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Differential Promotion of Glutamate Transporter Expression and Function by Glucocorticoids in Astrocytes from Various Brain Regions
Steroids that activate glucocorticoid receptors (GRs) and mineralocorticoid receptors have important regulatory effects on neural development, plasticity, and the body's stress response. Here, we investigated the role of corticosteroids in regulating the expression of the glial glutamate transp...
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Published in: | The Journal of biological chemistry 2005-10, Vol.280 (41), p.34924-34932 |
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description | Steroids that activate glucocorticoid receptors (GRs) and mineralocorticoid receptors have important regulatory effects on neural development, plasticity, and the body's stress response. Here, we investigated the role of corticosteroids in regulating the expression of the glial glutamate transporters glial glutamate transporter-1 (GLT-1) and glutamate-aspartate transporter (GLAST) in rat primary astrocytes. The synthetic glucocorticoid dexamethasone provoked a marked increase of GLT-1 transcription and protein levels in cortical astrocytes, whereas GLAST expression remained unaffected. Up-regulation of GLT-1 expression was accompanied by an enhanced glutamate uptake, which could be blocked by the specific GLT-1 inhibitor dihydrokainate. The promoting effect of dexamethasone on GLT-1 gene expression and function was abolished by the GR antagonist mifepristone. A predominant role of the GR was further supported by the observation that corticosterone could elevate GLT-1 expression in a dose-dependent manner, whereas aldosterone, the physiological ligand of the mineralocorticoid receptor, exerted only weak effects even when applied at high concentrations. Moreover, we monitored brain region-specific differences, since all corticosteroids used in this study failed to alter the expression of GLT-1 in midbrain and cerebellar glia, although expression levels of both corticosteroid receptor subtypes were similar in all brain regions analyzed. Dexamethasone, however, modestly enhanced GLT-1 expression in cerebellar glia in combination with the DNA methyltransferase inhibitor 5-aza-2-deoxycytidine, suggesting that suppression of GLT-1 expression in cerebellar cultures may at least in part be epigenetically mediated by a DNA methylation-dependent process. Taken together, our data highlight a potential role for glucocorticoids in regulating GLT-1 gene expression during central nervous system development or pathophysiogical processes including stress. |
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Here, we investigated the role of corticosteroids in regulating the expression of the glial glutamate transporters glial glutamate transporter-1 (GLT-1) and glutamate-aspartate transporter (GLAST) in rat primary astrocytes. The synthetic glucocorticoid dexamethasone provoked a marked increase of GLT-1 transcription and protein levels in cortical astrocytes, whereas GLAST expression remained unaffected. Up-regulation of GLT-1 expression was accompanied by an enhanced glutamate uptake, which could be blocked by the specific GLT-1 inhibitor dihydrokainate. The promoting effect of dexamethasone on GLT-1 gene expression and function was abolished by the GR antagonist mifepristone. A predominant role of the GR was further supported by the observation that corticosterone could elevate GLT-1 expression in a dose-dependent manner, whereas aldosterone, the physiological ligand of the mineralocorticoid receptor, exerted only weak effects even when applied at high concentrations. Moreover, we monitored brain region-specific differences, since all corticosteroids used in this study failed to alter the expression of GLT-1 in midbrain and cerebellar glia, although expression levels of both corticosteroid receptor subtypes were similar in all brain regions analyzed. Dexamethasone, however, modestly enhanced GLT-1 expression in cerebellar glia in combination with the DNA methyltransferase inhibitor 5-aza-2-deoxycytidine, suggesting that suppression of GLT-1 expression in cerebellar cultures may at least in part be epigenetically mediated by a DNA methylation-dependent process. Taken together, our data highlight a potential role for glucocorticoids in regulating GLT-1 gene expression during central nervous system development or pathophysiogical processes including stress.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.M502581200</identifier><identifier>PMID: 16079146</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adrenal Cortex Hormones - metabolism ; Amino Acid Transport System X-AG - biosynthesis ; Amino Acid Transport System X-AG - metabolism ; Animals ; Astrocytes - cytology ; Astrocytes - metabolism ; Azacitidine - analogs & derivatives ; Azacitidine - pharmacology ; Blotting, Western ; Brain - metabolism ; Central Nervous System - pathology ; Cerebellum - pathology ; Corticosterone - metabolism ; Corticosterone - pharmacology ; Decitabine ; Detergents - pharmacology ; Dexamethasone - pharmacology ; DNA Methylation ; DNA Modification Methylases - metabolism ; DNA Primers - chemistry ; Dose-Response Relationship, Drug ; Fluorescent Dyes - pharmacology ; Glucocorticoids - chemistry ; Immunohistochemistry ; Kainic Acid - analogs & derivatives ; Kainic Acid - pharmacology ; Ligands ; Luciferases - metabolism ; Membrane Microdomains - metabolism ; Mifepristone - pharmacology ; Neuroglia - pathology ; Rats ; Rats, Sprague-Dawley ; Receptors, Mineralocorticoid - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Time Factors ; Transfection ; Up-Regulation</subject><ispartof>The Journal of biological chemistry, 2005-10, Vol.280 (41), p.34924-34932</ispartof><rights>2005 © 2005 ASBMB. Currently published by Elsevier Inc; originally published by American Society for Biochemistry and Molecular Biology.