Temporary loss of perivascular aquaporin-4 in neocortex after transient middle cerebral artery occlusion in mice

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dc.contributor.author Amiry-Moghaddam, M
dc.contributor.author Ottersen, O P
dc.contributor.author Agre, P
dc.contributor.author Rash, J E
dc.contributor.author Haug, F M
dc.contributor.author Laake, P
dc.contributor.author Skare, O
dc.contributor.author Zeynalov, E
dc.contributor.author Davidson, K G
dc.contributor.author Yasumura, T
dc.contributor.author Mylonakou, M N
dc.contributor.author Otsuka, T
dc.contributor.author Bhardwaj, A
dc.contributor.author Frydenlund, D S
dc.date.accessioned 2010-03-04T19:57:09Z
dc.date.available 2010-03-04T19:57:09Z
dc.date.issued 2006-09-05
dc.identifier.citation Proc Natl Acad Sci U S A. 2006 Sep 5;103(36):13532-6. Epub 2006 Aug 28. http://www.pnas.org/content/103/36/13532.abstract en
dc.identifier.uri http://jhir.library.jhu.edu/handle/1774.2/33887
dc.description.abstract The aquaporin-4 (AQP4) pool in the perivascular astrocyte membranes has been shown to be critically involved in the formation and dissolution of brain edema. Cerebral edema is a major cause of morbidity and mortality in stroke. It is therefore essential to know whether the perivascular pool of AQP4 is up- or down-regulated after an ischemic insult, because such changes would determine the time course of edema formation. Here we demonstrate by quantitative immunogold cytochemistry that the ischemic striatum and neocortex show distinct patterns of AQP4 expression in the reperfusion phase after 90 min of middle cerebral artery occlusion. The striatal core displays a loss of perivascular AQP4 at 24 hr of reperfusion with no sign of subsequent recovery. The most affected part of the cortex also exhibits loss of perivascular AQP4. This loss is of magnitude similar to that of the striatal core, but it shows a partial recovery toward 72 hr of reperfusion. By freeze fracture we show that the loss of perivascular AQP4 is associated with the disappearance of the square lattices of particles that normally are distinct features of the perivascular astrocyte membrane. The cortical border zone differs from the central part of the ischemic lesion by showing no loss of perivascular AQP4 at 24 hr of reperfusion but rather a slight increase. These data indicate that the size of the AQP4 pool that controls the exchange of fluid between brain and blood during edema formation and dissolution is subject to large and region-specific changes in the reperfusion phase. en
dc.description.provenance Submitted by Janice Chen (janice.chen@jhu.edu) on 2010-03-04T16:46:57Z No. of bitstreams: 1 PNAS-2006-Frydenlund-13532-6.pdf: 1713827 bytes, checksum: a69ed70b65abed24708f5c3280b16c06 (MD5) en
dc.description.provenance Approved for entry into archive by David Reynolds(davidr@jhu.edu) on 2010-03-04T19:57:09Z (GMT) No. of bitstreams: 1 PNAS-2006-Frydenlund-13532-6.pdf: 1713827 bytes, checksum: a69ed70b65abed24708f5c3280b16c06 (MD5) en
dc.description.provenance Made available in DSpace on 2010-03-04T19:57:09Z (GMT). No. of bitstreams: 1 PNAS-2006-Frydenlund-13532-6.pdf: 1713827 bytes, checksum: a69ed70b65abed24708f5c3280b16c06 (MD5) Previous issue date: 2006-09-05 en
dc.language.iso en_US en
dc.publisher National Academy of Sciences en
dc.subject Neocortex/metabolism en
dc.subject Infarction, Middle Cerebral Artery/metabolism en
dc.subject Aquaporin 4/metabolism en
dc.title Temporary loss of perivascular aquaporin-4 in neocortex after transient middle cerebral artery occlusion in mice en
dc.type Article en

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