| Literature DB >> 24896566 |
Be'eri Niego1, Robert L Medcalf1.
Abstract
Plasmin, the principal downstream product of tissue-type plasminogen activator (tPA), is known for its potent fibrin-degrading capacity but is also recognized for many non-fibrinolytic activities. Curiously, plasmin has not been conclusively linked to blood-brain barrier (BBB) disruption during recombinant tPA (rtPA)-induced thrombolysis in ischemic stroke. This is surprising given the substantial involvement of tPA in the modulation of BBB permeability and the co-existence of tPA and plasminogen in both blood and brain throughout the ischemic event. Here, we review the work that argues a role for plasmin together with endogenous tPA or rtPA in BBB alteration, presenting the overall controversy around the topic yet creating a rational case for an involvement of plasmin in this process.Entities:
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Year: 2014 PMID: 24896566 PMCID: PMC4126105 DOI: 10.1038/jcbfm.2014.99
Source DB: PubMed Journal: J Cereb Blood Flow Metab ISSN: 0271-678X Impact factor: 6.200