LEMPIT

LEUKOCYTE MICRODOMAINS AND PLATELET INTERACTIONS IN THROMBO-INFLAMMATORY INJURY

 Coordinatore 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: Stefan
Cognome: Jungbluth
Email: send email
Telefono: 34914531200
Fax: +3491 453 12 45

 Nazionalità Coordinatore Spain [ES]
 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-PEOPLE-2009-RG
 Funding Scheme MC-IRG
 Anno di inizio 2010
 Periodo (anno-mese-giorno) 2010-01-01   -   2013-12-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    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: Stefan
Cognome: Jungbluth
Email: send email
Telefono: 34914531200
Fax: +3491 453 12 45

ES (MADRID) coordinator 100˙000.00

Mappa


 Word cloud

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leukocytes    polarization    uropod    interactions    edge    platelets    domains    vascular    inflammatory    molecular   

 Obiettivo del progetto (Objective)

'During the inflammatory response, leukocytes accumulate in the vascular lumen and undergo a morphological and molecular polarization characterized by the formation of discrete domains (a leading edge and an uropod) that allows their directional migration. We aim to understand how and when this polarization originates, as well as the endothelial signals that induce it under physiological conditions. We propose to use a novel intravital microscopy system to image these domains in real-time. Recent observations have shown that leukocytes that are adherent on the endothelium interact with other blood components, including platelets, and that these interactions contribute to the vascular and tissue injuries associated to inflammatory processes. We therefore propose to characterize the subcellular domains and receptors present in polarized leukocytes and platelets that mediate these interactions. We will also investigate the contribution of the interactions mediated by each leukocyte domain (leading edge or uropod) in the normal and pathogenic inflammatory response, using various transgenic mouse lines and different models of inflammation. These studies will allow a better understanding of the inflammatory response at the cellular and molecular levels, and may lead to the rational design of therapies targeting this group of complications that so overwhelmingly threat our quality of life.'

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