
• Ventricular Remodeling (genetics)