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Mechanisms underlying AQP4 accumulation in astrocyte endfeet
Author(s) -
Camassa Laura Maria Azzurra,
Lunde Lisa K.,
Hoddevik Eystein H.,
Stensland Maria,
Boldt Henning B.,
De Souza Gustavo A.,
Ottersen Ole P.,
AmiryMoghaddam Mahmood
Publication year - 2015
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.22878
Subject(s) - basal lamina , dystroglycan , agrin , biology , astrocyte , anatomy , extracellular matrix , basement membrane , neuroscience , aquaporin 4 , microbiology and biotechnology , blood–brain barrier , homeostasis , biophysics , ultrastructure , biochemistry , central nervous system , laminin , postsynaptic potential , receptor
The brain–blood interface holds the key to our understanding of how cerebral blood flow is regulated and how water and solutes are exchanged between blood and brain. The highly specialized astrocytic membranes that enwrap brain microvessels are salient constituents of the brain‐blood interface. These endfoot membranes contain a distinct set of molecules that is anchored to the subendothelial basal lamina forming an endfoot‐basal lamina junctional complex. Here we explore the mechanisms underpinning the formation of this complex. By use of a tailor made model system we show that endothelial cells promote AQP4 accumulation by exerting an inductive effect through extracellular matrix components such as agrin, as well as through a direct mechanical interaction with the endfoot processes. Through the compounds they secrete, the endothelial cells also increase AQP4 expression. The present data suggest that the highly specialized gliovascular interface is established through inductive processes that include both chemical and mechanical factors. GLIA 2015;63:2073–2091