Syndecan‐1 expression is upregulated in degenerating articular cartilage in a transgenic mouse model for osteoarthritis

Author： Salminen H. Säämänen A. Jalkanen M. Vuorio E. Pirilä L.

ISSN： 0300-9742

Source： Scandinavian Journal of Rheumatology, Vol.34, Iss.6, 2005-11, pp. : 469-474

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Abstract

Objective: Mice heterozygous for the Del1 transgene locus with a short deletion mutation in the type II collagen gene develop early‐onset degenerative changes in the knee joints that progress to end‐stage osteoarthritis by the age of 12–15 months. This study focuses on the expression and distribution of syndecan‐1, a cell‐surface heparan sulfate proteoglycan, during the development of osteoarthritic cartilage degeneration, to better understand its role in this disease. Methods: Northern analyses of total RNA extracted from knee joints of transgenic Del1 mice and their nontransgenic controls were used to monitor changes in syndecan‐1 mRNA levels during development, growth, ageing, and cartilage degeneration. Immunohistochemistry was used to study the distribution of syndecan‐1 in the knee joints at different stages of cartilage degeneration. Results: Syndecan‐1 mRNA was present in knee joints throughout life, with the highest mRNA levels in ageing knee joints. In Del1 mice, a transient upregulation of syndecan‐1 mRNA synthesis was observed at the age of 6 months coinciding with early stages of cartilage degeneration and a period of attempted repair. Immunostaining for syndecan‐1 was most intense in chondrocytes of superficial and intermediate zones of articular cartilage adjacent to defect areas. Chondrocyte clusters also stained strongly for syndecan‐1. Conclusion: The present temporospatial expression data on upregulation of syndecan‐1 in articular cartilage during early stages of cartilage degeneration suggest that this molecule is involved in the attempted repair of cartilage fibrillations. Combined with the known role of syndecan‐1 during skeletal development and wound healing, this interesting finding warrants further validation.