Facial nerve lesion response; strain differences but no involvement of IFN-γ, STAT4 or STAT6
Facial nerve lesions lead to a retrograde response characterized by activation of glia surrounding axotomized motoneurons and up-regulation of immunological cell surface molecules such as major histocompatibility complex (MHC) antigens. Cytokines, in particular interferon-γ, are potent inducers of M...
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| Veröffentlicht in: | Neuroreport 2002-09, Vol.13 (13), p.1589-1593 |
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| creator | Lidman, Olle Fraidakis, Matt Lycke, Nils Olson, Lars Olsson, Tomas Piehl, Fredrik |
| description | Facial nerve lesions lead to a retrograde response characterized by activation of glia surrounding axotomized motoneurons and up-regulation of immunological cell surface molecules such as major histocompatibility complex (MHC) antigens. Cytokines, in particular interferon-γ, are potent inducers of MHC expression and glial activation. We have here tested whether axotomy-induced activation is changed in transgenic mouse strains lacking components of the IFN-γ signaling pathway, STAT4 or STAT6. No differences regarding astrocyte activation, ß2-microglobulin or MHC class I expression were discernible as compared to wild type controls. In contrast, there were conspicuous differences in the reaction between the examined wild type strains (C57BL/6J, BALB/c and 129/SvJ), suggesting considerable polymorphisms in the genetic regulation of these events, however, not involving IFN-γ, STAT4 or STAT6. |
| doi_str_mv | 10.1097/00001756-200209160-00003 |
| format | Article |
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Cytokines, in particular interferon-γ, are potent inducers of MHC expression and glial activation. We have here tested whether axotomy-induced activation is changed in transgenic mouse strains lacking components of the IFN-γ signaling pathway, STAT4 or STAT6. No differences regarding astrocyte activation, ß2-microglobulin or MHC class I expression were discernible as compared to wild type controls. In contrast, there were conspicuous differences in the reaction between the examined wild type strains (C57BL/6J, BALB/c and 129/SvJ), suggesting considerable polymorphisms in the genetic regulation of these events, however, not involving IFN-γ, STAT4 or STAT6.</description><identifier>ISSN: 0959-4965</identifier><identifier>EISSN: 1473-558X</identifier><identifier>DOI: 10.1097/00001756-200209160-00003</identifier><identifier>PMID: 12352607</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins, Inc</publisher><subject>Animals ; Axotomy ; beta 2-Microglobulin - genetics ; Biological and medical sciences ; Development. Senescence. Regeneration. Transplantation ; DNA-Binding Proteins - genetics ; DNA-Binding Proteins - immunology ; Facial Nerve Injuries - genetics ; Facial Nerve Injuries - immunology ; Female ; Fundamental and applied biological sciences. Psychology ; GAP-43 Protein - genetics ; Gene Expression Regulation - physiology ; Glial Fibrillary Acidic Protein - genetics ; Gliosis - genetics ; Gliosis - immunology ; Histocompatibility Antigens - genetics ; Histocompatibility Antigens - immunology ; Interferon Regulatory Factor-1 ; Interferon-gamma - genetics ; Interferon-gamma - immunology ; Male ; Mice ; Mice, Inbred Strains - genetics ; Mice, Inbred Strains - growth & development ; Mice, Knockout ; Motor Neurons - immunology ; Motor Neurons - metabolism ; Motor Neurons - pathology ; Neuroglia - immunology ; Neuroglia - metabolism ; Phosphoproteins - genetics ; Retrograde Degeneration - genetics ; Retrograde Degeneration - immunology ; RNA, Messenger - metabolism ; Signal Transduction - genetics ; Signal Transduction - immunology ; STAT4 Transcription Factor ; STAT6 Transcription Factor ; Trans-Activators - genetics ; Trans-Activators - immunology ; Up-Regulation - physiology ; Vertebrates: nervous system and sense organs</subject><ispartof>Neuroreport, 2002-09, Vol.13 (13), p.1589-1593</ispartof><rights>2002 Lippincott Williams & Wilkins, Inc.</rights><rights>2002 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4553-39f90b03aa511c122fe7160ff254ffb2804996ab3fe941ce11eb82a2596deadb3</citedby><cites>FETCH-LOGICAL-c4553-39f90b03aa511c122fe7160ff254ffb2804996ab3fe941ce11eb82a2596deadb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13962309$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12352607$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:1943260$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Lidman, Olle</creatorcontrib><creatorcontrib>Fraidakis, Matt</creatorcontrib><creatorcontrib>Lycke, Nils</creatorcontrib><creatorcontrib>Olson, Lars</creatorcontrib><creatorcontrib>Olsson, Tomas</creatorcontrib><creatorcontrib>Piehl, Fredrik</creatorcontrib><title>Facial nerve lesion response; strain differences but