Suppression of canonical TGF- β signaling enables GATA4 to interact with H3K27me3 demethylase JMJD3 to promote cardiomyogenesis

Direct reprogramming of fibroblasts into cardiomyocytes (CMs) represents a promising strategy to regenerate CMs lost after ischemic heart injury. Overexpression of GATA4, HAND2, MEF2C, TBX5, miR-1, and miR-133 (GHMT2m) along with transforming growth factor beta (TGF- β) inhibition efficiently promotes reprogramming. However, the mechanisms by which TGF-β blockade promotes cardiac reprogramming remain unknown. Here, we identify interactions between the histone H3 lysine 27 trimethylation (H3K27me3) – demethylase JMJD3, the SWI/SNF remodeling complex subunit B RG1, and cardiac transcription factors.

Source: Journal of Molecular and Cellular Cardiology - December 24, 2020 Category: Cytology Authors: Andrew S. Riching, Etienne Danis, Yuanbiao Zhao, Yingqiong Cao, Congwu Chi, Rushita A. Bagchi, Brianna J. Klein, Hongyan Xu, Tatiana G. Kutateladze, Timothy A. McKinsey, Peter M. Buttrick, Kunhua Song Source Type: research