Coordinatore | KAROLINSKA INSTITUTET
Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie. |
Nazionalità Coordinatore | Sweden [SE] |
Totale costo | 1˙750˙000 € |
EC contributo | 1˙750˙000 € |
Programma | FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) |
Code Call | ERC-2012-StG_20111109 |
Funding Scheme | ERC-SG |
Anno di inizio | 2013 |
Periodo (anno-mese-giorno) | 2013-02-01 - 2018-01-31 |
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1 |
KAROLINSKA INSTITUTET
Organization address
address: Nobels Vag 5 contact info |
SE (STOCKHOLM) | hostInstitution | 1˙750˙000.00 |
2 |
KAROLINSKA INSTITUTET
Organization address
address: Nobels Vag 5 contact info |
SE (STOCKHOLM) | hostInstitution | 1˙750˙000.00 |
Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.
'Damage to the central nervous system (CNS) often leads to persistent functional deficits, causing great individual suffering and enormous cost to society. The manifestation of these deficits is believed to be associated with the scar tissue that forms locally at lesions, causing permanent tissue alteration and blocking regeneration. Research on CNS scar tissue has primarily focused on astrocytes and it is often referred to as the glial scar. However, although it has received much less attention, there is also a connective tissue or stromal, non-glial, component of the scar. While studying spinal cord injury-induced scarring, I recently discovered a new subpopulation of perivascular cells, named type A pericytes, as a major source of connective scar tissue. Type A pericytes are embedded in the vascular wall but proliferate and leave the blood vessel upon injury, differentiating into fibroblast-like cells that deposit extracellular matrix to seal the lesion and form the persistent stromal scar core. The aim of the proposal is to determine whether type A pericytes are a general source of pathological connective tissue in the CNS, to understand the nature of type A pericytes, and to uncover the signaling mechanisms mediating their recruitment. By comparing several different injury and disease models the proposed research intends to uncover common mechanisms of scarring and fibrosis and to identify new targets for human treatment after CNS injury.'