Differential regulation of Kir4.1 and Kir2.1 expression in the ischemic rat retina
Ischemia–reperfusion of the rat retina causes gliosis of Müller cells that is associated with a decrease of their K + conductance. By using quantitative PCR and immunohistochemical staining of retinal slices, we investigated the effect of transient ischemia–reperfusion on retinal expression of two i...
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| Veröffentlicht in: | Neuroscience letters 2006-03, Vol.396 (2), p.97-101 |
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| creator | Iandiev, Ianors Tenckhoff, Solveig Pannicke, Thomas Biedermann, Bernd Hollborn, Margrit Wiedemann, Peter Reichenbach, Andreas Bringmann, Andreas |
| description | Ischemia–reperfusion of the rat retina causes gliosis of Müller cells that is associated with a decrease of their K
+ conductance. By using quantitative PCR and immunohistochemical staining of retinal slices, we investigated the effect of transient ischemia–reperfusion on retinal expression of two inward-rectifying K
+ (Kir) channels, Kir4.1 and Kir2.1. In control retinas, Müller cells prominently expressed both Kir4.1 and Kir2.1 proteins. At 7 days after reperfusion, the expression of Kir4.1 protein was strongly downregulated, while the Kir2.1 protein expression remained unaltered. The expression of Kir4.1 mRNA was reduced by 55% after ischemia while the expression of Kir2.1 mRNA was not altered. The data suggest that the glial expression of distinct Kir channels is differentially regulated after retinal ischemia, with deletarious consequences for K
+ ion and water homeostasis. |
| doi_str_mv | 10.1016/j.neulet.2005.11.016 |
| format | Article |
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+ conductance. By using quantitative PCR and immunohistochemical staining of retinal slices, we investigated the effect of transient ischemia–reperfusion on retinal expression of two inward-rectifying K
+ (Kir) channels, Kir4.1 and Kir2.1. In control retinas, Müller cells prominently expressed both Kir4.1 and Kir2.1 proteins. At 7 days after reperfusion, the expression of Kir4.1 protein was strongly downregulated, while the Kir2.1 protein expression remained unaltered. The expression of Kir4.1 mRNA was reduced by 55% after ischemia while the expression of Kir2.1 mRNA was not altered. The data suggest that the glial expression of distinct Kir channels is differentially regulated after retinal ischemia, with deletarious consequences for K
+ ion and water homeostasis.</description><identifier>ISSN: 0304-3940</identifier><identifier>EISSN: 1872-7972</identifier><identifier>DOI: 10.1016/j.neulet.2005.11.016</identifier><identifier>PMID: 16330144</identifier><identifier>CODEN: NELED5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Animals ; Biological and medical sciences ; Cells, Cultured ; Eye and associated structures. Visual pathways and centers. Vision ; Fundamental and applied biological sciences. Psychology ; Gene Expression Regulation ; Glia ; Ischemia ; Ischemia - metabolism ; Medical sciences ; Müller cell ; Neuroglia - metabolism ; Ophthalmology ; Optic Neuropathy, Ischemic ; Potassium channels ; Potassium Channels, Inwardly Rectifying - metabolism ; Rats ; Rats, Long-Evans ; Retina ; Retina - metabolism ; Retinal Vessels - metabolism ; Retinopathies ; RT-PCR ; Tissue Distribution ; Vertebrates: nervous system and sense organs</subject><ispartof>Neuroscience letters, 2006-03, Vol.396 (2), p.97-101</ispartof><rights>2005 Elsevier Ireland