CIP, a Cardiac Isl1-Interacting Protein, Represses Cardiomyocyte Hypertrophy

• DOI: 10.1161/circresaha.111.259663
• Publication Date: 2012-02-17T05:54:18Z
• Authors: Zhan-Peng Huang; Hee Young Seok; Bin Zhou; Jinghai Chen; Jian-Fu Chen; Yazhong Tao; William T. Pu; Da-Zhi Wang
• Keywords: Pressure overload; GATA4; Mef2; Cardiac myocyte

Mammalian heart has minimal regenerative capacity. In response to mechanical or pathological stress, the undergoes cardiac remodeling. Pressure and volume overload in cause increased size (hypertrophic growth) of cardiomyocytes. Whereas regulatory pathways that activate hypertrophy have been well-established, molecular events inhibit repress are less known.To identify investigate novel regulators modulate hypertrophy.Here, we report identification, characterization, functional examination a Isl1-interacting protein (CIP). CIP was identified from bioinformatic search for cardiac-expressed genes mouse embryonic hearts. encodes nuclear without recognizable motifs. Northern blotting, situ hybridization, reporter gene tracing demonstrated is highly expressed cardiomyocytes developing adult Yeast two-hybrid screening Isl1, LIM/homeodomain transcription factor essential specification progenitor cells second field, as cofactor CIP. directly interacted with mapped domains these two proteins, which mediate their interaction. We show represses transcriptional activity Isl1 activation myocyte enhancer 2C. The expression dramatically reduced hypertrophic Most importantly, overexpression repressed agonist-induced cardiomyocyte hypertrophy.Our studies therefore regulator hypertrophy.