P2X(7) receptor-mRNA and -protein in the mouse retina; changes during retinal degeneration in BALBCrds mice
A combined real-time PCR/immunohistochemistry study was carried out to investigate whether P2X(7) receptors, known to induce apoptosis and necrosis, may be causally related to the process of retinal degeneration in BALBCrds mice. In the retinae of BALBCrds mice, P2X(7) receptor-mRNA was the highest...
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description | A combined real-time PCR/immunohistochemistry study was carried out to investigate whether P2X(7) receptors, known to induce apoptosis and necrosis, may be causally related to the process of retinal degeneration in BALBCrds mice. In the retinae of BALBCrds mice, P2X(7) receptor-mRNA was the highest at an age of 20-40 days, and declined afterwards. At the same time, the P2X(7) receptor-message was constantly low in the retina of control BALBC mice until postnatal day 100. The receptor-mRNA in total brain tissue of both strains of mice was comparable with that of BALBCrds retinae. Double immunofluorescence in combination with laser scanning microscopy was used to study the distribution of P2X(7) receptor-immunoreactivity (IR) on neurons and different glial cell types of the retina. An exclusively neuronal localization of P2X(7)-IR in the ganglion cell layer was found by using either anti-neuronal nuclei or microtubule associated protein-2 as neuronal markers. There was a slight age-dependent decrease in the abundance of neuronal P2X(7)-IR both in BALBCrds or BALBC mice. P2X(7)-IR failed to co-localize with any of the non-neuronal markers used to stain microglial or Müller glial cells. No P2X(7) receptor-IR was found in the retinal ganglion cell layer of P2X(7)(-/-) animals, when compared with the control littermates. Hence, we suggest that, in BALBCrds mice, an early up-regulation of neuronal P2X(7) receptors may cause injury of retinal neurons and thereby functionally contribute to the retinal damage. |
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In the retinae of BALBCrds mice, P2X(7) receptor-mRNA was the highest at an age of 20-40 days, and declined afterwards. At the same time, the P2X(7) receptor-message was constantly low in the retina of control BALBC mice until postnatal day 100. The receptor-mRNA in total brain tissue of both strains of mice was comparable with that of BALBCrds retinae. Double immunofluorescence in combination with laser scanning microscopy was used to study the distribution of P2X(7) receptor-immunoreactivity (IR) on neurons and different glial cell types of the retina. An exclusively neuronal localization of P2X(7)-IR in the ganglion cell layer was found by using either anti-neuronal nuclei or microtubule associated protein-2 as neuronal markers. There was a slight age-dependent decrease in the abundance of neuronal P2X(7)-IR both in BALBCrds or BALBC mice. P2X(7)-IR failed to co-localize with any of the non-neuronal markers used to stain microglial or Müller glial cells. No P2X(7) receptor-IR was found in the retinal ganglion cell layer of P2X(7)(-/-) animals, when compared with the control littermates. Hence, we suggest that, in BALBCrds mice, an early up-regulation of neuronal P2X(7) receptors may cause injury of retinal neurons and thereby functionally contribute to the retinal damage.</description><identifier>ISSN: 0197-0186</identifier><identifier>DOI: 10.1016/j.neuint.2005.04.022</identifier><identifier>PMID: 15964665</identifier><language>eng</language><publisher>England</publisher><subject>Aging - metabolism ; Animals ; Biomarkers - metabolism ; Disease Models, Animal ; Down-Regulation - physiology ; Female ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Neurologic Mutants ; Microtubule-Associated Proteins - metabolism ; Nerve Degeneration - genetics ; Nerve Degeneration - metabolism ; Nerve Degeneration - physiopathology ; Nerve Tissue Proteins - metabolism ; Neuroglia - metabolism ; Neuroglia - pathology ; Nuclear Proteins - metabolism ; Receptors, Purinergic P2 - genetics ; Receptors, Purinergic P2 - metabolism ; Receptors, Purinergic P2X7 ; Retina - metabolism ; Retina - pathology ; Retina - physiopathology ; Retinal Degeneration - genetics ; Retinal Degeneration - metabolism ; Retinal Degeneration - physiopathology ; Retinal Ganglion Cells - metabolism ; Retinal Ganglion Cells - pathology ; RNA, Messenger - metabolism ; Up-Regulation - physiology</subject><ispartof>Neurochemistry international, 2005-09, Vol.47 (4), p.235-242</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15964665$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Franke, Heike</creatorcontrib><creatorcontrib>Klimke, Kerstin</creatorcontrib><creatorcontrib>Brinckmann, Ute</creatorcontrib><creatorcontrib>Grosche, Jens</creatorcontrib><creatorcontrib>Francke, Mike</creatorcontrib><creatorcontrib>Sperlagh, Beata</creatorcontrib><creatorcontrib>Reichenbach, Andreas</creatorcontrib><creatorcontrib>Liebert, Uwe