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Thrombin Mutant W215A/E217A Treatment Improves Neurological Outcome and Reduces Cerebral Infarct Size in a Mouse Model of Ischemic Stroke
Author(s) -
Michelle A. BernyLang,
Sawan Hurst,
Erik I. Tucker,
Leslie A. Pelc,
Ruikang K. Wang,
Patricia D. Hurn,
Enrico Di,
Owen J. T. McCarty,
András Gruber
Publication year - 2011
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/strokeaha.110.603811
Subject(s) - medicine , middle cerebral artery , hemostasis , tissue plasminogen activator , stroke (engine) , anesthesia , plasminogen activator , ischemia , cerebral infarction , occlusion , cardiology , mechanical engineering , engineering
Treatment of ischemic stroke by activation of endogenous plasminogen using tissue plasminogen activator is limited by bleeding side effects. In mice, treatment of experimental ischemic stroke with activated protein C improves outcomes; however, activated protein C also has bleeding side effects. In contrast, activation of endogenous protein C using thrombin mutant W215A/E217A (WE) is antithrombotic without hemostasis impairment in primates. Therefore, we investigated the outcome of WE-treated experimental ischemic stroke in mice.

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