no involvement of IFN-γ, STAT4 or STAT6</title><title>Neuroreport</title><addtitle>Neuroreport</addtitle><description>Facial nerve lesions lead to a retrograde response characterized by activation of glia surrounding axotomized motoneurons and up-regulation of immunological cell surface molecules such as major histocompatibility complex (MHC) antigens. Cytokines, in particular interferon-γ, are potent inducers of MHC expression and glial activation. We have here tested whether axotomy-induced activation is changed in transgenic mouse strains lacking components of the IFN-γ signaling pathway, STAT4 or STAT6. No differences regarding astrocyte activation, ß2-microglobulin or MHC class I expression were discernible as compared to wild type controls. In contrast, there were conspicuous differences in the reaction between the examined wild type strains (C57BL/6J, BALB/c and 129/SvJ), suggesting considerable polymorphisms in the genetic regulation of these events, however, not involving IFN-γ, STAT4 or STAT6.</description><subject>Animals</subject><subject>Axotomy</subject><subject>beta 2-Microglobulin - genetics</subject><subject>Biological and medical sciences</subject><subject>Development. Senescence. Regeneration. Transplantation</subject><subject>DNA-Binding Proteins - genetics</subject><subject>DNA-Binding Proteins - immunology</subject><subject>Facial Nerve Injuries - genetics</subject><subject>Facial Nerve Injuries - immunology</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>GAP-43 Protein - genetics</subject><subject>Gene Expression Regulation - physiology</subject><subject>Glial Fibrillary Acidic Protein - genetics</subject><subject>Gliosis - genetics</subject><subject>Gliosis - immunology</subject><subject>Histocompatibility Antigens - genetics</subject><subject>Histocompatibility Antigens - immunology</subject><subject>Interferon Regulatory Factor-1</subject><subject>Interferon-gamma - genetics</subject><subject>Interferon-gamma - immunology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred Strains - genetics</subject><subject>Mice, Inbred Strains - growth & development</subject><subject>Mice, Knockout</subject><subject>Motor Neurons - immunology</subject><subject>Motor Neurons - metabolism</subject><subject>Motor Neurons - pathology</subject><subject>Neuroglia - immunology</subject><subject>Neuroglia - metabolism</subject><subject>Phosphoproteins - genetics</subject><subject>Retrograde Degeneration - genetics</subject><subject>Retrograde Degeneration - immunology</subject><subject>RNA, Messenger - metabolism</subject><subject>Signal Transduction - genetics</subject><subject>Signal Transduction - immunology</subject><subject>STAT4 Transcription Factor</subject><subject>STAT6 Transcription Factor</subject><subject>Trans-Activators - genetics</subject><subject>Trans-Activators - immunology</subject><subject>Up-Regulation - physiology</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0959-4965</issn><issn>1473-558X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFks1uEzEUhS0EoqHwCsgbWDHg_7HFqqpIqVTBgiCxQZZncq2aOnawZxLxXLxHn4lJM7QrxN346ui718c6RghT8pYS074jU9FWqoYRwoihijQHiT9CCypa3kipvz1GC2KkaYRR8gQ9q_XHRBhC9VN0QhmXTJF2gb4vXR9cxAnKDnCEGnLCBeo2pwrvcR2KCwmvg_dQIPVQcTcOOGUc0i7HHWwgDTh7fLn81Nz-foO_rM5WAudy16jn6Il3scKL-TxFX5cfVucfm6vPF5fnZ1dNL6TkDTfekI5w5ySlPWXMQzu9yXsmhfcd00QYo1zHPRhBe6AUOs0ck0atwa07foqa4966h-3Y2W0JG1d-2eyCnaWbqQMrDRNKT_zrI78t-ecIdbCbUHuI0SXIY7Uto0xJY_4LUq20VvwA6iPYl1xrAX_vgRJ7yMz-zczeZ3Yn8Wn05XzH2G1g_TA4hzQBr2bA1d5FX1zqQ33guFGMk4MHceT2OQ5Q6k0c91DsNbg4XNt__Rn-B9v6rc0</recordid><startdate>20020916</startdate><enddate>20020916</enddate><creator>Lidman, Olle</creator><creator>Fraidakis, Matt</creator><creator>Lycke, Nils</creator><creator>Olson, Lars</creator><creator>Olsson, Tomas</creator><creator>Piehl, Fredrik</creator><general>Lippincott Williams & Wilkins, Inc</general><general>Lippincott Williams and Wilkins</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>7TK</scope><scope>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope></search><sort><creationdate>20020916</creationdate><title>Facial nerve lesion response; strain differences but no involvement of IFN-γ, STAT4 or STAT6</title><author>Lidman, Olle ; Fraidakis, Matt ; Lycke, Nils ; Olson, Lars ; Olsson, Tomas ; Piehl, Fredrik</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4553-39f90b03aa511c122fe7160ff254ffb2804996ab3fe941ce11eb82a2596deadb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Axotomy</topic><topic>beta 2-Microglobulin - genetics</topic><topic>Biological and medical sciences</topic><topic>Development. Senescence. Regeneration. Transplantation</topic><topic>DNA-Binding Proteins - genetics</topic><topic>DNA-Binding Proteins - immunology</topic><topic>Facial Nerve Injuries - genetics</topic><topic>Facial Nerve Injuries - immunology</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>GAP-43 