LUEDDE-MED3-AACHEN

The Function of inflammatory signalling pathways in acute and chronic liver disease and liver cancer

Coordinatore	UNIVERSITAETSKLINIKUM AACHEN    more Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
Nazionalità Coordinatore	Germany [DE]
Totale costo	1˙600˙356 €
EC contributo	1˙600˙356 €
Programma	FP7-IDEAS-ERC Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	ERC-2007-StG
Funding Scheme	ERC-SG
Anno di inizio	2008
Periodo (anno-mese-giorno)	2008-09-01   -   2014-08-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	UNIVERSITAETSKLINIKUM AACHEN  Organization address address: Pauwelsstrasse 30 city: AACHEN postcode: 52074 contact info Titolo: Dr. Nome: Tom Cognome: Luedde Email: send email Telefono: +49 241 80 35609 Fax: +49 241 80 82455	DE (AACHEN)	hostInstitution	0.00
2	UNIVERSITAETSKLINIKUM AACHEN  Organization address address: Pauwelsstrasse 30 city: AACHEN postcode: 52074 contact info Titolo: Mr. Nome: Volker Cognome: Legewie Email: send email Telefono: +49 241 80 88494 Fax: +49 241 80 82051	DE (AACHEN)	hostInstitution	0.00

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 Obiettivo del progetto (Objective)

'The aim of this proposal is to examine the role of inflammatory signalling pathways in murine models of liver and biliary disease by application of conditional gene targeting using cre/loxP technology. Previous studies have provided evidence that the NF-kB pathway and its activating kinase complex – consisting of three subunits: IKK1, IKK2 and NEMO – are crucial regulators of liver physiology and pathology, but their differential, cell specific functions in the liver are currently only poorly understood. The first part of this proposal will focus on the evaluation of molecular mechanisms underlying the development of hepatocellular carcinoma in a setting of chronic hepatitis. By using a novel mouse model of spontaneous liver cancer based on conditional deletion of NEMO in hepatocytes, the functions of cytokines, specific intracellular signalling pathways, the innate and adaptive immune system and the role of hepatic stem cells in hepatitis and carcinogenesis will be examined. In the second part of this proposal, we will extend these studies by evaluating the function of NEMO/NF-kB in other hepatic cell compartments, specifically the function of NEMO in hepatic stellate cells and liver fibrosis, the endothelial function of NEMO/NF-kB in an in vivo model of hepatic ischemia-reperfusion injury and the role of the NF-kB pathway in biliary epithelial cells and inflammatory biliary diseases. Finally, in the third part of this proposal we will analyse the unknown intrahepatic role of non-canonical, IKK1-dependent signalling pathways and the function of TAK1 – a molecule at the interface between inflammatory and developmental pathways – in liver injury, fatty-liver-disease and insulin-resistance. Knowledge gained by these studies and the further understanding of the cell specific hepatic function of NF-kB and related pathways might build the basis for the development of novel pharmacological approaches for the future treatment of liver diseases and cancer in humans.'