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• W2039145424 endingPage "971" @default.
• W2039145424 startingPage "964" @default.
• W2039145424 abstract "Cardiovascular and neurologic surgeries often involve a temporary reduction in cerebral blood flow. In these conditions, as well as during cerebral ischemia and traumatic brain injury, the temporary loss of oxygen and glucose initiates a cascade of cellular events that culminate in neuronal death and damage. Understanding the mechanisms that contribute to neuronal death after hypoxia/ischemia is critically important for treatment of such brain injury. Here, we use a model of combined cerebral hypoxia/ischemia (H/I) to examine the role of protease-activated receptor-1 (PAR-1) in hypoxic/ischemic neuronal damage. Our data show that PAR-1-deficient mice have smaller lesion volumes than wild-type controls after 45 minutes of H/I. The results of the genetic block of PAR-1 were corroborated using a PAR-1 antagonist, which decreased infarct volume in wild-type C57Bl6 mice. Examination of cellular responses to H/I reveals that PAR-1 -/- animals have less cellular death and diminished glial fibrillary acidic protein expression. Additionally, PAR-1 -/- mice exhibit less motor behavior impairment in rotorod and inverted wire-hang tests. These data suggest that PAR-1 contributes to hypoxic/ischemic brain injury and are consistent with other studies that implicate serine proteases and their receptors in neuropathology after cerebral insults." @default.
• W2039145424 created "2016-06-24" @default.
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• W2039145424 date "2004-09-01" @default.
• W2039145424 modified "2023-10-18" @default.
• W2039145424 title "PAR-1 Deficiency Protects against Neuronal Damage and Neurologic Deficits after Unilateral Cerebral Hypoxia/Ischemia" @default.
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• W2039145424 doi "https://doi.org/10.1097/01.wcb.0000128266.87474.bf" @default.
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• W2039145424 hasPublicationYear "2004" @default.
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