RHOA IN INFLAMMATION

"role of a small GTPase, RhoA, in skin inflammation"

Coordinatore	more  Organization address postcode: 1017 contact info Titolo: Mr. Nome: Ivan Cognome: Kristoffersen Email: send email Telefono: +45 353222626 Fax: -35324567
Nazionalità Coordinatore	Non specificata
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-PEOP
Anno di inizio	2009
Periodo (anno-mese-giorno)	2009-11-01   -   2014-05-30

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	KOBENHAVNS UNIVERSITET	DK	coordinator	100˙000.00

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 Obiettivo del progetto (Objective)

'Psoriasis is a common immune-mediated disease, characterized by aberrant epidermal differentiation, surface scale formation and marked cutaneous inflammation. It affects about 1% of the European population and has currently no effective treatment. The visible nature of the disease ensures that patients have both physical and psychosocial effects intruding their life style. Using genetically modified mice, engineered to have a keratinocyte-restricted deletion of the RhoA gene, we found for the first time that RhoA regulates the sensitivity of skin to inflammatory stress in vivo. Moreover, around a metal ear tag, those mice develop a severe skin defect bearing similarities to psoriasis. Our goal is to understand the role of RhoA in skin inflammation and the possible involvement of decreased RhoA signaling in the development of psoriasis. To achieve our goal we propose to investigate gene expression in vivo through an array on freshly prepared primary keratinocytes and to test if the induced gene expression is cell autonomous by using a lentivirus strategy. A lentiviral knockdown sublibrary will help us to determine which signaling mechanisms contribute to those changes in gene expression. Moreover, we want to use our model to investigate the sensitivity of RhoA null skin to an irritant contact dermatis model and to induce an allergic contact dermatis. We will then analyze the infiltrating cells and determine the mechanisms involved in the inflammation. Using tissue sections from our mice and from psoriasis patients we will study the similarities between ear tag lesions and psoriatic lesions by establishing new immunostaining protocols. Our work will increase our understanding of psoriasis development and identify new drug targets that are needed to improve the current psoriasis therapies.'

Introduzione (Teaser)

European researchers worked to unveil the molecular aetiology of inflammation-related skin conditions such as psoriasis. The findings of the study have the potential to lead to novel treatments.