Attenuated hypertrophic response to pressure overload in a lamin A/C haploinsufficiency mouse.

Journal of Molecular and Cellular Cardiology
Mihaela CupesiJan Lammerding

Abstract

Inherited mutations cause approximately 30% of all dilated cardiomyopathy cases, with autosomal dominant mutations in the LMNA gene accounting for more than one third of these. The LMNA gene encodes the nuclear envelope proteins lamins A and C, which provide structural support to the nucleus and also play critical roles in transcriptional regulation. Functional deletion of a single allele is sufficient to trigger dilated cardiomyopathy in humans and mice. However, whereas Lmna(-/-) mice develop severe muscular dystrophy and dilated cardiomyopathy and die by 8 weeks of age, heterozygous Lmna(+/-) mice have a much milder phenotype, with changes in ventricular function and morphology only becoming apparent at 1 year of age. Here, we studied 8- to 20-week-old Lmna(+/-) mice and wild-type littermates in a pressure overload model to examine whether increased mechanical load can accelerate or exacerbate myocardial dysfunction in the heterozygotes. While overall survival was similar between genotypes, Lmna(+/-) animals had a significantly attenuated hypertrophic response to pressure overload as evidenced by reduced ventricular mass and myocyte size. Analysis of pressure overload-induced transcriptional changes suggested that the reduce...Continue Reading

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Citations

Dec 7, 2013·Trends in Cell Biology·Patricia M Davidson, Jan Lammerding
Jan 1, 2013·Rare Diseases·Chin Yee HoJan Lammerding
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Aug 28, 2021·International Journal of Molecular Sciences·Chun Chou, Michael T Chin

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