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      Time course of aquaporin expression after transient focal cerebral ischemia in mice.

      Journal of Neuroscience Research
      Animals, Aquaporin 4, metabolism, Aquaporins, Astrocytes, Blood-Brain Barrier, physiopathology, Brain Edema, etiology, Cerebral Cortex, Cerebral Infarction, complications, Disease Models, Animal, Ischemic Attack, Transient, Male, Mice, Mice, Inbred ICR, Microtubule-Associated Proteins, Time Factors, Up-Regulation, physiology

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          Abstract

          Cerebral edema contributes to morbidity and mortality in stroke. Aquaporins (AQPs)-1, -4, and -9 have been identified as the three main water channels in the brain. To clarify their role in water movement, we have compared their expression patterns with brain swelling after transient focal brain ischemia. There were two peaks of maximal hemispheric swelling at 1 hr and at 48 hr after ischemia, coinciding with two peaks of AQP4 expression. At 1 hr after occlusion, AQP4 expression was significantly increased on astrocyte endfeet in the core and in the border of the lesion. At 48 hr, AQP4 expression was increased in astrocytes in the border of the lesion over the whole cell. AQP9 showed a significant induction at 24 hr that increased gradually with time, without correlation with the swelling. The expression of AQP1 remained unchanged. These results suggest that AQP4, but not AQP1 or AQP9, may play an important role in water movement associated with the pathophysiology of edema after transient cerebral ischemia in the mouse. Copyright 2006 Wiley-Liss, Inc.

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