Secreted protein acidic and rich in cysteine (SPARC) in human skeletal muscle

Louise Helskov Jørgensen, Stine Juhl Petersson, Jeeva Sellathurai, Ditte C. Andersen, Susanne Thayssen, Dorte J Sant, Charlotte Harken Jensen, Henrik Daa Schrøder

Publikation: Bidrag til tidsskriftTidsskriftsartikelForskningpeer review

Abstract

Secreted protein acidic and rich in cysteine (SPARC)/osteonectin is expressed in different tissues during remodeling and repair, suggesting a function in regeneration. Several gene expression studies indicated that SPARC was expressed in response to muscle damage. Studies on myoblasts further indicated a function of SPARC in skeletal muscle. We therefore found it of interest to study SPARC expression in human skeletal muscle during development and in biopsies from Duchenne and Becker muscular dystrophy and congenital muscular dystrophy, congenital myopathy, inclusion body myositis, and polymyositis patients to analyze SPARC expression in a selected range of inherited and idiopathic muscle wasting diseases. SPARC-positive cells were observed both in fetal and neonatal muscle, and in addition, fetal myofibers were observed to express SPARC at the age of 15-16 weeks. SPARC protein was detected in the majority of analyzed muscle biopsies (23 of 24), mainly in mononuclear cells of which few were pax7 positive. Myotubes and regenerating myofibers also expressed SPARC. The expression-degree seemed to reflect the severity of the lesion. In accordance with these in vivo findings, primary human-derived satellite cells were found to express SPARC both during proliferation and differentiation in vitro. In conclusion, this study shows SPARC expression both during muscle development and in regenerating muscle. The expression is detected both in satellite cells/myoblasts and in myotubes and muscle fibers, indicating a role for SPARC in the skeletal muscle compartment.

OriginalsprogEngelsk
TidsskriftJournal of Histochemistry and Cytochemistry
Vol/bind57
Udgave nummer1
Sider (fra-til)29-39
Antal sider11
ISSN0022-1554
DOI
StatusUdgivet - jan. 2009

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