Galectin-3/MAC-2 in Experimental Allergic Encephalomyelitis
The removal of degenerating myelin by phagocytosis is central to pathogenesis and repair in traumatized and diseased nervous system. Galectin-3/MAC-2 is a differentiation and activation marker of murine and human monocytes/macrophages/microglia. Galectin-3/MAC-2, along with MAC-1 that mediates myeli...
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| Veröffentlicht in: | Experimental neurology 1999-12, Vol.160 (2), p.508-514 |
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| description | The removal of degenerating myelin by phagocytosis is central to pathogenesis and repair in traumatized and diseased nervous system. Galectin-3/MAC-2 is a differentiation and activation marker of murine and human monocytes/macrophages/microglia. Galectin-3/MAC-2, along with MAC-1 that mediates myelin phagocytosis, marks an in vivo activation state in macrophages, which are involved in myelin degeneration and phagocytosis in injured mouse peripheral nerves. In contrast, high levels of MAC-1 but extremely low levels of Galectin-3/MAC-2 are expressed in vivo in injured CNS where myelin degeneration and phagocytosis progress extremely slowly. The present study was aimed at testing whether an activation state marked by Galectin-3/MAC-2 is present in vivo in the CNS of EAE mice concomitant with autoimmune induced myelin degeneration and phagocytosis. EAE was inflicted by mouse spinal cord homogenate. Demyelination was assessed by light microscopy and Galectin-3/MAC-2, MAC-1, and F4/80 expression by immunocytochemistry. We presently document that Galectin-3/MAC-2 expression is up regulated, along with MAC-1 and F4/80, in spinal cords and optic nerves of EAE mice in areas of demyelination and myelin degeneration, in myelin phagocytosing microglia and macrophages. Copolymer 1 (Glatiramer acetate) suppresses EAE, demyelination, and Galectin-3/MAC-2 expression. EAE pathogenesis thus involves a state of activation in microglia and macrophages characterized by the expression Galectin-3/MAC-2 along with MAC-1. Furthermore, the in vivo responses to injury and autoimmune challenge in the CNS differ in the activation pattern of microglia and macrophages with regard to Galectin-3/MAC-2 expression and the corresponding occurrence of myelin degeneration and phagocytosis. |
| doi_str_mv | 10.1006/exnr.1999.7229 |
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Galectin-3/MAC-2 is a differentiation and activation marker of murine and human monocytes/macrophages/microglia. Galectin-3/MAC-2, along with MAC-1 that mediates myelin phagocytosis, marks an in vivo activation state in macrophages, which are involved in myelin degeneration and phagocytosis in injured mouse peripheral nerves. In contrast, high levels of MAC-1 but extremely low levels of Galectin-3/MAC-2 are expressed in vivo in injured CNS where myelin degeneration and phagocytosis progress extremely slowly. The present study was aimed at testing whether an activation state marked by Galectin-3/MAC-2 is present in vivo in the CNS of EAE mice concomitant with autoimmune induced myelin degeneration and phagocytosis. EAE was inflicted by mouse spinal cord homogenate. Demyelination was assessed by light microscopy and Galectin-3/MAC-2, MAC-1, and F4/80 expression by immunocytochemistry. We presently document that Galectin-3/MAC-2 expression is up regulated, along with MAC-1 and F4/80, in spinal cords and optic nerves of EAE mice in areas of demyelination and myelin degeneration, in myelin phagocytosing microglia and macrophages. Copolymer 1 (Glatiramer acetate) suppresses EAE, demyelination, and Galectin-3/MAC-2 expression. EAE pathogenesis thus involves a state of activation in microglia and macrophages characterized by the expression Galectin-3/MAC-2 along with MAC-1. Furthermore, the in vivo responses to injury and autoimmune challenge in the CNS differ in the activation pattern of microglia and macrophages with regard to Galectin-3/MAC-2 expression and the corresponding occurrence of myelin degeneration and phagocytosis.</description><identifier>ISSN: 0014-4886</identifier><identifier>EISSN: 1090-2430</identifier><identifier>DOI: 10.1006/exnr.1999.7229</identifier><identifier>PMID: 10619568</identifier><identifier>CODEN: EXNEAC</identifier><language>eng</language><publisher>Amsterdam: Elsevier Inc</publisher><subject>Animals ; Antigens, Differentiation - analysis ; Antigens, Differentiation - metabolism ; Biological and medical sciences ; CR3 ; Crosses, Genetic ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; EAE ; Encephalomyelitis, Autoimmune, Experimental - metabolism ; Encephalomyelitis, Autoimmune, Experimental - pathology ; Female ; Galectin 3 ; Galectin-3/MAC-2 ; Glatiramer acetate/copolymer 1 ; Humans ; Immunohistochemistry ; MAC-1 ; Macrophage-1 Antigen - metabolism ; macrophage/microglia ; Macrophages - metabolism ; Macrophages - pathology ; Male ; Medical sciences ; Membrane Glycoproteins - metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred