STIFFMATRIXVASC

From extracellular matrix rigidity to vascular aging

 Coordinatore INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE (INSERM) 

 Organization address address: 101 Rue de Tolbiac
city: PARIS
postcode: 75654

contact info
Titolo: Ms.
Nome: Fatima
Cognome: Baghdali
Email: send email
Telefono: +33 2 40358679
Fax: +33 2 40477701

 Nazionalità Coordinatore France [FR]
 Totale costo 75˙000 €
 EC contributo 75˙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 2013
 Periodo (anno-mese-giorno) 2013-09-01   -   2016-08-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE (INSERM)

 Organization address address: 101 Rue de Tolbiac
city: PARIS
postcode: 75654

contact info
Titolo: Ms.
Nome: Fatima
Cognome: Baghdali
Email: send email
Telefono: +33 2 40358679
Fax: +33 2 40477701

FR (PARIS) coordinator 75˙000.00

Mappa


 Word cloud

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

mechanical    suggesting    vascular    stiffness    ecs    affects    regulate    found    physical    ecm    larg       cvd    arterial    cells    gef    stiffening   

 Obiettivo del progetto (Objective)

'The extracellular matrix (ECM) affects many aspects of cell growth and behavior. Not only do cells respond to the composition of the ECM, but they also respond to its physical properties, adjusting to the stiffness of their physical environment by generating tension within the cytoskeleton. In the vascular system, the large arteries from the central arterial system become stiffer with age. It is now well established that arterial stiffening significantly contributes to cardiovascular disease (CVD) development. Recent studies have highlighted that ECM stiffness affects endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) differentiation, proliferation and motility, suggesting that the cellular response to ECM stiffness may play an important role during the development of aging-associated CVD. We recently found that LARG and GEF-H1 regulate the mechanical response to force on integrins. In preliminary results we found that these two proteins are activated in response to ECM stiffness, suggesting that LARG and GEF-H1 may also regulate the mechanical response to ECM stiffness. In this proposal we will test this hypothesis and we will investigate the role of LARG and GEF-H1 in ECs and VSCMs during arterial stiffening.'

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