Dystrophin-dependent and -independent AQP4 pools are expressed in the mouse brain

In a recent study, we demonstrated that in the plasma membrane AQP4 is organized into several distinct large multisubunit complexes. In this study, we analysed whether these pools are similarly affected in dystrophin‐deficient mice and immunolocalized the sites of dystrophin‐dependent and ‐independe...

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Bibliographic Details
Published in:Glia 2008-06, Vol.56 (8), p.869-876
Main Authors: Nicchia, Grazia Paola, Rossi, Andrea, Nudel, Uri, Svelto, Maria, Frigeri, Antonio
Format: Article
Language:English
Subjects:
Animals
Aquaporin 4 - metabolism
Aquaporin-4
BN-PAGE
Brain - anatomy & histology
Brain - metabolism
Calcium-Binding Proteins - metabolism
DGC
Dystroglycans - metabolism
Dystrophin - deficiency
Dystrophin - physiology
Gene Expression Regulation - genetics
Gene Expression Regulation - physiology
mdx
Membrane Proteins - metabolism
Mice
Mice, Inbred C57BL
Mice, Transgenic
Muscle Proteins - metabolism
neuromuscular system
OAPs
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Summary:In a recent study, we demonstrated that in the plasma membrane AQP4 is organized into several distinct large multisubunit complexes. In this study, we analysed whether these pools are similarly affected in dystrophin‐deficient mice and immunolocalized the sites of dystrophin‐dependent and ‐independent AQP4 pools. Western blot performed on two‐dimensional Blue Native/SDS‐PAGE membranes indicated that, among the AQP4 pools, it was mainly a large multisubunit complex that was specifically affected in dystrophin‐deficient mice (DP71 and mdx3cv mice). This dystrophin‐dependent AQP4 pool was immunolocalized in perivascular astrocytes, since it was found to be significantly altered in both types of dystrophin‐deficient mice. Dystrophin‐independent pools were immunolocalized in the granular cell layer of the cerebellum and in the subpial endfoot layer and ependymal cells in the brain. These data provide a better understanding on the association between AQP4 and the dystrophin‐glycoprotein complex in the central nervous system. © 2008 Wiley‐Liss, Inc.
ISSN:0894-1491
1098-1136
DOI:10.1002/glia.20661