Source:http://linkedlifedata.com/resource/pubmed/id/18335407
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2008-3-12
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| pubmed:abstractText |
Preferential atrophy of Type-II muscle fibres occurs in several clinical situations, including cachexia, muscle disuse, chronic glucocorticoid treatment, remote neoplasia, and sometimes as an aspect of recent-denervation. For the patient, the Type-II atrophy itself might be unfavourable (as a glucocorticoid side-effect) or favourable (survivalistic via the muscle-alanine liver-gluconeogenesis pathway in starvation). The cellular mechanisms underlying Type-II fibre atrophy are unclear. Myostatin (Mstn) is physiologically a negative regulator of muscle mass and strength. In this study we evaluated a possible role of Mstn in Type-II fibre atrophy in human muscle. Mstn and Mstn precursor protein (MstnPP) were studied in 10-muscle biopsies containing Type-II fibre atrophy and in 17 disease and normal control muscle biopsies. When comparison was made with normal control fibres, we found the following: 1) by immunocytochemistry, diffusely increased Mstn/MstnPP in the atrophic Type-II muscle fibres; 2) by immunoblots, Mstn/MstnPP increased individually; 3) by RT-PCR, no increase in MstnPP mRNA. In conclusion, our results a) suggest that Mstn/ /MstnPP might play a role in the pathogenic cascade of Type-II muscle fibre atrophy; b) broaden our previously-described associations of Mstn in human muscle pathology, and c) could possibly lead to clinical prevention when Type-II muscle fibre atrophy is unfavourable, for instance in glucocorticoid therapy.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphatases,
http://linkedlifedata.com/resource/pubmed/chemical/Biological Markers,
http://linkedlifedata.com/resource/pubmed/chemical/Glucocorticoids,
http://linkedlifedata.com/resource/pubmed/chemical/MSTN protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Myostatin,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Precursors,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta
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| pubmed:status |
MEDLINE
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| pubmed:month |
Feb
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| pubmed:issn |
0015-5659
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
67
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
6-12
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:18335407-Adenosine Triphosphatases,
pubmed-meshheading:18335407-Adult,
pubmed-meshheading:18335407-Aged,
pubmed-meshheading:18335407-Aged, 80 and over,
pubmed-meshheading:18335407-Biological Markers,
pubmed-meshheading:18335407-Biopsy,
pubmed-meshheading:18335407-Glucocorticoids,
pubmed-meshheading:18335407-Humans,
pubmed-meshheading:18335407-Immunohistochemistry,
pubmed-meshheading:18335407-Middle Aged,
pubmed-meshheading:18335407-Muscle, Skeletal,
pubmed-meshheading:18335407-Muscle Fibers, Fast-Twitch,
pubmed-meshheading:18335407-Muscular Atrophy,
pubmed-meshheading:18335407-Myostatin,
pubmed-meshheading:18335407-Protein Precursors,
pubmed-meshheading:18335407-RNA, Messenger,
pubmed-meshheading:18335407-Transforming Growth Factor beta,
pubmed-meshheading:18335407-Up-Regulation
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| pubmed:year |
2008
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| pubmed:articleTitle |
Myostatin and its precursor protein are increased in the skeletal muscle of patients with Type-II muscle fibre atrophy.
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| pubmed:affiliation |
USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, Los Angeles, CA 90017-1912, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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