Plasminogen Deficiency Delays the Onset and Protects from Demyelination and Paralysis in Autoimmune Neuroinflammatory Disease.

ABSTRACT: Multiple sclerosis (MS) is a neuroinflammatory, demyelinating disease of the CNS. Fibrinogen deposition at sites of blood-brain barrier breakdown is a prominent feature of neuroinflammatory disease and contributes to disease severity. Plasminogen, the primary fibrinolytic enzyme, also modifies inflammatory processes. We used a murine model of MS, experimental autoimmune encephalomyelitis (EAE), to evaluate the hypothesis that the loss of plasminogen would exacerbate neuroinflammatory disease. However, contrary to initial expectations, EAE-challenged plasminogen-deficient (Plg^-) mice developed significantly delayed disease onset and reduced disease severity compared with wild-type (Plg⁺) mice. Similarly, pharmacologic inhibition of plasmin activation with tranexamic ac

SUBMITTER: Shaw MA 

PROVIDER: S-EPMC5394895 | biostudies-literature | 2017 Apr

REPOSITORIES: biostudies-literature