MYCMACS

Role of c-Myc in atherosclerotic macrophages

 Coordinatore UNIVERSITY COLLEGE LONDON 

 Organization address address: GOWER STREET
city: LONDON
postcode: WC1E 6BT

contact info
Titolo: Ms.
Nome: Kamila
Cognome: Kolasinska
Email: send email
Telefono: 442031000000
Fax: 442078000000

 Nazionalità Coordinatore United Kingdom [UK]
 Totale costo 50˙000 €
 EC contributo 50˙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-PEOPLE-2011-CIG
 Funding Scheme MC-CIG
 Anno di inizio 2012
 Periodo (anno-mese-giorno) 2012-03-01   -   2014-02-28

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITY COLLEGE LONDON

 Organization address address: GOWER STREET
city: LONDON
postcode: WC1E 6BT

contact info
Titolo: Ms.
Nome: Kamila
Cognome: Kolasinska
Email: send email
Telefono: 442031000000
Fax: 442078000000

UK (LONDON) coordinator 18˙750.00
2    FUNDACION CENTRO NACIONAL DE INVESTIGACIONES CARDIOVASCULARES CARLOS III

 Organization address address: C/ MELCHOR FERNANDEZ ALMAGRO 3
city: MADRID
postcode: 28029

contact info
Titolo: Dr.
Nome: David
Cognome: Sayago
Email: send email
Telefono: 34914531318

ES (MADRID) participant 31˙250.00

Mappa


 Word cloud

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

atherosclerotic    world    activated    macrophages    activation    expression    cardiovascular    macrophage    myc    atherosclerosis    transcription    disease      

 Obiettivo del progetto (Objective)

'Atherosclerosis and associated cardiovascular disease are the leading causes of mortality in developed countries and the World Health Organization has estimated that by 2020 these disorders will be the main sanitary and socio-economic problem world-wide due in part to the progressive aging of our societies. Atherosclerosis is a complex chronic inflammatory process triggered and perpetuated by cardiovascular risk factors which cause endothelial dysfunction and leukocyte infiltration within the subendothelial space in the artery wall. The most prominent immune cells that invade lesions are monocytes/macrophages (comprising up to 60% of atheromata mass) and T-lymphocytes. Recent evidences suggest that different atherosclerotic stages are associated with distinct macrophage subtypes, principally the classically-activated (M1) and alternatively-activated (M2) populations. The main obstacle to the anti-atherosclerotic therapy based on targeting atherosclerotic macrophage is that very little is known about the intracellular pathways and transcription factors involved in macrophage activation. I recently demonstrated that the transcription factor c-Myc is specifically induced in human macrophages during M2 alternative activation and controls the expression of around 50% of M2-specific markers. The main goal of this project is to elucidate the role thatc-Myc plays in macrophage functions that are relevant in atherosclerosis (eg., proliferation, apoptosis, migration, lipid uptake) and the effects of ablating macrophage c-Myc expression on disease initiation and progression.'

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