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Taurine chloramine inhibits proliferation of rheumatoid arthritis synoviocytes by triggering a p53-dependent pathway

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Abstract.

Objective and Design

Taurine chloramine (Tau-Cl), originating from activated neutrophils, possesses antiinflammatory activities. Fibroblast-like synoviocytes (FLS) participate in the chronic synovitis and synovial membrane hyperplasia that are characteristic pathological features of rheumatoid arthritis (RA). The present study was conducted to investigate the mechanism of the Tau-Cl effect on the proliferation of these cells in culture.

Materials and methods

FLS were stimulated in vitro with platelet derived growth factor (PDGF) alone or together with Tau-Cl. Cell proliferation was evaluated by counting the total and dividing cell numbers and by measurement of 3H-thymidine incorporation. Expression of the key cell-cycle regulators was evaluated at the protein (Western blotting) and/or mRNA (RT-PCR) levels.

Results

Treatment of RA FLS with Tau-Cl (200–500 μM) resulted in an early nuclear accumulation of p53 tumor suppressor protein. Moreover, Tau-Cl inhibited PDGF-triggered cell proliferation (IC50 value ≈ 250–300 μM), accompanied by characteristic modulation of p53 transcriptional targets: down-regulation of proliferating cell nuclear antigen (PCNA) and survivin, and concomitant up-regulation of p21 mitotic inhibitor.

Conclusion

We propose that Tau-Cl inhibits proliferation of RA FLS by triggering a p53-dependent cell-cycle arrest and conclude that this compound suppresses pathways in FLS that are known to contribute to the pathology of RA.

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Correspondence to E. Kontny.

Additional information

Received 30 May 2005; returned for revision 6 January 2006; returned for final revision 21 February 2006; accepted by J. Skotnicki and J. Di Battista 17 May 2006

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Kontny, E., Rudnicka, W., Chorąży-Massalska, M. et al. Taurine chloramine inhibits proliferation of rheumatoid arthritis synoviocytes by triggering a p53-dependent pathway. Inflamm. res. 55, 446–455 (2006). https://doi.org/10.1007/s00011-006-5067-5

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  • DOI: https://doi.org/10.1007/s00011-006-5067-5

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