open access

Vol 67, No 1 (2008)
ORIGINAL ARTICLES
Published online: 2007-12-03
Submitted: 2012-02-06
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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.

open access

Vol 67, No 1 (2008)
ORIGINAL ARTICLES
Published online: 2007-12-03
Submitted: 2012-02-06

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)
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Keywords

Type-II muscle fibre atrophy; myostatin; myostatin precursor protein; GDF-8; human muscle

About this article
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)

Pages

8-14

Published online

2007-12-03

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

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