Limited Energy Supply in Müller Cells Alters Glutamate Uptake
The viability of retinal ganglion cells (RGC) is essential for the maintenance of visual function. RGC homeostasis is maintained by the surrounding retinal glial cells, the Müller cells, which buffer the extracellular concentration of neurotransmitters and provide the RGCs with energy. This study ev...
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| Veröffentlicht in: | Neurochemical research 2014-05, Vol.39 (5), p.941-949 |
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| creator | Toft-Kehler, Anne Katrine Skytt, Dorte Marie Poulsen, Kristian Arild Brændstrup, Charlotte Taul Gegelashvili, Georgi Waagepetersen, Helle Kolko, Miriam |
| description | The viability of retinal ganglion cells (RGC) is essential for the maintenance of visual function. RGC homeostasis is maintained by the surrounding retinal glial cells, the Müller cells, which buffer the extracellular concentration of neurotransmitters and provide the RGCs with energy. This study evaluates if glucose-deprivation of Müller cells interferes with their ability to remove glutamate from the extracellular space. The human Müller glial cell line, Moorfields/Institute of Ophthalmology-Müller 1, was used to study changes in glutamate uptake. Excitatory amino acid transporter (EAAT) proteins were up-regulated in glucose-deprived Müller cells and glutamate uptake was significantly increased in the absence of glucose. The present findings revealed an up-regulation of EAAT1 and EAAT2 in glucose-deprived Müller cells as well as an increased ability to take up glutamate. Hence, glucose deprivation may result in an increased ability to protect RGCs from glutamate-induced excitotoxicity, whereas malfunction of glutamate uptake in Müller cells may contribute to retinal neurodegeneration. |
| doi_str_mv | 10.1007/s11064-014-1289-z |
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RGC homeostasis is maintained by the surrounding retinal glial cells, the Müller cells, which buffer the extracellular concentration of neurotransmitters and provide the RGCs with energy. This study evaluates if glucose-deprivation of Müller cells interferes with their ability to remove glutamate from the extracellular space. The human Müller glial cell line, Moorfields/Institute of Ophthalmology-Müller 1, was used to study changes in glutamate uptake. Excitatory amino acid transporter (EAAT) proteins were up-regulated in glucose-deprived Müller cells and glutamate uptake was significantly increased in the absence of glucose. The present findings revealed an up-regulation of EAAT1 and EAAT2 in glucose-deprived Müller cells as well as an increased ability to take up glutamate. Hence, glucose deprivation may result in an increased ability to protect RGCs from glutamate-induced excitotoxicity, whereas malfunction of glutamate uptake in Müller cells may contribute to retinal neurodegeneration.</description><identifier>ISSN: 0364-3190</identifier><identifier>EISSN: 1573-6903</identifier><identifier>DOI: 10.1007/s11064-014-1289-z</identifier><identifier>PMID: 24700282</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Cell Line ; Cell Survival - drug effects ; D-Aspartic Acid - metabolism ; Ependymoglial Cells - physiology ; Excitatory Amino Acid Transporter 1 - metabolism ; Excitatory Amino Acid Transporter 2 - metabolism ; Glucose - deficiency ; Glutamic Acid - metabolism ; Humans ; Neurochemistry ; Neurology ; Neurosciences ; Original Paper ; Up-Regulation</subject><ispartof>Neurochemical research, 2014-05, Vol.39 (5), p.941-949</ispartof><rights>Springer Science+Business Media New York 2014</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c442t-22f32c14ebbacfa3d9c580957c2555ee8f1badfb326953aedec5c0783e11b2603</citedby><cites>FETCH-LOGICAL-c442t-22f32c14ebbacfa3d9c580957c2555ee8f1badfb326953aedec5c0783e11b2603</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11064-014-1289-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11064-014-1289-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24700282$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Toft-Kehler, Anne Katrine</creatorcontrib><creatorcontrib>Skytt, Dorte Marie</creatorcontrib><creatorcontrib>Poulsen, Kristian Arild</creatorcontrib><creatorcontrib>Brændstrup, Charlotte Taul</creatorcontrib><creatorcontrib>Gegelashvili, Georgi</creatorcontrib><creatorcontrib>Waagepetersen, Helle</creatorcontrib><creatorcontrib>Kolko, Miriam</creatorcontrib><title>Limited Energy Supply in Müller Cells Alters Glutamate Uptake</title><title>Neurochemical research</title><addtitle>Neurochem Res</addtitle><addtitle>Neurochem Res</addtitle><description>The viability of retinal ganglion cells (RGC) is essential for the maintenance of visual function. 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RGC homeostasis is maintained by the surrounding retinal glial cells, the Müller cells, which buffer the extracellular concentration of neurotransmitters and provide the RGCs with energy. This study evaluates if glucose-deprivation of Müller cells interferes with their ability to remove glutamate from the extracellular space. The human Müller glial cell line, Moorfields/Institute of Ophthalmology-Müller 1, was used to study changes in glutamate uptake. Excitatory amino acid transporter (EAAT) proteins were up-regulated in glucose-deprived Müller cells and glutamate uptake was significantly increased in the absence of glucose. The present findings revealed an up-regulation of EAAT1 and EAAT2 in glucose-deprived Müller cells as well as an increased ability to take up glutamate. Hence, glucose deprivation may result in an increased ability to protect RGCs from glutamate-induced excitotoxicity, whereas malfunction of glutamate uptake in Müller cells may contribute to retinal neurodegeneration.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>24700282</pmid><doi>10.1007/s11064-014-1289-z</doi><tpages>9</tpages></addata></record> |
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| subjects | Biochemistry Biomedical and Life Sciences Biomedicine Cell Biology Cell Line Cell Survival - drug effects D-Aspartic Acid - metabolism Ependymoglial Cells - physiology Excitatory Amino Acid Transporter 1 - metabolism Excitatory Amino Acid Transporter 2 - metabolism Glucose - deficiency Glutamic Acid - metabolism Humans Neurochemistry Neurology Neurosciences Original Paper Up-Regulation |
| title | Limited Energy Supply in Müller Cells Alters Glutamate Uptake |
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