Gerd</creatorcontrib><creatorcontrib>Illes, Peter</creatorcontrib><title>P2X(7) receptor-mRNA and -protein in the mouse retina; changes during retinal degeneration in BALBCrds mice</title><title>Neurochemistry international</title><addtitle>Neurochem Int</addtitle><description>A combined real-time PCR/immunohistochemistry study was carried out to investigate whether P2X(7) receptors, known to induce apoptosis and necrosis, may be causally related to the process of retinal degeneration in BALBCrds mice. In the retinae of BALBCrds mice, P2X(7) receptor-mRNA was the highest at an age of 20-40 days, and declined afterwards. At the same time, the P2X(7) receptor-message was constantly low in the retina of control BALBC mice until postnatal day 100. The receptor-mRNA in total brain tissue of both strains of mice was comparable with that of BALBCrds retinae. Double immunofluorescence in combination with laser scanning microscopy was used to study the distribution of P2X(7) receptor-immunoreactivity (IR) on neurons and different glial cell types of the retina. An exclusively neuronal localization of P2X(7)-IR in the ganglion cell layer was found by using either anti-neuronal nuclei or microtubule associated protein-2 as neuronal markers. There was a slight age-dependent decrease in the abundance of neuronal P2X(7)-IR both in BALBCrds or BALBC mice. P2X(7)-IR failed to co-localize with any of the non-neuronal markers used to stain microglial or Müller glial cells. No P2X(7) receptor-IR was found in the retinal ganglion cell layer of P2X(7)(-/-) animals, when compared with the control littermates. Hence, we suggest that, in BALBCrds mice, an early up-regulation of neuronal P2X(7) receptors may cause injury of retinal neurons and thereby functionally contribute to the retinal damage.</description><subject>Aging - metabolism</subject><subject>Animals</subject><subject>Biomarkers - metabolism</subject><subject>Disease Models, Animal</subject><subject>Down-Regulation - physiology</subject><subject>Female</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Neurologic Mutants</subject><subject>Microtubule-Associated Proteins - metabolism</subject><subject>Nerve Degeneration - genetics</subject><subject>Nerve Degeneration - metabolism</subject><subject>Nerve Degeneration - physiopathology</subject><subject>Nerve Tissue Proteins - metabolism</subject><subject>Neuroglia - metabolism</subject><subject>Neuroglia - pathology</subject><subject>Nuclear Proteins - metabolism</subject><subject>Receptors, Purinergic P2 - genetics</subject><subject>Receptors, Purinergic P2 - metabolism</subject><subject>Receptors, Purinergic P2X7</subject><subject>Retina - metabolism</subject><subject>Retina - pathology</subject><subject>Retina - physiopathology</subject><subject>Retinal Degeneration - genetics</subject><subject>Retinal Degeneration - metabolism</subject><subject>Retinal Degeneration - physiopathology</subject><subject>Retinal Ganglion Cells - metabolism</subject><subject>Retinal Ganglion Cells - pathology</subject><subject>RNA, Messenger - metabolism</subject><subject>Up-Regulation - physiology</subject><issn>0197-0186</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1kE9LxDAQxXNQ3HX1G4jkJHponaRp0uJpd_EfLCqi4K2kzXS3a5uuSXrw21t05Q0MPH4z8B4hZwxiBkxeb2OLQ2NDzAHSGEQMnB-QKbBcRcAyOSHH3m8BQOWQHpEJS3MppEyn5POFf1yqK-qwwl3oXdS9Ps2ptoZGO9cHbCwdJ2yQdv3gceRCY_UNrTbartFTM7jGrvd2Sw2u0aLToel_Dxfz1WLpjKddU-EJOax16_F0v2fk_e72bfkQrZ7vH5fzVbRjSR6iRECtM6UYpjrLNahUKxQllrkWnBvFKiilSpOEC-R1UgtmDMMK6kTzUTKZkYu_v2OCrwF9KLrGV9i22uIYopAZcJblYgTP9-BQdmiKnWs67b6L_3qSH4_2ZqQ</recordid><startdate>200509</startdate><enddate>200509</enddate><creator>Franke, Heike</creator><creator>Klimke, Kerstin</creator><creator>Brinckmann, Ute</creator><creator>Grosche, Jens</creator><creator>Francke, Mike</creator><creator>Sperlagh, Beata</creator><creator>Reichenbach, Andreas</creator><creator>Liebert, Uwe Gerd</creator><creator>Illes, Peter</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>200509</creationdate><title>P2X(7) receptor-mRNA and -protein in the mouse retina; changes during retinal degeneration in BALBCrds mice</title><author>Franke, Heike ; Klimke, Kerstin ; Brinckmann, Ute ; Grosche, Jens ; Francke, Mike ; Sperlagh, Beata ; Reichenbach, Andreas ; Liebert, Uwe Gerd ; Illes, Peter</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p139t-340fa8771e5a89a075a7e4beb9a422d71c0b6753324e2f3f41dd1ec0f3a2a2a63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Aging - metabolism</topic><topic>Animals</topic><topic>Biomarkers - metabolism</topic><topic>Disease Models, Animal</topic><topic>Down-Regulation - physiology</topic><topic>Female</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Neurologic