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Rheumatoid arthritis

PIAS3 inhibition blocks FLS activity

Nature Reviews Rheumatology volume 12, pages 70–71 (2016)Cite this article

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The authors showed that FLSs isolated from patients with RA, but not those from patients with osteoarthritis, expressed higher levels of PIAS3 than those from healthy controls. A series of in vitro experiments in which PIAS3 expression was knocked down by specific short-hairpin RNA (shRNA) showed that the ability of RA FLSs to migrate towards a chemoattractant, infiltrate a gel-coated trans-well membrane and form lamellipodia is partially dependent on PIAS3.

Importantly, TNF-mediated upregulation and secretion of matrix metalloproteinases MMP3, MMP9 and MMP13 — enzymes that are associated with the invasive behaviour of FLSs — and activation of the cell-motility regulators Rac1 (Ras-related C3 botulinum toxin substrate 1), p21-activated kinase 1 and c-Jun N-terminal kinase was also decreased by PIAS3 knockdown. Finally, the authors also observed that knockdown of PIAS3 prevented TNF-mediated accumulation of Rac1–SUMO-1.

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References

  1. Lao, M. et al. Protein inhibitor of activated STAT3 regulates migration, invasion, and activation of fibroblast-like synoviocytes in rheumatoid arthritis. J. Immunol. http://dx.doi.org/10.4049/jimmunol.1403254

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  1. João H. Duarte
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Duarte, J. PIAS3 inhibition blocks FLS activity. Nat Rev Rheumatol 12, 70–71 (2016). https://doi.org/10.1038/nrrheum.2015.182

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  • DOI: https://doi.org/10.1038/nrrheum.2015.182

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