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Isolation and Culture of Neonatal Mouse Cardiomyocytes
Published on: September 6, 2013
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ADAP1 limits neonatal cardiomyocyte hypertrophy by reducing integrin cell surface expression
Hugo Giguère1, Audrey-Ann Dumont2, Jonathan Berthiaume1
1Département de Pharmacologie et Physiologie, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, Sherbrooke, QC, Canada.
Scientific Reports
|September 13, 2018
Summary
ArfGAP with dual PH domains 1 (ADAP1) acts as an anti-hypertrophic factor in cardiomyocytes. ADAP1 limits cardiac hypertrophy by reorganizing α-actinin and reducing β1-integrin surface expression.
Area of Science:
- Cardiovascular Biology
- Cellular Signaling
- Molecular Cardiology
Background:
- The ArfGAP with dual PH domains 1 (ADAP1) is known to regulate the ERK1/2 pathway in non-cardiomyocytes.
- Its specific role in cardiomyocytes and cardiac hypertrophy remains uncharacterized.
Purpose of the Study:
- To investigate the function of ADAP1 in the hypertrophic process of cardiomyocytes.
- To elucidate the molecular mechanisms underlying ADAP1's effects in cardiac cells.
Main Methods:
- Assessed ADAP1 expression in rat hearts using RT-qPCR and Western blotting.
- Utilized adenoviral-mediated overexpression of ADAP1 in cultured rat neonatal ventricular cardiomyocytes.
- Analyzed cardiomyocyte hypertrophy, protein synthesis, ERK1/2 pathway activation, fetal gene program, α-actinin organization, and β1-integrin surface expression.
Main Results:
- ADAP1 is preferentially expressed in cardiomyocytes.
- ADAP1 overexpression limited serum-induced hypertrophy and completely blocked phenylephrine- and Mek1ca-induced hypertrophy.
- The anti-hypertrophic effect was independent of protein synthesis, ERK1/2 pathway, or fetal gene program activation.
- ADAP1 reorganized α-actinin and reduced surface β1-integrin, effects potentiated by Mek1ca.
Conclusions:
- ADAP1 possesses anti-hypertrophic properties in cardiomyocytes.
- ADAP1 influences cardiomyocyte structure by altering α-actinin organization and β1-integrin localization.
- These findings reveal a novel role for ADAP1 in regulating cardiac hypertrophy.
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