RHOA IN INFLAMMATION

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

 Coordinatore  

 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

Mappa


 Word cloud

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

patients    vivo    model    psoriasis    disease    dermatis    tag    sensitivity    rhoa    mechanisms    skin    lesions    ear    moreover    gene    determine    similarities    inflammation    mice    signaling    contact    expression   

 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.

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