Premium
Time course of aquaporin expression after transient focal cerebral ischemia in mice
Author(s) -
de Castro Ribeiro Marlise,
Hirt Lorenz,
Bogousslavsky Julien,
Regli Luca,
Badaut Jérôme
Publication year - 2006
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.20819
Subject(s) - ischemia , aquaporin 4 , astrocyte , edema , lesion , pathophysiology , cerebral edema , brain edema , stroke (engine) , aquaporin , brain ischemia , pathology , aquaporin 1 , medicine , neuroscience , water channel , biology , central nervous system , physiology , mechanical engineering , engineering , inlet
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. © 2006 Wiley‐Liss, Inc.