Depletion of lamina-associated polypeptide 1 from cardiomyocytes causes cardiac dysfunction in mice.

ABSTRACT: We previously showed that striated muscle-selective depletion of lamina-associated polypeptide 1 (LAP1), an integral inner nuclear membrane protein, leads to profound muscular dystrophy with premature death in mice. As LAP1 is also depleted in hearts of these mice, we examined their cardiac phenotype. Striated muscle-selective LAP1 knockout mice display ventricular systolic dysfunction with abnormal induction of genes encoding cardiomyopathy related proteins. To eliminate possible confounding effects due to skeletal muscle pathology, we generated a new mouse line in which LAP1 is deleted in a cardiomyocyte-selective manner. These mice had no skeletal muscle pathology and appeared overtly normal at 20 weeks of age. However, cardiac echocardiography revealed that they developed left ventricu

SUBMITTER: Shin JY 

PROVIDER: S-EPMC4133221 | biostudies-literature | 2014 May-Jun

REPOSITORIES: biostudies-literature