CARTILAGE TGF-BETA

Functional role of endogenous latent TGF-beta activation in the intrinsic repair of mechanically loaded articular cartilage

Coordinatore	IMPERIAL COLLEGE OF SCIENCE, TECHNOLOGY AND MEDICINE    more  Organization address address: SOUTH KENSINGTON CAMPUS EXHIBITION ROAD city: LONDON postcode: SW7 2AZ contact info Titolo: Mr. Nome: Shaun Cognome: Power Email: send email Telefono: +44 207 594 8773 Fax: +44 207 594 8609
Nazionalità Coordinatore	United Kingdom [UK]
Totale costo	221˙606 €
EC contributo	221˙606 €
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-2013-IIF
Funding Scheme	MC-IIF
Anno di inizio	2014
Periodo (anno-mese-giorno)	2014-04-07   -   2016-04-06

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	IMPERIAL COLLEGE OF SCIENCE, TECHNOLOGY AND MEDICINE  Organization address address: SOUTH KENSINGTON CAMPUS EXHIBITION ROAD city: LONDON postcode: SW7 2AZ contact info Titolo: Mr. Nome: Shaun Cognome: Power Email: send email Telefono: +44 207 594 8773 Fax: +44 207 594 8609	UK (LONDON)	coordinator	221˙606.40

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 Obiettivo del progetto (Objective)

'Articular cartilage serves as a load bearing material for synovial joints, transmitting loads while maintaining low friction and wear. Progressive degeneration of the tissue leads to osteoarthritis (OA), a debilitating condition characterized by pain and severe limitations in mobility. OA is highly prevalent amongst the EU population and is associated with significant economic burdens. An improved understanding of the underlying mechanisms that defeat normal tissue maintenance and lead to joint degeneration is critical for the development of successful treatment strategies. This project examines a newly hypothesized intrinsic repair mechanism in articular cartilage, mediated by the extracellular activation of large stores of latent (inactive) TGF-beta through the action of chondrocyte-secreted proteases. This proposal hypothesizes that this mechanism maintains cartilage homeostasis in response to a wide range of physiologic mechanical loading conditions, but is unable to maintain tissue subjected to excessive loading, as seen in OA associated risk factors (e.g., joint instability, high impact activities). This hypothesized mechanism will be investigated through the implementation of an in vitro experimental model system, consisting of the mechanical loading of articular cartilage explants and the sophisticated biochemical analysis of resulting TGF-beta activation and microstructural alterations to the cartilage ECM. This state-of-the-art proposal represents an exciting, unique opportunity to bring together the complementary skillsets of the candidate and the Stevens Group, with their respective expertise in biomechanics and biochemistry, to uncover fundamental mechanisms in cartilage mechanobiology. This mutually beneficial cooperation between Europe and the U.S. can promote the development of successful treatments for OA, including tissue engineering and molecular intervention strategies that will impact the EU community at large.'