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Cardiomyocyte-Specific Expression of Lamin A Improves Cardiac Function in Lmna−/− Mice
Journal article   Open access   Peer reviewed

Cardiomyocyte-Specific Expression of Lamin A Improves Cardiac Function in Lmna−/− Mice

Richard L Frock, Steven C Chen, Dao-Fu Da, Ellie Frett, Carmen Lau, Christina Brown, Diana N Pak, Yuexia Wang, Antoine Muchir, Howard J Worman, …
PloS one, Vol.7(8), e42918
08/15/2012
DOI: 10.1371/journal.pone.0042918
PMCID: PMC3419749
PMID: 22905185
url
https://doi.org/10.1371/journal.pone.0042918View
Published (Version of record) Open Access

Abstract

Lmna−/− mice display multiple tissue defects and die by 6–8 weeks of age reportedly from dilated cardiomyopathy with associated conduction defects. We sought to determine whether restoration of lamin A in cardiomyocytes improves cardiac function and extends the survival of Lmna−/− mice. We observed increased total desmin protein levels and disorganization of the cytoplasmic desmin network in ∼20% of Lmna−/− ventricular myocytes, rescued in a cell-autonomous manner in Lmna−/− mice expressing a cardiac-specific lamin A transgene (Lmna−/−; Tg). Lmna−/−; Tg mice displayed significantly increased contractility and preservation of myocardial performance compared to Lmna−/− mice. Lmna−/−; Tg mice attenuated ERK1/2 phosphorylation relative to Lmna−/− mice, potentially underlying the improved localization of connexin43 to the intercalated disc. Electrocardiographic recordings from Lmna−/− mice revealed arrhythmic events and increased frequency of PR interval prolongation, which is partially rescued in Lmna−/−; Tg mice. These findings support our observation that Lmna−/−; Tg mice have a 12% median extension in lifespan compared to Lmna−/− mice. While significant, Lmna−/−; Tg mice only have modest improvement in cardiac function and survival likely stemming from the observation that only 40% of Lmna−/−; Tg cardiomyocytes have detectable lamin A expression. Cardiomyocyte-specific restoration of lamin A in Lmna−/− mice improves heart-specific pathology and extends lifespan, demonstrating that the cardiac pathology of Lmna−/− mice limits survival. The expression of lamin A is sufficient to rescue certain cellular defects associated with loss of A-type lamins in cardiomyocytes in a cell-autonomous fashion
Medicine Biology

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