Myostatin is increased and complexes with amyloid-beta within sporadic inclusion-body myositis muscle fibers
Myostatin is a negative regulator of muscle mass and strength. Sporadic inclusion-body myositis (s-IBM) is the most common degenerative muscle disease of older persons and is characterized by pronounced muscle wasting. s-IBM is of unknown etiology and pathogenesis, and it lacks definitive treatment....
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| Veröffentlicht in: | Acta neuropathologica 2005-08, Vol.110 (2), p.173-177 |
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| container_title | Acta neuropathologica |
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| creator | Wójcik, Sławomir Engel, W King McFerrin, Janis Askanas, Valerie |
| description | Myostatin is a negative regulator of muscle mass and strength. Sporadic inclusion-body myositis (s-IBM) is the most common degenerative muscle disease of older persons and is characterized by pronounced muscle wasting. s-IBM is of unknown etiology and pathogenesis, and it lacks definitive treatment. We have now demonstrated in samples from 12 s-IBM biopsies that: (1) by light and electron microscopic immunocytochemistry, myostatin/myostatin precursor is accumulated within muscle fibers and co-localized with amyloid-beta (Abeta); (2) by immunoblots, both myostatin and myostatin precursor are increased; and (3) by immunoprecipitation, myostatin precursor complexes with Abeta. Our study suggests that myostatin/myostatin precursor, either alone, or bound to Abeta, may play a novel role in the pathogenesis of s-IBM. |
| doi_str_mv | 10.1007/s00401-005-1035-3 |
| format | Article |
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Our study suggests that myostatin/myostatin precursor, either alone, or bound to Abeta, may play a novel role in the pathogenesis of s-IBM.</description><subject>Amyloid beta-Peptides - metabolism</subject><subject>Humans</subject><subject>Immunoblotting</subject><subject>Immunohistochemistry</subject><subject>Immunoprecipitation</subject><subject>Microscopy, Immunoelectron</subject><subject>Muscle, Skeletal - metabolism</subject><subject>Muscle, Skeletal - pathology</subject><subject>Myositis, Inclusion Body - metabolism</subject><subject>Myositis, Inclusion Body - pathology</subject><subject>Myostatin</subject><subject>Transforming Growth Factor beta - metabolism</subject><issn>0001-6322</issn><issn>1432-0533</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkMtOwzAQRS0EoqXwAWyQV-wMfibOElW8pCI23Vt-RRglcckkgvw9Ka3EajQz99zFQeia0TtGaXkPlErKCKWKMCoUESdoyaTghCohTtGS0vlbCM4X6ALgc954KdU5WjBVaaG5XqLmbcow2CF1OAFOne-jhRiw7QL2ud018ScC_k7DB7bt1OQUiIuD_bvMDOxyb0Pye7IZIeWOuBwm3M6taZgb2xF8E3GdXOzhEp3VtoF4dZwrtH163K5fyOb9-XX9sCGeV9VAtPPKBaWclJL6WnkbuCuocFJoIaK1uuTcRqUrV1TS1pLLSqtSSh1Y7UqxQreH2l2fv8YIg2kT-Ng0tot5BFNoJRgr9Bxkh6DvM0Afa7PrU2v7yTBq9obNwbCZDZu9YSNm5uZYPro2hn_iqFT8AqPIeMg</recordid><startdate>200508</startdate><enddate>200508</enddate><creator>Wójcik, Sławomir</creator><creator>Engel, W King</creator><creator>McFerrin, Janis</creator><creator>Askanas, Valerie</creator><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>200508</creationdate><title>Myostatin is increased and complexes with amyloid-beta within sporadic inclusion-body myositis muscle fibers</title><author>Wójcik, Sławomir ; Engel, W King ; McFerrin, Janis ; Askanas, Valerie</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c299t-8bc5bd55b4440cf5cad2b603b43833eaa8722ae589b694af4249857448d1fb73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Amyloid beta-Peptides - metabolism</topic><topic>Humans</topic><topic>Immunoblotting</topic><topic>Immunohistochemistry</topic><topic>Immunoprecipitation</topic><topic>Microscopy, Immunoelectron</topic><topic>Muscle, Skeletal - metabolism</topic><topic>Muscle, Skeletal - pathology</topic><topic>Myositis, Inclusion Body - metabolism</topic><topic>Myositis, Inclusion Body - pathology</topic><topic>Myostatin</topic><topic>Transforming Growth Factor beta - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wójcik, Sławomir</creatorcontrib><creatorcontrib>Engel, W King</creatorcontrib><creatorcontrib>McFerrin, Janis</creatorcontrib><creatorcontrib>Askanas, Valerie</creatorcontrib><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>Acta neuropathologica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wójcik, Sławomir</au><au>Engel, W King</au><au>McFerrin, Janis</au><au>Askanas, Valerie</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Myostatin is increased and complexes with amyloid-beta within sporadic inclusion-body myositis muscle fibers</atitle><jtitle>Acta neuropathologica</jtitle><addtitle>Acta Neuropathol</addtitle><date>2005-08</date><risdate>2005</risdate><volume>110</volume><issue>2</issue><spage>173</spage><epage>177</epage><pages>173-177</pages><issn>0001-6322</issn><eissn>1432-0533</eissn><abstract>Myostatin is a negative regulator of muscle mass and strength. 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| ispartof | Acta neuropathologica, 2005-08, Vol.110 (2), p.173-177 |
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| subjects | Amyloid beta-Peptides - metabolism Humans Immunoblotting Immunohistochemistry Immunoprecipitation Microscopy, Immunoelectron Muscle, Skeletal - metabolism Muscle, Skeletal - pathology Myositis, Inclusion Body - metabolism Myositis, Inclusion Body - pathology Myostatin Transforming Growth Factor beta - metabolism |
| title | Myostatin is increased and complexes with amyloid-beta within sporadic inclusion-body myositis muscle fibers |
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