4.2 Article

Taurine chloramine differentially inhibits matrix metalloproteinase 1 and 13 synthesis in interleukin-1 beta stimulated fibroblast-like synoviocytes

Journal

ARTHRITIS RESEARCH & THERAPY
Volume 9, Issue 4, Pages -

Publisher

BMC
DOI: 10.1186/ar2279

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It has been suggested that taurine chloramine (TauCl) plays an important role in the downregulation of proinflammatory mediators. However, little is known about its effect on the expression of matrix metalloproteinases ( MMPs). In this study, we investigated the effects of TauCl on synovial expression of MMPs. The effects of TauCl on MMP expression in IL-1 beta stimulated fibroblast-like synoviocytes (FLSs) were studied using the following techniques. Real-time PCR and semi-quantitative PCR were employed to analyze the mRNA expression of MMPs. ELISA was used to determine protein levels of MMPs. Western blot analyses were performed to analyze the mitogen-activated protein kinase and inhibitor of nuclear factor-kappa B (I kappa B) kinase signalling pathways. Finally, electrophoretic mobility shift assay and immunohistochemistry were used to assess localization of transcription factors. IL-1 beta increased the transcriptional and translational levels of MMP-1 and MMP-13 in rheumatoid arthritis FLSs, whereas the levels of MMP-2 and MMP-9 were unaffected. TauCl at a concentration of 400 to 600 mu mol/l greatly inhibited the transcriptional and translational expression of MMP-13, but the expression of MMP-1 was significantly inhibited at 800 mol/l. At a concentration of 600 mol/l, TauCl did not significantly inhibit phosphorylation of mitogen-activated protein kinase or I kappa B degradation in IL-1 beta stimulated rheumatoid arthritis FLSs. The degradation of I kappa B was significantly inhibited at a TauCl concentration of 800 mu mol/ I. The inhibitory effect of TauCl on I kappa B degradation was confirmed by electrophoretic mobility shift assay and immunochemical staining for localization of nuclear factor-kappa B. TauCl differentially inhibits the expression of MMP-1 and MMP-13, and inhibits expression of MMP-1 primarily through the inhibition of I kappa B degradation, whereas it inhibits expression of MMP-13 through signalling pathways other than the I kappa B pathway.

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