WT1HEART

Identification of new targets of Wt1 during cardiovascular development

 Coordinatore UNIVERSITAT DE BARCELONA 

 Organization address address: GRAN VIA DE LES CORTS CATALANES 585
city: BARCELONA
postcode: 8007

contact info
Titolo: Mr.
Nome: Xavier
Cognome: Gutierrez
Email: send email
Telefono: 34934035385
Fax: 34934489434

 Nazionalità Coordinatore Spain [ES]
 Totale costo 100˙000 €
 EC contributo 100˙000 €
 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-CIG
 Funding Scheme MC-CIG
 Anno di inizio 2012
 Periodo (anno-mese-giorno) 2012-04-02   -   2016-04-01

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITAT DE BARCELONA

 Organization address address: GRAN VIA DE LES CORTS CATALANES 585
city: BARCELONA
postcode: 8007

contact info
Titolo: Mr.
Nome: Xavier
Cognome: Gutierrez
Email: send email
Telefono: 34934035385
Fax: 34934489434

ES (BARCELONA) coordinator 100˙000.00

Mappa


 Word cloud

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

cardiovascular    cells    ko    deletion    gene    heart    plays    coronary    epicardium    epicardial    wt    mechanisms    regulate    cardiomyocyte    proliferation    mouse    repair    tissue   

 Obiettivo del progetto (Objective)

'The epicardium is a mesothelial tissue that plays a crucial role during heart development, by contributing to the formation of cardiovascular precursor cells and by producing growth factors important for heart formation. Wt1 gene encodes a zinc finger protein, which plays a critical role in normal development of several organs such as kidney, gonads, spleen and heart. During heart formation, Wt1 is mainly expressed in the epicardium and epicardial derived cells. Deletion of Wt1 gene in an epicardial specific manner lead to a KO mouse with profound defect in both cardiomyocyte proliferation and coronary vascular development, suggesting that Wt1 KO epicardial cells constitute a good model to study the putative growth factors and signalling produced by epicardial cells. The principal objectives of the proposed project are to identify new targets of Wt1 during cardiovascular development, to explore their role in the formation of coronary blood vessels and cardiomyocyte proliferation and to dissect some of the mechanisms involved. We propose to study how Wt1 deletion, in vitro and in vivo, induced expression or repression of chemokines and growth factors and how this influences heart morphogenesis. The molecular mechanisms that regulate the development of the cardiovascular system in mouse embryos are comparable with those that regulate repair in adult tissue. The identification of new Wt1 targets during epicardium development, would allow us to design new strategies to activate those pathways during regeneration and repair of damaged hearts'

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