Mutants</topic><topic>Microtubule-Associated Proteins - metabolism</topic><topic>Nerve Degeneration - genetics</topic><topic>Nerve Degeneration - metabolism</topic><topic>Nerve Degeneration - physiopathology</topic><topic>Nerve Tissue Proteins - metabolism</topic><topic>Neuroglia - metabolism</topic><topic>Neuroglia - pathology</topic><topic>Nuclear Proteins - metabolism</topic><topic>Receptors, Purinergic P2 - genetics</topic><topic>Receptors, Purinergic P2 - metabolism</topic><topic>Receptors, Purinergic P2X7</topic><topic>Retina - metabolism</topic><topic>Retina - pathology</topic><topic>Retina - physiopathology</topic><topic>Retinal Degeneration - genetics</topic><topic>Retinal Degeneration - metabolism</topic><topic>Retinal Degeneration - physiopathology</topic><topic>Retinal Ganglion Cells - metabolism</topic><topic>Retinal Ganglion Cells - pathology</topic><topic>RNA, Messenger - metabolism</topic><topic>Up-Regulation - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Franke, Heike</creatorcontrib><creatorcontrib>Klimke, Kerstin</creatorcontrib><creatorcontrib>Brinckmann, Ute</creatorcontrib><creatorcontrib>Grosche, Jens</creatorcontrib><creatorcontrib>Francke, Mike</creatorcontrib><creatorcontrib>Sperlagh, Beata</creatorcontrib><creatorcontrib>Reichenbach, Andreas</creatorcontrib><creatorcontrib>Liebert, Uwe Gerd</creatorcontrib><creatorcontrib>Illes, Peter</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Neurochemistry international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Franke, Heike</au><au>Klimke, Kerstin</au><au>Brinckmann, Ute</au><au>Grosche, Jens</au><au>Francke, Mike</au><au>Sperlagh, Beata</au><au>Reichenbach, Andreas</au><au>Liebert, Uwe Gerd</au><au>Illes, Peter</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>P2X(7) receptor-mRNA and -protein in the mouse retina; changes during retinal degeneration in BALBCrds mice</atitle><jtitle>Neurochemistry international</jtitle><addtitle>Neurochem Int</addtitle><date>2005-09</date><risdate>2005</risdate><volume>47</volume><issue>4</issue><spage>235</spage><epage>242</epage><pages>235-242</pages><issn>0197-0186</issn><abstract>A combined real-time PCR/immunohistochemistry study was carried out to investigate whether P2X(7) receptors, known to induce apoptosis and necrosis, may be causally related to the process of retinal degeneration in BALBCrds mice. In the retinae of BALBCrds mice, P2X(7) receptor-mRNA was the highest at an age of 20-40 days, and declined afterwards. At the same time, the P2X(7) receptor-message was constantly low in the retina of control BALBC mice until postnatal day 100. The receptor-mRNA in total brain tissue of both strains of mice was comparable with that of BALBCrds retinae. Double immunofluorescence in combination with laser scanning microscopy was used to study the distribution of P2X(7) receptor-immunoreactivity (IR) on neurons and different glial cell types of the retina. An exclusively neuronal localization of P2X(7)-IR in the ganglion cell layer was found by using either anti-neuronal nuclei or microtubule associated protein-2 as neuronal markers. There was a slight age-dependent decrease in the abundance of neuronal P2X(7)-IR both in BALBCrds or BALBC mice. P2X(7)-IR failed to co-localize with any of the non-neuronal markers used to stain microglial or Müller glial cells. No P2X(7) receptor-IR was found in the retinal ganglion cell layer of P2X(7)(-/-) animals, when compared with the control littermates. Hence, we suggest that, in BALBCrds mice, an early up-regulation of neuronal P2X(7) receptors may cause injury of retinal neurons and thereby functionally contribute to the retinal damage.</abstract><cop>England</cop><pmid>15964665</pmid><doi>10.1016/j.neuint.2005.04.022</doi><tpages>8</tpages></addata></record> |
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subjects | Aging - metabolism Animals Biomarkers - metabolism Disease Models, Animal Down-Regulation - physiology Female Male Mice Mice, Inbred BALB C Mice, Neurologic Mutants Microtubule-Associated Proteins - metabolism Nerve Degeneration - genetics Nerve Degeneration - metabolism Nerve Degeneration - physiopathology Nerve Tissue Proteins - metabolism Neuroglia - metabolism Neuroglia - pathology Nuclear Proteins - metabolism Receptors, Purinergic P2 - genetics Receptors, Purinergic P2 - metabolism Receptors, Purinergic P2X7 Retina - metabolism Retina - pathology Retina - physiopathology Retinal Degeneration - genetics Retinal Degeneration - metabolism Retinal Degeneration - physiopathology Retinal Ganglion Cells - metabolism Retinal Ganglion Cells - pathology RNA, Messenger - metabolism Up-Regulation - physiology |
title | P2X(7) receptor-mRNA and -protein in the mouse retina; changes during retinal degeneration in BALBCrds mice |
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