Scar formation is a common response to many central nervous system (CNS) disorders and a major obstacle blocking axonal regeneration in CNS disease. Previous work identified perivascular fibroblasts as a novel source of the “fibrotic” non-neural lesion scar in CNS disease. However, factors regulating fibrotic scar formation in CNS disease remain unknown. This study will identify the role of a changed environment in CNS disease with vasculature rupture and deposition of the circulating blood-derived coagulation factor fibrinogen on perivascular fibroblast activation and ECM deposition. We will potentially discover mechanisms applicable to control perivascular fibroblast fate and functions tailored to promote a wide range of CNS diseases with fibrotic scar formation.
 

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