WNT VASCULAR REMODEL

Molecular control of vascular remodelling: A role for Wnt signalling

Coordinatore	more  Organization address address: ST JOHN STREET 407 ANGEL BUILDING city: LONDON postcode: EC1V 4AD contact info Titolo: Ms. Nome: Holly Cognome: Elphinstone Email: send email Telefono: +44 20 7269 3524 Fax: +44 20 7269 3585
Nazionalità Coordinatore	Non specificata
Totale costo	173˙240 €
EC contributo	173˙240 €
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)
Anno di inizio	0
Periodo (anno-mese-giorno)	0000-00-00   -   0000-00-00

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	CANCER RESEARCH UK  Organization address address: ST JOHN STREET 407 ANGEL BUILDING city: LONDON postcode: EC1V 4AD contact info Titolo: Ms. Nome: Holly Cognome: Elphinstone Email: send email Telefono: +44 20 7269 3524 Fax: +44 20 7269 3585	UK (LONDON)	coordinator	173˙240.80

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 Obiettivo del progetto (Objective)

'A functional network of blood vessels is essential for all aspects of growth and organ function during embryonic development and adult life. A wide number of human disorders are related to vascular defects like cancer, diabetic retinopathy or stroke. During vascular remodelling, superfluous blood vessels regress in a process named vascular pruning. In contrast to the molecular mechanisms controlling vascular sprouting, vascular pruning has been less studied and very little is known about the cellular and molecular mechanisms controlling this process in vivo. Accumulating evidence indicates that Wnt signalling regulates multiple aspects of endothelial cell behaviour during vascular morphogenesis including vascular regression. However, the precise cellular mechanism of vessel pruning as well as the expression and function of relevant Wnt signalling components in this process remain undefined. The present proposal therefore aims to elucidate the cellular mechanism of Wnt signalling during vascular pruning. Targeted inactivation of Wnt ligands and receptors in different cell population in mouse, in combination with pharmacological activation or inhibition of the Wnt pathway, will be used for deciphering the Wnt contribution in vascular pruning, both in retinal and zebrafish angiogenesis. In addition, we aim also to implement an ex-vivo model of vascular remodelling, which will be used to perform a pharmacological screen for drugs that can stabilise or induce vascular remodelling, regression or apoptosis. Improving the knowledge of the molecular regulation of vascular morphogenesis, particularly in vascular pruning and the contribution of Wnt signalling in angiogenesis, will facilitate the development of new therapeutic strategies for diseases related to vascular defects such as cancer and retinopathies.'