Retinal Colocalization and In Vitro Interaction of the Glutamate Receptor EAAT3 and the Serum- and Glucocorticoid-Inducible Kinase SGK1

dc.contributor.authorSchniepp, Roman
dc.contributor.authorKohler, Konrad
dc.contributor.authorLadewig, Thomas
dc.contributor.authorGuenther, Elke
dc.contributor.authorHenke, Guido
dc.contributor.authorPalmada, Monica
dc.contributor.authorBoehmer, C
dc.contributor.authorRothstein, Jeffrey
dc.contributor.authorBroer, Stefan
dc.contributor.authorLang, Florian
dc.date.accessioned2015-12-13T23:07:33Z
dc.date.available2015-12-13T23:07:33Z
dc.date.issued2004
dc.date.updated2015-12-12T08:09:28Z
dc.description.abstractPURPOSE. The serum- and glucocorticoid-inducible kinase SGK1 regulates several epithelial channels and transporters, the related protein kinase B (PKB) regulates glucose transport. SGK1 is expressed in the brain and could thus regulate glial and/or neuronal transport processes. The present study explores whether SGK1 is expressed in the retina and whether it regulates EAAT3, a Na+-coupled glutamate transporter. EAAT3 is expressed in retinal ganglion cells and accomplishes the clearance of glutamate from synaptic clefts. METHODS. Immunohistochemistry was performed to test for retinal SGK1 expression. For functional analysis, cRNA encoding EAAT3 was injected into Xenopus oocytes with or without additional injection of wild-type SGK1, constitutively active S422DSGK1, inactive K127NSGK1, and/or constitutively active T308D,S473DPKB. Glutamate induced current (IGLU) was taken as a measure for transport. RESULTS. SGK1 is indeed expressed in several retinal cells including retinal ganglion cells where it is colocalized with EAAT3. In EAAT3-expressing Xenopus oocytes, glutamate-induced current was stimulated by coexpression of wild-type SGK1, constitutively active S422DSGK1, and constitutively active T308D,S473DPKB, but not by inactive K127NSGK1. CONCLUSIONS. SGK1 and EAAT3 are coexpressed in retinal neurons, and SGK1 serves to stimulate EAAT3. This function is shared by protein kinase B (PKB). The experiments reveal a novel mechanism regulating EAAT3, which may be essential for the function of the retinal ganglion cells.
dc.identifier.issn1552-5783
dc.identifier.urihttp://hdl.handle.net/1885/86260
dc.publisherAssociation for Research in Vision and Opthalmology
dc.sourceInvestigative Ophthalmology and Visual Science
dc.subjectKeywords: complementary RNA; glutamate receptor; glutamate receptor eaat3; glutamic acid; protein kinase B; serum and glucocorticoid regulated kinase 1; unclassified drug; complementary RNA; cotransporter; excitatory amino acid transporter 3; glutamate transporter;
dc.titleRetinal Colocalization and In Vitro Interaction of the Glutamate Receptor EAAT3 and the Serum- and Glucocorticoid-Inducible Kinase SGK1
dc.typeJournal article
local.bibliographicCitation.issue5
local.bibliographicCitation.lastpage1449
local.bibliographicCitation.startpage1442
local.contributor.affiliationSchniepp, Roman, University of Tubingen
local.contributor.affiliationKohler, Konrad, University of Tubingen
local.contributor.affiliationLadewig, Thomas, University of Tubingen
local.contributor.affiliationGuenther, Elke, University of Tubingen
local.contributor.affiliationHenke, Guido, University of Tubingen
local.contributor.affiliationPalmada, Monica, Rhine-Waal University of Applied Sciences
local.contributor.affiliationBoehmer, C, University of Tubingen
local.contributor.affiliationRothstein, Jeffrey, Johns Hopkins University
local.contributor.affiliationBroer, Stefan, College of Medicine, Biology and Environment, ANU
local.contributor.affiliationLang, Florian, University of Tubingen
local.contributor.authoremailu4009041@anu.edu.au
local.contributor.authoruidBroer, Stefan, u4009041
local.description.notesImported from ARIES
local.description.refereedYes
local.identifier.absfor060105 - Cell Neurochemistry
local.identifier.ariespublicationMigratedxPub15076
local.identifier.citationvolume45
local.identifier.doi10.1167/iovs.03-0062
local.identifier.scopusID2-s2.0-2442709321
local.identifier.uidSubmittedByMigrated
local.type.statusPublished Version

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