MODOPCFATE

Modulation of oligodendrocyte precursor cells differentiation fate during CNS remyelination

 Coordinatore INSTYTUT BIOLOGII DOSWIADCZALNEJ IM. M. NENCKIEGO POLSKIEJ AKADEMII NAUK 

 Organization address address: UL. LUDWIKA PASTEURA 3
city: WARSZAWA
postcode: 02 093

contact info
Titolo: Mrs.
Nome: Marta
Cognome: Rucinska
Email: send email
Telefono: 48225892330
Fax: 48228225342

 Nazionalità Coordinatore Poland [PL]
 Totale costo 45˙000 €
 EC contributo 45˙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-ERG
 Anno di inizio 2009
 Periodo (anno-mese-giorno) 2009-10-01   -   2013-03-03

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    INSTYTUT BIOLOGII DOSWIADCZALNEJ IM. M. NENCKIEGO POLSKIEJ AKADEMII NAUK

 Organization address address: UL. LUDWIKA PASTEURA 3
city: WARSZAWA
postcode: 02 093

contact info
Titolo: Mrs.
Nome: Marta
Cognome: Rucinska
Email: send email
Telefono: 48225892330
Fax: 48228225342

PL (WARSZAWA) coordinator 45˙000.00

Mappa


 Word cloud

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

precursor    fate    differentiation    cells    schwann    hypothesis    multiple    progressive    demyelinated    axons    opcs    molecular    cellular    remyelination    sheaths    myelin    demonstrated    oligodendrocyte    mechanisms    adult    sclerosis    cns   

 Obiettivo del progetto (Objective)

'The aim of this project is to identify the microenviromental factors and their downstream cellular effectors determining the fate of adult CNS precursor cells which could be modulated in order to control remyelination process. Remyelination is the best example of regenerative processes in adult CNS, in which new myelin sheaths are restored to axons that have been demyelinated as a result of oligodendrocyte death. However, the efficiency of remyelination decreases with age and in multiple sclerosis, a disease that can afflict a patient for several decades, there is a progressive decline in remyelination. The consequence of remyelination failure is progressive loss of the chronically demyelinated axons. Therefore, there is an urgent need to understand the cellular and molecular mechanisms involved in remyelination. New oligodendrocytes are derived from proliferating oligodendrocyte precursor cells (OPCs). However, we have demonstrated, in the lineage fate mapping study, that this name does not fully reflect their differentiation potential; under appropriate conditions they can also give rise to astrocytes and Schwann cells. We demonstrated that Schwann cells, derived form OPCs, occupied almost exclusively the tissue around blood vessels in astrocyte-deficient areas. Therefore the hypothesis postulating the occurrence of specific niches creating microenvironment that regulate or determine the alternative fate of precursor cells during remyelination arises. Our vascular-niche hypothesis, which will be investigated, predicts a causative role of BMP pathway in prompting OPCs to differentiation into Schwann cells or in blocking them in the proliferation phase.'

Introduzione (Teaser)

Myelin sheaths provide insulation and structural support in neuronal axons. Understanding the molecular mechanisms of natural myelin production could help to design treatment regimes for disorders such as multiple sclerosis.

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