Fig 3.

Proposed models for the interaction of lncRNA-Chaer/TINCR and PRC2. In normal cases, PRC2 inhibits gene activation by trimethylation of H3K27 at the promoters. EZH2, EED, and SUZ12 are core components of PRC2 complex. A: Under stress stimulation, lncRNA-Chaer directly interacts with the catalytic subunit (EZH2) of PRC2 and interferes with PRC2 genomic targeting, thereby activating hypertrophic gene expression. B: LncRNA-TINCR binds to PRC2 and provokes EZH2-mediated H3K27me3 modification by recruiting it to the promoter of CaMKII, which functions as an inducer of cardiac hypertrophy.