Abstract 101: FHL2 -null Mice Showing Less Cardiac Remodeling

Abstract

The four and a half Lin11, Isl-1 and Mec-3 (LIM) domain protein 2 (FHL2) is a member of the four and a half LIM domain-only (FHL) gene family, and has been shown to play an important role in cardiac remodeling. Here, we tested the hypothesis that isoproterenol-induced myocardial fibrosis in mice lacking FHL2 is related to resistant to myocardial fibrosis. We compared the cardiac phenotypes of FHL2 -null mice. Extra-cellular matrix remodeling and apoptosis are examined to determine the roles of FHL2 on cardiac fibrosis induced by isoproterenol. Compared to wild type littermates, FHL2 -null mice exhibited lower mortality. Masson’s Trichrome and silver stains showed significantly less severe ventricle fibrosis in FHL2-null mice. In addition, FHL2 -null mice exhibited lower levels of TGF-β, collagen I/III, but higher membrane-type matrix metalloproteinase-1 (MT1-MMP/MMP-14) during cardiac remodeling. This study shows that alternations of FHL2 might be implicated in the pathogenesis of cardiac fibrosis and suggests FHL2 as novel targets for cardiac fibrosis therapy. Further studies are required to define the mechanism by which FHL2 modulates cardiac remodeling.