Ltd</rights><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-ed3bb8f009099d746ce88b4689d770ae25d272d9f5a4536622d216dfd40acacc3</citedby><cites>FETCH-LOGICAL-c456t-ed3bb8f009099d746ce88b4689d770ae25d272d9f5a4536622d216dfd40acacc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0304394005012966$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17573262$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16330144$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Iandiev, Ianors</creatorcontrib><creatorcontrib>Tenckhoff, Solveig</creatorcontrib><creatorcontrib>Pannicke, Thomas</creatorcontrib><creatorcontrib>Biedermann, Bernd</creatorcontrib><creatorcontrib>Hollborn, Margrit</creatorcontrib><creatorcontrib>Wiedemann, Peter</creatorcontrib><creatorcontrib>Reichenbach, Andreas</creatorcontrib><creatorcontrib>Bringmann, Andreas</creatorcontrib><title>Differential regulation of Kir4.1 and Kir2.1 expression in the ischemic rat retina</title><title>Neuroscience letters</title><addtitle>Neurosci Lett</addtitle><description>Ischemia–reperfusion of the rat retina causes gliosis of Müller cells that is associated with a decrease of their K
+ conductance. By using quantitative PCR and immunohistochemical staining of retinal slices, we investigated the effect of transient ischemia–reperfusion on retinal expression of two inward-rectifying K
+ (Kir) channels, Kir4.1 and Kir2.1. In control retinas, Müller cells prominently expressed both Kir4.1 and Kir2.1 proteins. At 7 days after reperfusion, the expression of Kir4.1 protein was strongly downregulated, while the Kir2.1 protein expression remained unaltered. The expression of Kir4.1 mRNA was reduced by 55% after ischemia while the expression of Kir2.1 mRNA was not altered. The data suggest that the glial expression of distinct Kir channels is differentially regulated after retinal ischemia, with deletarious consequences for K
+ ion and water homeostasis.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cells, Cultured</subject><subject>Eye and associated structures. Visual pathways and centers. Vision</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Regulation</subject><subject>Glia</subject><subject>Ischemia</subject><subject>Ischemia - metabolism</subject><subject>Medical sciences</subject><subject>Müller cell</subject><subject>Neuroglia - metabolism</subject><subject>Ophthalmology</subject><subject>Optic Neuropathy, Ischemic</subject><subject>Potassium channels</subject><subject>Potassium Channels, Inwardly Rectifying - metabolism</subject><subject>Rats</subject><subject>Rats, Long-Evans</subject><subject>Retina</subject><subject>Retina - metabolism</subject><subject>Retinal Vessels - metabolism</subject><subject>Retinopathies</subject><subject>RT-PCR</subject><subject>Tissue Distribution</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0304-3940</issn><issn>1872-7972</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1rGzEQhkVoiR2n_6CEvbS33eprpd1LILhtEmIIlPYsZGlUy6y1jqQN7b-PjA2-5aTRzPMOw4PQZ4Ibgon4tm0CTAPkhmLcNoQ0pXmB5qSTtJa9pB_QHDPMa9ZzPENXKW1xAUnLL9GMCMYw4XyOfn33zkGEkL0eqgh_p0FnP4ZqdNWTj7whlQ72UNJSwr99hJQOcx-qvIHKJ7OBnTdV1LnEsw_6Gn10ekjw6fQu0J-fP34vH-rV8_3j8m5VG96KXINl63XnMO5x31vJhYGuW3PRlY_EGmhrqaS2d63mLROCUkuJsM5yrI02hi3Q1-PefRxfJkhZ7co1MAw6wDglJaToGetlAfkRNHFMKYJT--h3Ov5XBKuDS7VVR5fq4FIRokqzxG5O-6f1Duw5dJJXgC8nQCejBxd1MD6dOdlKRgUt3O2Rg2Lj1UNUyXgIBqyPYLKyo3__kjfe5JMy</recordid><startdate>20060327</startdate><enddate>20060327</enddate><creator>Iandiev, Ianors</creator><creator>Tenckhoff, Solveig</creator><creator>Pannicke, Thomas</creator><creator>Biedermann, Bernd</creator><creator>Hollborn, Margrit</creator><creator>Wiedemann, Peter</creator><creator>Reichenbach, Andreas</creator><creator>Bringmann, Andreas</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20060327</creationdate><title>Differential regulation of Kir4.1 and Kir2.1 expression in the ischemic rat retina</title><author>Iandiev, Ianors ; Tenckhoff, Solveig ; Pannicke, Thomas ; Biedermann, Bernd ; Hollborn, Margrit ; Wiedemann, Peter ; Reichenbach, Andreas ; Bringmann, Andreas</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-ed3bb8f009099d746ce88b4689d770ae25d272d9f5a4536622d216dfd40acacc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cells, Cultured</topic><topic>Eye and associated structures. Visual pathways and centers. Vision</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression Regulation</topic><topic>Glia</topic><topic>Ischemia</topic><topic>Ischemia - metabolism</topic><topic>Medical sciences</topic><topic>Müller cell</topic><topic>Neuroglia - metabolism</topic><topic>Ophthalmology</topic><topic>Optic Neuropathy, Ischemic</topic><topic>Potassium channels</topic><topic>Potassium Channels, Inwardly Rectifying - metabolism</topic><topic>Rats</topic><topic>Rats, Long-Evans</topic><topic>Retina</topic><topic>Retina - metabolism</topic><topic>Retinal Vessels - metabolism</topic><topic>Retinopathies</topic><topic>RT-PCR</topic><topic>Tissue Distribution</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Iandiev, Ianors</creatorcontrib><creatorcontrib>Tenckhoff, Solveig</creatorcontrib><creatorcontrib>Pannicke, Thomas</creatorcontrib><creatorcontrib>Biedermann, Bernd</creatorcontrib><creatorcontrib>Hollborn, Margrit</creatorcontrib><creatorcontrib>Wiedemann, Peter</creatorcontrib><creatorcontrib>Reichenbach, Andreas</creatorcontrib><creatorcontrib>Bringmann, Andreas</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Neuroscience letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Iandiev, Ianors</au><au>Tenckhoff, Solveig</au><au>Pannicke, Thomas</au><au>Biedermann, Bernd</au><au>Hollborn, Margrit</au><au>Wiedemann, Peter</au><au>Reichenbach, Andreas</au><au>Bringmann, Andreas</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differential regulation of Kir4.1 and Kir2.1 expression in the ischemic rat retina</atitle><jtitle>Neuroscience letters</jtitle><addtitle>Neurosci Lett</addtitle><date>2006-03-27</date><risdate>2006</risdate><volume>396</volume><issue>2</issue><spage>97</spage><epage>101</epage><pages>97-101</pages><issn>0304-3940</issn><eissn>1872-7972</eissn><coden>NELED5</coden><abstract>Ischemia–reperfusion of the rat retina causes gliosis of Müller cells that is associated with a decrease of their K
+ conductance. By using quantitative PCR and immunohistochemical staining of retinal slices, we investigated the effect of transient ischemia–reperfusion on retinal expression of two inward-rectifying K
+ (Kir) channels, Kir4.1 and Kir2.1. In control retinas, Müller cells prominently expressed both Kir4.1 and Kir2.1 proteins. At 7 days after reperfusion, the expression of Kir4.1 protein was strongly downregulated, while the Kir2.1 protein expression remained unaltered. The expression of Kir4.1 mRNA was reduced by 55% after ischemia while the expression of Kir2.1 mRNA was not altered. The data suggest that the glial expression of distinct Kir channels is differentially regulated after retinal ischemia, with deletarious consequences for K
+ ion and water homeostasis.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>16330144</pmid><doi>10.1016/j.neulet.2005.11.016</doi><tpages>5</tpages></addata></record> |
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| subjects | Animals Biological and medical sciences Cells, Cultured Eye and associated structures. Visual pathways and centers. Vision Fundamental and applied biological sciences. Psychology Gene Expression Regulation Glia Ischemia Ischemia - metabolism Medical sciences Müller cell Neuroglia - metabolism Ophthalmology Optic Neuropathy, Ischemic Potassium channels Potassium Channels, Inwardly Rectifying - metabolism Rats Rats, Long-Evans Retina Retina - metabolism Retinal Vessels - metabolism Retinopathies RT-PCR Tissue Distribution Vertebrates: nervous system and sense organs |
| title | Differential regulation of Kir4.1 and Kir2.1 expression in the ischemic rat retina |
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