4.6 Article

Effects of physical stimulation with electromagnetic field and insulin growth factor-I treatment on proteoglycan synthesis of bovine articular cartilage

Journal

OSTEOARTHRITIS AND CARTILAGE
Volume 12, Issue 10, Pages 793-800

Publisher

ELSEVIER SCI LTD
DOI: 10.1016/j.joca.2004.06.012

Keywords

EMF; IGF-I; articular cartilage; proteoglycan

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Objective: To investigate the single and combined effects of electromagnetic field (EMF) exposure and the insulin growth factor-I (IGF-I) on proteoglycan (PG) synthesis of bovine articular cartilage explants and chondrocytes cultured in monolayers. Design: Bovine articular cartilage explants and chondrocyte monolayers were exposed to EMF (75 Hz; 1.5 mT) for 24 h in the absence and in the presence of both 10% fetal bovine serum (FBS) and IGF-I (1-100 ng/ml). PG synthesis was determined by Na-2- (SO4)-S-35 incorporation. PG release into culture medium was determined by the dimethylmethylene blue (DMMB) assay. Results: In cartilage explants, EMF significantly increased S-35-sulfate incorporation both in the absence and in the presence of 10% FBS. Similarly, IGF-I increased S-35-sulfate incorporation in a dose-dependent manner both in 0% and 10% FIBS. At all doses of IGF-I, the combined effects of the two stimuli resulted additive. No effect was observed on medium PG release. Also in chondrocyte monolayers, IGF-I stimulated S-35-sulfate incorporation in a dose-dependent manner, both in 0% and 10% FBS, however, this was not modified by EMF exposure. Conclusions: The results of this study show that EMF can act in concert with IGF-I in stimulating PG synthesis in bovine articular cartilage explants. As this effect is not maintained in chondrocyte monolayers, the native cell-matrix interactions in the tissue may be fundamental in driving the EMF effects. These data suggest that in vivo the combination of both EMF and IGF may exert a more chondroprotective effect than either treatment alone on articular cartilage. (C) 2004 OsteoArthritis Research Society International. Published by Elsevier Ltd. All rights reserved.

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