PubMed:15815585 JSONTXT 5 Projects

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Id Subject Object Predicate Lexical cue
T1 0-169 DRI_Background denotes Endothelin-1 overexpression leads to further water accumulation and brain edema after middle cerebral artery occlusion via aquaporin 4 expression in astrocytic end-feet.
T2 170-297 DRI_Background denotes Stroke patients have increased levels of endothelin-1 (ET-1), a strong vasoconstrictor, in their plasma or cerebrospinal fluid.
T3 298-392 DRI_Outcome denotes Previously, we showed high level of ET-1 mRNA expression in astrocytes after hypoxia/ischemia.
T4 393-514 DRI_Challenge denotes It is unclear whether the contribution of ET-1 induction in astrocytes is protective or destructive in cerebral ischemia.
T5 515-563 DRI_Outcome denotes Here, we generated a transgenic mouse model that
T6 564-580 Token_Label.OUTSIDE denotes overexpress ET-1
T7 581-793 DRI_Outcome denotes in astrocytes (GET-1) using the glial fibrillary acidic protein promoter to examine the role of astrocytic ET-1 in ischemic stroke by challenging these mice with transient middle cerebral artery occlusion (MCAO).
T8 794-992 DRI_Background denotes Under normal condition, GET-1 mice showed no abnormality in brain morphology, cerebrovasculature, absolute cerebral blood flow, blood-brain barrier (BBB) integrity, and mean arterial blood pressure.
T9 993-1197 DRI_Background denotes Yet, GET-1 mice subjected to transient MCAO showed more severe neurologic deficits and increased infarct, which were partially normalized by administration of ABT-627 (ET(A) antagonist) 5 mins after MCAO.
T10 1198-1402 DRI_Outcome denotes In addition, GET-1 brains exhibited more Evans blue extravasation and showed decreased endothelial occludin expression after MCAO, correlating with higher brain water content and increased cerebral edema.
T11 1403-1519 DRI_Background denotes Aquaporin 4 expression was also more pronounced in astrocytic end-feet on blood vessels in GET-1 ipsilateral brains.
T12 1520-1700 DRI_Challenge denotes Our current data suggest that astrocytic ET-1 has deleterious effects on water homeostasis, cerebral edema and BBB integrity, which contribute to more severe ischemic brain injury.