FRB3AR

Functional role of the beta3-adrenoceptor in modulating the remodeling of the myocardium submitted to stress

Coordinatore	UNIVERSITE CATHOLIQUE DE LOUVAIN    more  Organization address address: Place De L'Universite 1 city: LOUVAIN LA NEUVE postcode: 1348 contact info Titolo: Prof. Nome: Jean-Luc Cognome: Balligand Email: send email Telefono: +32 2 764 5260 Fax: +32 2 764 5269
Nazionalità Coordinatore	Belgium [BE]
Totale costo	169˙800 €
EC contributo	169˙800 €
Programma	FP7-PEOPLE Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	FP7-PEOPLE-2011-IEF
Funding Scheme	MC-IEF
Anno di inizio	2012
Periodo (anno-mese-giorno)	2012-12-01   -   2014-11-30

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	UNIVERSITE CATHOLIQUE DE LOUVAIN  Organization address address: Place De L'Universite 1 city: LOUVAIN LA NEUVE postcode: 1348 contact info Titolo: Prof. Nome: Jean-Luc Cognome: Balligand Email: send email Telefono: +32 2 764 5260 Fax: +32 2 764 5269	BE (LOUVAIN LA NEUVE)	coordinator	169˙800.00

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 Obiettivo del progetto (Objective)

'This project investigates the role of the beta3 adrenoceptor (β3-AR) in modulating the remodeling of the myocardium submitted to stress. Promising advances have been made in the host laboratory in showing that overexpression of the β3-AR in cardiac myocytes confers protection from pro-hypertrophic stimulus induced-remodeling. Preliminary data suggest that nitric oxide (NO) production by NO synthase (NOS), which is known to be coupled to the β3-AR signalling in the heart, is necessary for this protection to occur. Our central hypothesis therefore is that the activation of the β3-AR protects against hypertrophic remodeling of the heart through NOS and, possibly protein kinase G (PKG) -dependent mechanisms. The following stages of the research project will aim at 1) exploring the ability of the β3-AR to regulate remodeling in response to hemodynamic stresses of different severity; 2) ascertaining the specific role of the NOS isoform(s) in this protection; 3) unravelling the downstream effectors involved in the protective effects conferred by β3-AR activation; 4) investigating the co-localization of these key effectors with β3-AR in cellular microdomains, including caveolae; 5) studying the stage-specific- role of β3-AR signalling in the regulation of remodelling and function of stressed hearts from an inducible, cardiac specific, knockout mouse model. These experiments will enhance our understanding of the pathophysiologic role of beta3-adrenoceptors, which are upregulated in the remodeling heart, opening the way for new therapeutic modalities for cardiac remodeling using agonists at these receptors.'