Mechanism of myelin breakdown in experimental demyelination : A putative role for calpain
Although calpain has been extensively studied, its physiological function is poorly understood. In contrast, its role in the pathophysiology of various diseases has been implicated, including that of experimental allergic encephalomyelitis (EAE), an animal model of the demyelinating disease multiple...
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| Veröffentlicht in: | Neurochemical research 2001-06, Vol.26 (6), p.731-737 |
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| creator | SCHAECHER, K. E SHIELDS, D. C BANIK, N. L |
| description | Although calpain has been extensively studied, its physiological function is poorly understood. In contrast, its role in the pathophysiology of various diseases has been implicated, including that of experimental allergic encephalomyelitis (EAE), an animal model of the demyelinating disease multiple sclerosis (MS). In EAE, calpain degrades myelin proteins, including myelin basic protein (MBP), suggesting a role for calpain in the breakdown of myelin in this disease. Subsequent studies revealed increased calpain activity and expression in the glial and inflammatory cells concomitant with loss of axon and myelin proteins. This suggested a crucial role for calpain in demyelinating diseases. |
| doi_str_mv | 10.1023/A:1010903823668 |
| format | Article |
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This suggested a crucial role for calpain in demyelinating diseases.</description><identifier>ISSN: 0364-3190</identifier><identifier>EISSN: 1573-6903</identifier><identifier>DOI: 10.1023/A:1010903823668</identifier><identifier>PMID: 11519732</identifier><identifier>CODEN: NEREDZ</identifier><language>eng</language><publisher>New York, NY: Springer</publisher><subject>Animals ; Biological and medical sciences ; Calpain - metabolism ; Demyelinating Diseases - metabolism ; Encephalomyelitis, Autoimmune, Experimental - metabolism ; Humans ; Immunohistochemistry ; Medical sciences ; Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. 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E</creatorcontrib><creatorcontrib>SHIELDS, D. C</creatorcontrib><creatorcontrib>BANIK, N. L</creatorcontrib><title>Mechanism of myelin breakdown in experimental demyelination : A putative role for calpain</title><title>Neurochemical research</title><addtitle>Neurochem Res</addtitle><description>Although calpain has been extensively studied, its physiological function is poorly understood. In contrast, its role in the pathophysiology of various diseases has been implicated, including that of experimental allergic encephalomyelitis (EAE), an animal model of the demyelinating disease multiple sclerosis (MS). In EAE, calpain degrades myelin proteins, including myelin basic protein (MBP), suggesting a role for calpain in the breakdown of myelin in this disease. Subsequent studies revealed increased calpain activity and expression in the glial and inflammatory cells concomitant with loss of axon and myelin proteins. This suggested a crucial role for calpain in demyelinating diseases.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Calpain - metabolism</subject><subject>Demyelinating Diseases - metabolism</subject><subject>Encephalomyelitis, Autoimmune, Experimental - metabolism</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Medical sciences</subject><subject>Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis</subject><subject>Myelin Sheath - metabolism</subject><subject>Neurology</subject><subject>Tissue Distribution</subject><issn>0364-3190</issn><issn>1573-6903</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqF0MtLxDAQBvAgirs-zt4kiHirziRtmu5tEV-w4kEvnkqaTrHaprVpffz3BlwRvHgavuHHwHyMHSCcIgh5tlwgIGQgtZBK6Q02xySVkQqbTTYHqeJIYgYztuP9MwQKArfZDDHBLJVizh5vyT4ZV_uWdxVvP6mpHS8GMi9l9-54CPTR01C35EbT8JK-iRnrzvEFX_J-GkN4Iz50DfGqG7g1TW9qt8e2KtN42l_PXXZ_efFwfh2t7q5uzperyMoYxghlTFTopChQ6bjMhJYlaaWEhiKBzBalAZRElCYCrCBdGolglUYbCpC77OT7aj90rxP5MW9rb6lpjKNu8nmKKACy5F-IGtM02ACP_sDnbhpceCEXAtNEikwFdLhGU9FSmfehITN85j_FBnC8BsaHQqrBOFv7XwdpnAX2BbvthZw</recordid><startdate>20010601</startdate><enddate>20010601</enddate><creator>SCHAECHER, K. E</creator><creator>SHIELDS, D. C</creator><creator>BANIK, N. 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E ; SHIELDS, D. C ; BANIK, N. L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c340t-134eeb85bb1684d9283de866280b509cbda013eee7520c2e8da310c681c0233</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Calpain - metabolism</topic><topic>Demyelinating Diseases - metabolism</topic><topic>Encephalomyelitis, Autoimmune, Experimental - metabolism</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Medical sciences</topic><topic>Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis</topic><topic>Myelin Sheath - metabolism</topic><topic>Neurology</topic><topic>Tissue Distribution</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SCHAECHER, K. E</creatorcontrib><creatorcontrib>SHIELDS, D. 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E</au><au>SHIELDS, D. C</au><au>BANIK, N. L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanism of myelin breakdown in experimental demyelination : A putative role for calpain</atitle><jtitle>Neurochemical research</jtitle><addtitle>Neurochem Res</addtitle><date>2001-06-01</date><risdate>2001</risdate><volume>26</volume><issue>6</issue><spage>731</spage><epage>737</epage><pages>731-737</pages><issn>0364-3190</issn><eissn>1573-6903</eissn><coden>NEREDZ</coden><abstract>Although calpain has been extensively studied, its physiological function is poorly understood. In contrast, its role in the pathophysiology of various diseases has been implicated, including that of experimental allergic encephalomyelitis (EAE), an animal model of the demyelinating disease multiple sclerosis (MS). In EAE, calpain degrades myelin proteins, including myelin basic protein (MBP), suggesting a role for calpain in the breakdown of myelin in this disease. 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| subjects | Animals Biological and medical sciences Calpain - metabolism Demyelinating Diseases - metabolism Encephalomyelitis, Autoimmune, Experimental - metabolism Humans Immunohistochemistry Medical sciences Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis Myelin Sheath - metabolism Neurology Tissue Distribution |
| title | Mechanism of myelin breakdown in experimental demyelination : A putative role for calpain |
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