Strains ; multiple sclerosis ; Myelin Sheath - pathology ; Nerve Degeneration ; Neurology ; Optic Nerve - metabolism ; Optic Nerve - pathology ; Phagocytosis ; Spinal Cord - immunology ; Spinal Cord - metabolism ; Spinal Cord - pathology</subject><ispartof>Experimental neurology, 1999-12, Vol.160 (2), p.508-514</ispartof><rights>1999 Academic Press</rights><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c369t-81fbf411bfed222cd2b32fce6db61cb466d07d9a846bb7ac8bc4f1338ed59bb3</citedby><cites>FETCH-LOGICAL-c369t-81fbf411bfed222cd2b32fce6db61cb466d07d9a846bb7ac8bc4f1338ed59bb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0014488699972291$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1254849$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10619568$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Reichert, Fanny</creatorcontrib><creatorcontrib>Rotshenker, Shlomo</creatorcontrib><title>Galectin-3/MAC-2 in Experimental Allergic Encephalomyelitis</title><title>Experimental neurology</title><addtitle>Exp Neurol</addtitle><description>The removal of degenerating myelin by phagocytosis is central to pathogenesis and repair in traumatized and diseased nervous system. Galectin-3/MAC-2 is a differentiation and activation marker of murine and human monocytes/macrophages/microglia. Galectin-3/MAC-2, along with MAC-1 that mediates myelin phagocytosis, marks an in vivo activation state in macrophages, which are involved in myelin degeneration and phagocytosis in injured mouse peripheral nerves. In contrast, high levels of MAC-1 but extremely low levels of Galectin-3/MAC-2 are expressed in vivo in injured CNS where myelin degeneration and phagocytosis progress extremely slowly. The present study was aimed at testing whether an activation state marked by Galectin-3/MAC-2 is present in vivo in the CNS of EAE mice concomitant with autoimmune induced myelin degeneration and phagocytosis. EAE was inflicted by mouse spinal cord homogenate. Demyelination was assessed by light microscopy and Galectin-3/MAC-2, MAC-1, and F4/80 expression by immunocytochemistry. We presently document that Galectin-3/MAC-2 expression is up regulated, along with MAC-1 and F4/80, in spinal cords and optic nerves of EAE mice in areas of demyelination and myelin degeneration, in myelin phagocytosing microglia and macrophages. Copolymer 1 (Glatiramer acetate) suppresses EAE, demyelination, and Galectin-3/MAC-2 expression. EAE pathogenesis thus involves a state of activation in microglia and macrophages characterized by the expression Galectin-3/MAC-2 along with MAC-1. Furthermore, the in vivo responses to injury and autoimmune challenge in the CNS differ in the activation pattern of microglia and macrophages with regard to Galectin-3/MAC-2 expression and the corresponding occurrence of myelin degeneration and phagocytosis.</description><subject>Animals</subject><subject>Antigens, Differentiation - analysis</subject><subject>Antigens, Differentiation - metabolism</subject><subject>Biological and medical sciences</subject><subject>CR3</subject><subject>Crosses, Genetic</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>EAE</subject><subject>Encephalomyelitis, Autoimmune, Experimental - metabolism</subject><subject>Encephalomyelitis, Autoimmune, Experimental - pathology</subject><subject>Female</subject><subject>Galectin 3</subject><subject>Galectin-3/MAC-2</subject><subject>Glatiramer acetate/copolymer 1</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>MAC-1</subject><subject>Macrophage-1 Antigen - metabolism</subject><subject>macrophage/microglia</subject><subject>Macrophages - metabolism</subject><subject>Macrophages - pathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Inbred Strains</subject><subject>multiple sclerosis</subject><subject>Myelin Sheath - pathology</subject><subject>Nerve Degeneration</subject><subject>Neurology</subject><subject>Optic Nerve - metabolism</subject><subject>Optic Nerve - pathology</subject><subject>Phagocytosis</subject><subject>Spinal Cord - immunology</subject><subject>Spinal Cord - metabolism</subject><subject>Spinal Cord - pathology</subject><issn>0014-4886</issn><issn>1090-2430</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kD1PwzAURS0EoqWwMqIOiC2t7biOLaaqKgWpiKW75Y8XMHKTYKeo_fckaiVYmN5y3tW9B6FbgicEYz6FfRUnREo5KSiVZ2hIsMQZZTk-R0OMCcuYEHyArlL6xBhLRotLNCCYEznjYogeVzqAbX2V5dPX-SKjY1-Nl_sGot9C1eownocA8d3b8bKy0HzoUG8PEHzr0zW6KHVIcHO6I7R5Wm4Wz9n6bfWymK8zm3PZZoKUpmSEmBIcpdQ6anJaWuDOcGIN49zhwkktGDem0FYYy0qS5wLcTBqTj9DDMbaJ9dcOUqu2PlkIQVdQ75LiMhfdyFkHTo6gjXVKEUrVdCt0PCiCVW9L9bZUb0v1trqHu1PyzmzB_cGPejrg_gToZHUoo66sT78cnTHB-hxxxKCz8O0hqmQ9dLqcj51c5Wr_X4Uf7euGAQ</recordid><startdate>19991201</startdate><enddate>19991201</enddate><creator>Reichert, Fanny</creator><creator>Rotshenker, Shlomo</creator><general>Elsevier Inc</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>19991201</creationdate><title>Galectin-3/MAC-2 in Experimental Allergic Encephalomyelitis</title><author>Reichert, Fanny ; Rotshenker, Shlomo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c369t-81fbf411bfed222cd2b32fce6db61cb466d07d9a846bb7ac8bc4f1338ed59bb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Antigens, Differentiation - analysis</topic><topic>Antigens, Differentiation - metabolism</topic><topic>Biological and medical sciences</topic><topic>CR3</topic><topic>Crosses, Genetic</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>EAE</topic><topic>Encephalomyelitis, Autoimmune, Experimental - metabolism</topic><topic>Encephalomyelitis, Autoimmune, Experimental - pathology</topic><topic>Female</topic><topic>Galectin 3</topic><topic>Galectin-3/MAC-2</topic><topic>Glatiramer acetate/copolymer 1</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>MAC-1</topic><topic>Macrophage-1 Antigen - metabolism</topic><topic>macrophage/microglia</topic><topic>Macrophages - metabolism</topic><topic>Macrophages - pathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Glycoproteins - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Inbred Strains</topic><topic>multiple sclerosis</topic><topic>Myelin Sheath - pathology</topic><topic>Nerve Degeneration</topic><topic>Neurology</topic><topic>Optic Nerve - metabolism</topic><topic>Optic Nerve - pathology</topic><topic>Phagocytosis</topic><topic>Spinal Cord - immunology</topic><topic>Spinal Cord - metabolism</topic><topic>Spinal Cord - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Reichert, Fanny</creatorcontrib><creatorcontrib>Rotshenker, Shlomo</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>Experimental neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Reichert, Fanny</au><au>Rotshenker, Shlomo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Galectin-3/MAC-2 in Experimental Allergic Encephalomyelitis</atitle><jtitle>Experimental neurology</jtitle><addtitle>Exp Neurol</addtitle><date>1999-12-01</date><risdate>1999</risdate><volume>160</volume><issue>2</issue><spage>508</spage><epage>514</epage><pages>508-514</pages><issn>0014-4886</issn><eissn>1090-2430</eissn><coden>EXNEAC</coden><abstract>The removal of degenerating myelin by phagocytosis is central to pathogenesis and repair in traumatized and diseased nervous system. Galectin-3/MAC-2 is a differentiation and activation marker of murine and human monocytes/macrophages/microglia. Galectin-3/MAC-2, along with MAC-1 that mediates myelin phagocytosis, marks an in vivo activation state in macrophages, which are involved in myelin degeneration and phagocytosis in injured mouse peripheral nerves. In contrast, high levels of MAC-1 but extremely low levels of Galectin-3/MAC-2 are expressed in vivo in injured CNS where myelin degeneration and phagocytosis progress extremely slowly. The present study was aimed at testing whether an activation state marked by Galectin-3/MAC-2 is present in vivo in the CNS of EAE mice concomitant with autoimmune induced myelin degeneration and phagocytosis. EAE was inflicted by mouse spinal cord homogenate. Demyelination was assessed by light microscopy and Galectin-3/MAC-2, MAC-1, and F4/80 expression by immunocytochemistry. We presently document that Galectin-3/MAC-2 expression is up regulated, along with MAC-1 and F4/80, in spinal cords and optic nerves of EAE mice in areas of demyelination and myelin degeneration, in myelin phagocytosing microglia and macrophages. Copolymer 1 (Glatiramer acetate) suppresses EAE, demyelination, and Galectin-3/MAC-2 expression. EAE pathogenesis thus involves a state of activation in microglia and macrophages characterized by the expression Galectin-3/MAC-2 along with MAC-1. Furthermore, the in vivo responses to injury and autoimmune challenge in the CNS differ in the activation pattern of microglia and macrophages with regard to Galectin-3/MAC-2 expression and the corresponding occurrence of myelin degeneration and phagocytosis.</abstract><cop>Amsterdam</cop><pub>Elsevier Inc</pub><pmid>10619568</pmid><doi>10.1006/exnr.1999.7229</doi><tpages>7</tpages></addata></record> |
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| subjects | Animals Antigens, Differentiation - analysis Antigens, Differentiation - metabolism Biological and medical sciences CR3 Crosses, Genetic Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases EAE Encephalomyelitis, Autoimmune, Experimental - metabolism Encephalomyelitis, Autoimmune, Experimental - pathology Female Galectin 3 Galectin-3/MAC-2 Glatiramer acetate/copolymer 1 Humans Immunohistochemistry MAC-1 Macrophage-1 Antigen - metabolism macrophage/microglia Macrophages - metabolism Macrophages - pathology Male Medical sciences Membrane Glycoproteins - metabolism Mice Mice, Inbred BALB C Mice, Inbred Strains multiple sclerosis Myelin Sheath - pathology Nerve Degeneration Neurology Optic Nerve - metabolism Optic Nerve - pathology Phagocytosis Spinal Cord - immunology Spinal Cord - metabolism Spinal Cord - pathology |
| title | Galectin-3/MAC-2 in Experimental Allergic Encephalomyelitis |
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