FRB3AR

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

 Coordinatore 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

 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

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

heart    hypertrophic    signalling    ar    activation    nos    protection    effectors    remodeling    cardiac    beta   

 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.'

Altri progetti dello stesso programma (FP7-PEOPLE)

MICROREB (2009)

Micro-dynamics of rebellions: An inquiry into the role of middle level commanders in Chad

Read More  

SENSOMETAL (2009)

Nanosensors to monitor metal dynamics in living plant cells

Read More  

HEALTHEVENT (2014)

Financial Protection against Health Risks - Evidence from an Emerging Country with Universal Coverage and Methodological Considerations

Read More