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Acta Neuropathol. 2005 Aug;110(2):173-7. Epub 2005 Jun 28.

Myostatin is increased and complexes with amyloid-beta within sporadic inclusion-body myositis muscle fibers.

Author information

1
USC Neuromuscular Center, Department of Neurology, University of Southern California Keck School of Medicine, Good Samaritan Hospital, 637 S. Lucas Ave, Los Angeles, CA, 90017-1912, USA.

Abstract

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.

PMID:
15983828
DOI:
10.1007/s00401-005-1035-3
[Indexed for MEDLINE]

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