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Erschienen in: Rheumatology International 11/2007

01.09.2007 | Original Article

Activin A suppresses interleukin-1-induced matrix metalloproteinase 3 secretion in human chondrosarcoma cells

verfasst von: Deh-Ming Chang, Shao-Hsiang Liu, Herng-Sheng Lee, Jenn-Hung Lai, Chen-Hung Chen

Erschienen in: Rheumatology International | Ausgabe 11/2007

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Abstract

The objective was to investigate the effect of activin A on matrix metalloproteinase 3 (MMP-3) production and to identify the role of activin A in chondroprotection. SW1353 cells, a human chondrosarcoma cell line, were stimulated with interleukin (IL) 1α and tumor necrosis factor (TNF) α, and the concentrations of activin A, follistatin, and MMP-3 secreted into the culture media were measured by enzyme-linked immunosorbent assay (ELISA). Activin A was added to cell cultures in the presence of IL-1α or TNFα to determine its effect on the production of MMP-3 and sulfated glycosaminoglycan (sGAG) (measured by Alcian blue assay). To study the mechanism responsible for the chondroprotective effects of activin A, the production of IL-1 receptor antagonist (IL-1ra) and tissue inhibitor for metalloproteinases 1 (TIMP-1) was examined by ELISA. Addition of IL-1α did not affect the production of activin A by cultured SW1353 cells. IL-1α and activin A inhibited the production of follistatin. Stimulation of SW1353 cells with activin A suppressed IL-1α-induced, but not TNFα-induced, MMP-3 expression. Activin A had no effect on the production of sGAG, IL-1ra, or TIMP-1, although it suppressed the induction of TIMP-1 and IL-1ra by IL-1α. This novel finding of MMP-3 inhibition by activin A suggests a new role of activin A in cartilage remodeling. Activin A may have therapeutic potential for preventing cartilage degradation.
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Metadaten
Titel
Activin A suppresses interleukin-1-induced matrix metalloproteinase 3 secretion in human chondrosarcoma cells
verfasst von
Deh-Ming Chang
Shao-Hsiang Liu
Herng-Sheng Lee
Jenn-Hung Lai
Chen-Hung Chen
Publikationsdatum
01.09.2007
Verlag
Springer-Verlag
Erschienen in
Rheumatology International / Ausgabe 11/2007
Print ISSN: 0172-8172
Elektronische ISSN: 1437-160X
DOI
https://doi.org/10.1007/s00296-007-0350-5

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