FIB

Molecular mechanisms of fibrinogen function regulating NSC differentiation in CNS injury or disease

 Coordinatore UNIVERSITAETSKLINIKUM FREIBURG 

 Organization address address: HUGSTETTER STRASSE 49
city: FREIBURG
postcode: 79106

contact info
Titolo: Mr.
Nome: Jürgen
Cognome: Dreyer
Email: send email
Telefono: 4976130000000
Fax: 4976130000000

 Nazionalità Coordinatore Germany [DE]
 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-2010-RG
 Funding Scheme MC-IRG
 Anno di inizio 2011
 Periodo (anno-mese-giorno) 2011-04-01   -   2015-03-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITAETSKLINIKUM FREIBURG

 Organization address address: HUGSTETTER STRASSE 49
city: FREIBURG
postcode: 79106

contact info
Titolo: Mr.
Nome: Jürgen
Cognome: Dreyer
Email: send email
Telefono: 4976130000000
Fax: 4976130000000

DE (FREIBURG) coordinator 100˙000.00

Mappa


 Word cloud

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

protein    receptors    molecular    regeneration    nervous    fate    nsc    neurogenesis    regulating    signalling    brain    cell    identification    disease    nscs    cns    differentiation    affects    cells    proliferation    blood    fibrinogen    central    injury   

 Obiettivo del progetto (Objective)

'After brain injury or neurologic disease, the ability of the central nervous system (CNS) to regenerate is limited. Neural stem cells (NSCs) have the potential to differentiate into neurons and glia, but neurogenesis is incomplete after CNS disease because of a changed extracellular environment. The identification of novel factors responsible for regulating NSC fate is necessary for the molecular understanding of NSC differentiation. In previous work, we have identified that fibrinogen, a blood-derived protein, which is deposited in the nervous system after perturbations of the neurovascular homeostasis, is an inhibitor of neuronal regeneration and an activator of astrocyte scar formation. Fibrinogen interacts with a plethora of receptors and mediates pathways that control cell proliferation and differentiation. Although the signalling machinery necessary for fibrinogen action is present in brain cells, such as NSCs, the role of fibrinogen on NSC differentiation has not been characterized. The central goal of this project is to understand the molecular basis of fibrinogen signalling on NSC proliferation, migration and differentiation. The studies in this project involve the identification and characterization of the NSC/progenitor cell populations, the receptors and signaling mechanisms used by fibrinogen to mediate its effects on regulating NSC fate using state-of-the-art in vivo and in vitro techniques. Understanding how fibrinogen affects neurogenesis at the cellular and molecular levels after CNS injury is important for developing novel therapeutic approaches to promote functional regeneration of the nervous system.'

Introduzione (Teaser)

Blood protein fibrinogen changes the microenvironment in the central nervous system (CNS) after traumatic brain injury or brain disease. A European study is investigating the role of fibrinogen as a new factor that affects brain regeneration.

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