Effects of Osteochondrin S and select connective tissue ribonucleinate components on human osteoclastsin vitro

CANTLEY, M D, RAINSFORD, Kim and HAYNES, D R (2013). Effects of Osteochondrin S and select connective tissue ribonucleinate components on human osteoclastsin vitro. Journal of Pharmacy and Pharmacology, 65 (8), 1214-1222.

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Official URL: http://dx.doi.org/10.1111/jphp.12088
Link to published version:: 10.1111/jphp.12088

Abstract

Objectives: Osteochondrin S, a natural product derived from connective tissues and yeast, is used to treat osteoarthritis. The aim of this study was to determine the effect of Osteochondrin S on human osteoclast activity in vitro. Methods: Osteoclasts were derived from human peripheral blood mononuclear cells stimulated with macrophage colony-stimulating factor and receptor activator of nuclear factor kappa B (RANK) ligand. Cells were treated with 23.5–587.2 ng/ml Osteochondrin S or 0.2–5 mg/ml of RNA components (synovia, placenta, intervertebral disc or cartilage). The effects on osteoclast formation and resorptive activity were assessed. Real-time polymerase chain reaction was conducted to assess the expression of key osteoclast genes. Key findings: Osteochondrin S and the individual RNA extracts resulted in a concentration-dependent inhibition of human osteoclast activity. Osteochondrin S did not affect RANK, nuclear factor of activated T cells (NFATc1), osteoclast-associated receptor or cathepsin K expression. However, there was a significant (P < 0.05) reduction in mRNA expression of calcitonin receptor. Osteochondrin S treatment also significantly increased the expression of osteoclast inhibitory factor interferon-β and, interestingly, increased the expression of tumour necrosis-α-like weak inducer of apoptosis (TWEAK). Conclusions: Osteochondrin S inhibited the resorptive ability of osteoclasts. These actions are likely to occur at a late stage during osteoclast formation, downstream of NFATc1. Overall, the findings show that Osteochondrin S inhibition of osteoclast activity may be responsible for its beneficial effects on diseases such as osteoarthritis.

Item Type: Article
Research Institute, Centre or Group: Biomolecular Sciences Research Centre
Identification Number: 10.1111/jphp.12088
Depositing User: Louise Vickers
Date Deposited: 31 Oct 2014 11:45
Last Modified: 31 Oct 2014 11:45
URI: http://shura.shu.ac.uk/id/eprint/8611

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