LUNG REPAIR MODEL

Modelling lung repair in health and disease

Coordinatore	THE UNIVERSITY OF BIRMINGHAM    more  Organization address address: Edgbaston city: BIRMINGHAM postcode: B15 2TT contact info Titolo: Ms. Nome: May Cognome: Chung Email: send email Telefono: 441214000000 Fax: 441214000000
Nazionalità Coordinatore	United Kingdom [UK]
Totale costo	200˙371 €
EC contributo	200˙371 €
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-2011-IEF
Funding Scheme	MC-IEF
Anno di inizio	2012
Periodo (anno-mese-giorno)	2012-09-01   -   2014-08-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	THE UNIVERSITY OF BIRMINGHAM  Organization address address: Edgbaston city: BIRMINGHAM postcode: B15 2TT contact info Titolo: Ms. Nome: May Cognome: Chung Email: send email Telefono: 441214000000 Fax: 441214000000	UK (BIRMINGHAM)	coordinator	200˙371.80

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 Obiettivo del progetto (Objective)

'Acute and chronic lung injury is a major cause of morbidity and mortality worldwide. During physiological repair of the damaged alveolar epithelium transdifferentiation of Alveolar Type II (ATII) cells occurs into Alveolar Type I (ATI) cells. Also, recently identified human multipotent lung stem cells (hLSCs) may participate in repair mechanisms of injured lung tissue by differentiating into multiple cell lineages in the lung. In pathological repair mechanisms, epithelial-mesenchymal transition (EMT) occurs, epithelial cells acquire mesenchymal phenotype, a process that is believed to be associated with aberrant repair and scar formation after epithelial injury. EMT contributes to fibrosis in the lung in both acute and chronic alveolar diseases (e.g. Acute Lung Injury (ALI) and Idiopathic pulmonary fibrosis (IPF). The proposed project aims to investigate the role of Wnt11 in the differentiation of alveolar epithelial cells (AECs) and hLSCs. A tissue engineered 3D lung tissue model has been developed to mimic intercellular interactions in the lung which dramatically alters ligand responses in alveolar epithelium. Preliminary results suggest that in 3D co-culture and in human lung explant cultures Wnt11 promotes Alveolar Type II (ATII) like differentiation and prevents Epithelial-Mesenchymal Transition (EMT) in human small airway epithelium. If our hypothesis is correct we will ascertain whether Wnt11 may have important role in lung tissue regeneration thus marking it as a potential therapeutic target to promote alveolar epithelial repair. The use of hLSC may allow novel 3D tissue engineering solutions to be developed to replace damaged alveolar epithelium.'

Introduzione (Teaser)

Acute and chronic lung injury is a major cause of morbidity and mortality worldwide. Understanding and modelling the mechanisms of lung tissue repair are needed to find ways to replace damaged alveolar epithelium.