Protein - genetics</topic><topic>Gene Expression Regulation - physiology</topic><topic>Glial Fibrillary Acidic Protein - genetics</topic><topic>Gliosis - genetics</topic><topic>Gliosis - immunology</topic><topic>Histocompatibility Antigens - genetics</topic><topic>Histocompatibility Antigens - immunology</topic><topic>Interferon Regulatory Factor-1</topic><topic>Interferon-gamma - genetics</topic><topic>Interferon-gamma - immunology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred Strains - genetics</topic><topic>Mice, Inbred Strains - growth & development</topic><topic>Mice, Knockout</topic><topic>Motor Neurons - immunology</topic><topic>Motor Neurons - metabolism</topic><topic>Motor Neurons - pathology</topic><topic>Neuroglia - immunology</topic><topic>Neuroglia - metabolism</topic><topic>Phosphoproteins - genetics</topic><topic>Retrograde Degeneration - genetics</topic><topic>Retrograde Degeneration - immunology</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal Transduction - genetics</topic><topic>Signal Transduction - immunology</topic><topic>STAT4 Transcription Factor</topic><topic>STAT6 Transcription Factor</topic><topic>Trans-Activators - genetics</topic><topic>Trans-Activators - immunology</topic><topic>Up-Regulation - physiology</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lidman, Olle</creatorcontrib><creatorcontrib>Fraidakis, Matt</creatorcontrib><creatorcontrib>Lycke, Nils</creatorcontrib><creatorcontrib>Olson, Lars</creatorcontrib><creatorcontrib>Olsson, Tomas</creatorcontrib><creatorcontrib>Piehl, Fredrik</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>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><collection>SwePub</collection><collection>SwePub Articles</collection><jtitle>Neuroreport</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lidman, Olle</au><au>Fraidakis, Matt</au><au>Lycke, Nils</au><au>Olson, Lars</au><au>Olsson, Tomas</au><au>Piehl, Fredrik</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Facial nerve lesion response; strain differences but no involvement of IFN-γ, STAT4 or STAT6</atitle><jtitle>Neuroreport</jtitle><addtitle>Neuroreport</addtitle><date>2002-09-16</date><risdate>2002</risdate><volume>13</volume><issue>13</issue><spage>1589</spage><epage>1593</epage><pages>1589-1593</pages><issn>0959-4965</issn><eissn>1473-558X</eissn><abstract>Facial nerve lesions lead to a retrograde response characterized by activation of glia surrounding axotomized motoneurons and up-regulation of immunological cell surface molecules such as major histocompatibility complex (MHC) antigens. Cytokines, in particular interferon-γ, are potent inducers of MHC expression and glial activation. We have here tested whether axotomy-induced activation is changed in transgenic mouse strains lacking components of the IFN-γ signaling pathway, STAT4 or STAT6. No differences regarding astrocyte activation, ß2-microglobulin or MHC class I expression were discernible as compared to wild type controls. In contrast, there were conspicuous differences in the reaction between the examined wild type strains (C57BL/6J, BALB/c and 129/SvJ), suggesting considerable polymorphisms in the genetic regulation of these events, however, not involving IFN-γ, STAT4 or STAT6.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins, Inc</pub><pmid>12352607</pmid><doi>10.1097/00001756-200209160-00003</doi><tpages>5</tpages></addata></record> |
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| subjects | Animals Axotomy beta 2-Microglobulin - genetics Biological and medical sciences Development. Senescence. Regeneration. Transplantation DNA-Binding Proteins - genetics DNA-Binding Proteins - immunology Facial Nerve Injuries - genetics Facial Nerve Injuries - immunology Female Fundamental and applied biological sciences. Psychology GAP-43 Protein - genetics Gene Expression Regulation - physiology Glial Fibrillary Acidic Protein - genetics Gliosis - genetics Gliosis - immunology Histocompatibility Antigens - genetics Histocompatibility Antigens - immunology Interferon Regulatory Factor-1 Interferon-gamma - genetics Interferon-gamma - immunology Male Mice Mice, Inbred Strains - genetics Mice, Inbred Strains - growth & development Mice, Knockout Motor Neurons - immunology Motor Neurons - metabolism Motor Neurons - pathology Neuroglia - immunology Neuroglia - metabolism Phosphoproteins - genetics Retrograde Degeneration - genetics Retrograde Degeneration - immunology RNA, Messenger - metabolism Signal Transduction - genetics Signal Transduction - immunology STAT4 Transcription Factor STAT6 Transcription Factor Trans-Activators - genetics Trans-Activators - immunology Up-Regulation - physiology Vertebrates: nervous system and sense organs |
| title | Facial nerve lesion response; strain differences but no involvement of IFN-γ, STAT4 or STAT6 |
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