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c553t-e3594c3b973a035c0656c5493b4754ebe58141b2e3daebfb38e44d835055d2233</citedby><cites>FETCH-LOGICAL-c553t-e3594c3b973a035c0656c5493b4754ebe58141b2e3daebfb38e44d835055d2233</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0021925820639321$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3549,27924,27925,45780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16079146$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zschocke, Jürgen</creatorcontrib><creatorcontrib>Bayatti, Nadhim</creatorcontrib><creatorcontrib>Clement, Albrecht M.</creatorcontrib><creatorcontrib>Witan, Heidrun</creatorcontrib><creatorcontrib>Figiel, Maciej</creatorcontrib><creatorcontrib>Engele, Jürgen</creatorcontrib><creatorcontrib>Behl, Christian</creatorcontrib><title>Differential Promotion of Glutamate Transporter Expression and Function by Glucocorticoids in Astrocytes from Various Brain Regions</title><title>The Journal of biological chemistry</title><addtitle>J Biol Chem</addtitle><description>Steroids that activate glucocorticoid receptors (GRs) and mineralocorticoid receptors have important regulatory effects on neural development, plasticity, and the body's stress response. Here, we investigated the role of corticosteroids in regulating the expression of the glial glutamate transporters glial glutamate transporter-1 (GLT-1) and glutamate-aspartate transporter (GLAST) in rat primary astrocytes. The synthetic glucocorticoid dexamethasone provoked a marked increase of GLT-1 transcription and protein levels in cortical astrocytes, whereas GLAST expression remained unaffected. Up-regulation of GLT-1 expression was accompanied by an enhanced glutamate uptake, which could be blocked by the specific GLT-1 inhibitor dihydrokainate. The promoting effect of dexamethasone on GLT-1 gene expression and function was abolished by the GR antagonist mifepristone. A predominant role of the GR was further supported by the observation that corticosterone could elevate GLT-1 expression in a dose-dependent manner, whereas aldosterone, the physiological ligand of the mineralocorticoid receptor, exerted only weak effects even when applied at high concentrations. Moreover, we monitored brain region-specific differences, since all corticosteroids used in this study failed to alter the expression of GLT-1 in midbrain and cerebellar glia, although expression levels of both corticosteroid receptor subtypes were similar in all brain regions analyzed. Dexamethasone, however, modestly enhanced GLT-1 expression in cerebellar glia in combination with the DNA methyltransferase inhibitor 5-aza-2-deoxycytidine, suggesting that suppression of GLT-1 expression in cerebellar cultures may at least in part be epigenetically mediated by a DNA methylation-dependent process. 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Here, we investigated the role of corticosteroids in regulating the expression of the glial glutamate transporters glial glutamate transporter-1 (GLT-1) and glutamate-aspartate transporter (GLAST) in rat primary astrocytes. The synthetic glucocorticoid dexamethasone provoked a marked increase of GLT-1 transcription and protein levels in cortical astrocytes, whereas GLAST expression remained unaffected. Up-regulation of GLT-1 expression was accompanied by an enhanced glutamate uptake, which could be blocked by the specific GLT-1 inhibitor dihydrokainate. The promoting effect of dexamethasone on GLT-1 gene expression and function was abolished by the GR antagonist mifepristone. A predominant role of the GR was further supported by the observation that corticosterone could elevate GLT-1 expression in a dose-dependent manner, whereas aldosterone, the physiological ligand of the mineralocorticoid receptor, exerted only weak effects even when applied at high concentrations. Moreover, we monitored brain region-specific differences, since all corticosteroids used in this study failed to alter the expression of GLT-1 in midbrain and cerebellar glia, although expression levels of both corticosteroid receptor subtypes were similar in all brain regions analyzed. Dexamethasone, however, modestly enhanced GLT-1 expression in cerebellar glia in combination with the DNA methyltransferase inhibitor 5-aza-2-deoxycytidine, suggesting that suppression of GLT-1 expression in cerebellar cultures may at least in part be epigenetically mediated by a DNA methylation-dependent process. Taken together, our data highlight a potential role for glucocorticoids in regulating GLT-1 gene expression during central nervous system development or pathophysiogical processes including stress.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>16079146</pmid><doi>10.1074/jbc.M502581200</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adrenal Cortex Hormones - metabolism Amino Acid Transport System X-AG - biosynthesis Amino Acid Transport System X-AG - metabolism Animals Astrocytes - cytology Astrocytes - metabolism Azacitidine - analogs & derivatives Azacitidine - pharmacology Blotting, Western Brain - metabolism Central Nervous System - pathology Cerebellum - pathology Corticosterone - metabolism Corticosterone - pharmacology Decitabine Detergents - pharmacology Dexamethasone - pharmacology DNA Methylation DNA Modification Methylases - metabolism DNA Primers - chemistry Dose-Response Relationship, Drug Fluorescent Dyes - pharmacology Glucocorticoids - chemistry Immunohistochemistry Kainic Acid - analogs & derivatives Kainic Acid - pharmacology Ligands Luciferases - metabolism Membrane Microdomains - metabolism Mifepristone - pharmacology Neuroglia - pathology Rats Rats, Sprague-Dawley Receptors, Mineralocorticoid - metabolism Reverse Transcriptase Polymerase Chain Reaction Time Factors Transfection Up-Regulation |
title | Differential Promotion of Glutamate Transporter Expression and Function by Glucocorticoids in Astrocytes from Various Brain Regions |
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