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

AI Article Synopsis

  • Researchers found that removing lamina-associated polypeptide 1 (LAP1) from striated muscles in mice caused serious muscle conditions and early death, also affecting heart health.
  • Examining the hearts of these mice revealed they had significant heart dysfunction and changes in gene expression linked to cardiomyopathy.
  • A new mouse model targeted LAP1 deletion specifically in heart cells, which appeared normal but still developed heart issues, indicating that LAP1 is crucial for proper heart function, similar to findings in a human with a LAP1 gene mutation.

Article 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 ventricular systolic dysfunction and cardiac gene expression analysis revealed abnormal induction of cardiomyopathy-related genes. Our results demonstrate that LAP1 expression in cardiomyocytes is required for normal left ventricular function, consistent with a report of cardiomyopathy in a human subject with mutation in the gene encoding LAP1.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4133221PMC
http://dx.doi.org/10.4161/nucl.29227DOI Listing

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