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cAMP-binding protein Epac induces cardiomyocyte hypertrophy
Eric Morel1, Andrea Marcantoni, Monique Gastineau
1Cardiologie Cellulaire et Moléculaire, Inserm U-446, IFR-75, Faculté de Pharmacie, Université Paris XI, 5 Rue JB Clément, 92296 Chātenay Malabry, France.
Circulation Research
|November 5, 2005
Summary
Epac, a cAMP-activated protein, triggers cardiac cell growth and gene expression changes. This pathway involves calcium, Rac, calcineurin, and NFAT, revealing new insights into cAMP signaling in the heart.
Area of Science:
- Cardiology
- Molecular Biology
- Cell Signaling
Background:
- Cyclic adenosine monophosphate (cAMP) is a crucial second messenger in cardiac function.
- Epac (Exchange protein directly activated by cAMP) is a guanine nucleotide exchange factor (GEF) activated by cAMP.
Purpose of the Study:
- To investigate the role of Epac in cardiac cells.
- To elucidate the signaling pathways regulated by Epac in cardiomyocytes.
Main Methods:
- Epac activation in cardiac cells.
- Assessment of morphological changes and cardiac hypertrophic markers.
- Analysis of Ca2+-dependent signaling pathways involving Rac, calcineurin, and NFAT.
Main Results:
- Epac activation induces cardiomyocyte hypertrophy and expression of cardiac hypertrophic markers.
- This process is mediated by Ca2+-dependent activation of Rac.
- Epac activates a prohypertrophic pathway involving calcineurin and NFAT, with Rac playing a role in Epac-induced NFAT-dependent hypertrophy.
Conclusions:
- Epac is a novel positive regulator of cardiac growth.
- Epac signaling pathways, involving calcineurin and Rac, are critical for cAMP-mediated biological effects in the heart.
- These findings provide new insights into the molecular mechanisms of cardiac hypertrophy.