ATHEROGAG

Macrophage Proteoglycans in Atherosclerosis

 Coordinatore KATHOLIEKE UNIVERSITEIT LEUVEN 

 Organization address address: Oude Markt 13
city: LEUVEN
postcode: 3000

contact info
Titolo: Dr.
Nome: Stijn
Cognome: Delauré
Email: send email
Telefono: +32 16 320 944
Fax: +32 16 324 198

 Nazionalità Coordinatore Belgium [BE]
 Totale costo 179˙390 €
 EC contributo 179˙390 €
 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-2010-IOF
 Funding Scheme MC-IOF
 Anno di inizio 2011
 Periodo (anno-mese-giorno) 2011-07-01   -   2015-06-18

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    KATHOLIEKE UNIVERSITEIT LEUVEN

 Organization address address: Oude Markt 13
city: LEUVEN
postcode: 3000

contact info
Titolo: Dr.
Nome: Stijn
Cognome: Delauré
Email: send email
Telefono: +32 16 320 944
Fax: +32 16 324 198

BE (LEUVEN) coordinator 179˙390.40

Mappa


 Word cloud

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

want    diseases    vivo    cvd    determine    arteries    cultures    societies    atherosclerosis    macrophage    cardiovascular    atherosclerotic    cell    western    proteoglycans    infiltration    lesion    complications    conversion    impact   

 Obiettivo del progetto (Objective)

'Cardiovascular diseases (CVD) are the leading cause of death in Western societies. CVD-related deaths are primarily caused by complications of atherosclerosis, a disease initiated via focal infiltration and retention of lipoproteins in the subendothelial matrix of arteries due to a combination of aggregation and interaction with proteoglycans produced by the arteries. Little is known about the in vivo contribution of macrophage-derived and -associated proteoglycans during atherosclerosis development and progression. Considering this dearth of knowledge we will address two objectives: First, we want to determine the in vivo impact of reduced sulfation of macrophage proteoglycans on atherosclerosis using conditional mouse models lacking macrophage-specific Ndst1 functionality on an LDLR-deficient background. Atherosclerotic lesion quantity and quality will be analyzed in conjunction with macrophage lesion infiltration and lesion apoptosis and efferocytosis. Secondly, we want to evaluate the importance of proteoglycans for macrophage foam cell conversion, another key event in atherogenesis. Using macrophage cell cultures from wild-type or mutant mice we want to determine the importance of biosynthetic genes involved and the array of proteoglycans expressed before and after conversion. In addition the cells will be used to identify a specific proteoglycan important for conversion which will be consequently evaluated for its impact on atherosclerosis in vivo. During his mobility, the applicant will receive didactic (glycobiology, management, intellectual property, grants) and hands-on (MS, macrophage cultures, qPCR, shRNA, flow assay) training as well as network opportunities which will be implemented in the European return institution. Altogether, the generated data should add to our understanding of macrophage proteoglycans and their importance for CVD and provide the opportunity for identifying drug targets and for transfer of US collaborations and know-how to the EU'

Introduzione (Teaser)

Western societies have high mortality rates arising from cardiovascular diseases (CVDs) associated with atherosclerotic complications.

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