Vol 67, No 1 (2008)
Original article
Submitted: 2012-02-06
Published online: 2007-12-03
Myostatin and its precursor protein are increased in the skeletal muscle of patients with Type-II muscle fibre atrophy
S. Wójcik, A. Nogalska, W.K. Engel, V. Askanas
Folia Morphol 2008;67(1):8-14.
Vol 67, No 1 (2008)
ORIGINAL ARTICLES
Submitted: 2012-02-06
Published online: 2007-12-03
Abstract
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.
(Folia Morphol 2008; 67: 1-7)
Abstract
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.
(Folia Morphol 2008; 67: 1-7)
Keywords
Type-II muscle fibre atrophy; myostatin; myostatin precursor protein; GDF-8; human muscle
Title
Myostatin and its precursor protein are increased in the skeletal muscle of patients with Type-II muscle fibre atrophy
Journal
Folia Morphologica
Issue
Vol 67, No 1 (2008)
Article type
Original article
Pages
8-14
Published online
2007-12-03
Page views
558
Article views/downloads
1364
Bibliographic record
Folia Morphol 2008;67(1):8-14.
Keywords
Type-II muscle fibre atrophy
myostatin
myostatin precursor protein
GDF-8
human muscle
Authors
S. Wójcik
A. Nogalska
W.K. Engel
V. Askanas