Open AccessEffects of hyaluronic acid on the release of proteoglycan from the cell matrix in rabbit chondrocyte cultures in the presence and absence of cytokines
Author(s) -
Shimazu Atsushi,
Jikko Akitoshi,
Iwamoto Masahiro,
Koike Tatsuya,
Yan Weiqun,
Okada Yasunori,
Shinmei Masayuki,
Nakamura Shigeo,
Kato Yukio
Publication year - 1993
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/art.1780360217
Subject(s) - proteoglycan , hyaluronic acid , chondrocyte , glucosamine , cartilage , chemistry , chondroitin sulfate , matrix (chemical analysis) , decorin , microbiology and biotechnology , biochemistry , glycosaminoglycan , immunology , extracellular matrix , biology , anatomy , in vitro , chromatography
Objective. To investigate the effects of hyaluronic acid (HA) on the release of proteoglycan by cultured rabbit chondrocytes. Methods. Articular cartilage chondrocytes were isolated from the knee joints of New Zealand white rabbits. Proteoglycan synthesis after incubation with HA was determined by measuring 35 S‐sulfate incorporation. Cells incubated with HA were labeled with 3 H‐glucosamine and applied to a Sepharose CL‐2B column. After incubation of confluent cells with 35 S‐sulfate and then with HA in various concentrations in the presence or absence of cytokines, proteoglycan release from the cell matrix layer was measured. Results. HA ( M r 3 × 10 5 to 19 × 10 5 ), at 10 μg/ml to 1 mg/ml, had little effect on the incorporation of 35 S‐sulfate or 3 H‐glucosamine into cartilage matrix proteoglycans, or on the hydrodynamic size of proteoglycan monomers, in rabbit chondrocyte cultures. However, at 10–1,000 μg/ml, HA suppressed the release of 35 S‐proteoglycans from the cell matrix layer into the medium in the presence and absence of interleukin‐1, tumor necrosis factor α, or basic fibroblast growth factor. Conclusion. These results suggest that HA is a potent inhibitor of the displacement of matrix proteoglycan into culture medium.