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Published on: February 10, 2013
Lamina-associated polypeptide 2alpha loss impairs heart function and stress response in mice
Ivana Gotic1, Michael Leschnik, Ursula Kolm
1Max F. Perutz Laboratories, Medical University of Vienna, Dr. Bohr-Gasse 9/3, A-1030 Vienna, Austria.
Circulation Research
|November 21, 2009
Summary
Lamina-associated polypeptide (LAP)2alpha is crucial for maintaining normal heart function. Its absence causes cardiac dysfunction, but compensatory pathways may slow disease progression in LAP2alpha-deficient hearts.
Area of Science:
- Cardiovascular Biology
- Molecular Cell Biology
- Genetics
Background:
- Lamina-associated polypeptide (LAP)2alpha is a nuclear protein interacting with A-type lamins.
- Mutations in lamins and LAP2alpha are linked to human cardiac disorders.
- LAP2alpha's role in heart development and homeostasis is largely unknown.
Purpose of the Study:
- To investigate the necessity of LAP2alpha for normal cardiac function.
- To elucidate the molecular mechanisms underlying LAP2alpha deficiency in the heart.
Main Methods:
- Analysis of heart structure and function in complete and conditional Lap2alpha knockout mice.
- Examination of Lap2alpha(-/-)/Mdx double mutants.
- Assessment of cardiac transcription factors and signaling pathways.
Main Results:
- Complete Lap2alpha knockout led to systolic dysfunction and fibrosis.
- Cardiac transcription factors GATA4 and MEF2c were deregulated.
- Compensatory pathways, including beta-adrenergic signaling downregulation, altered disease progression.
- Dystrophin deficiency partially rescued the Lap2alpha(-/-) phenotype.
Conclusions:
- LAP2alpha plays a significant role in maintaining cardiac function under normal and stress conditions.
- These findings highlight LAP2alpha as a potential therapeutic target for cardiac diseases.
