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SFRP5 Enhances Wnt5a Induced-Inflammation in Rheumatoid Arthritis Fibroblast-Like Synoviocytes.

Dorra Elhaj Mahmoud1, Wajih Kaabachi2, Nadia Sassi1

  • 1Immuno-Rheumatology Research Laboratory, Rheumatology Department, La Rabta Hospital, University of Tunis-El Manar, Tunis, Tunisia.

Frontiers in Immunology
|July 2, 2021
PubMed
Summary

Wnt5a promotes inflammation in rheumatoid arthritis fibroblast-like synoviocytes, and the inhibitor SFRP5 unexpectedly enhances this effect. Careful evaluation of Wnt5a and SFRP5 interactions is crucial for rheumatoid arthritis (RA) treatment strategies.

Keywords:
FLSWnt pathwayfibrocytesinflammationrheumatoid arthritis

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Area of Science:

  • Rheumatology
  • Molecular Biology
  • Cell Biology

Background:

  • Fibroblast-like synoviocytes (FLS) drive pannus formation and joint destruction in rheumatoid arthritis (RA).
  • Wnt5a signaling is implicated in RA pathogenesis and represents a potential therapeutic target.

Purpose of the Study:

  • Investigate Wnt5a signaling elements in RA FLS and precursor cells.
  • Determine the role of Wnt5a in RA FLS pro-inflammatory activity.
  • Assess if SFRP5 can counteract Wnt5a-induced synovial dysfunction in vitro.

Main Methods:

  • Quantified Wnt5a, SFRP5, receptors, and targets in cultured RA FLS, fluid-derived FLS, and fibrocytes via qPCR.
  • Assessed pro-inflammatory molecule expression after Wnt5a and SFRP5 stimulation of RA FLS.

Main Results:

  • RA FLS, fluid-derived FLS, and fibrocytes express similar Wnt5a and receptor levels.
  • Wnt5a stimulated pro-inflammatory targets (IL1β, IL8, IL6) in RA FLS.
  • SFRP5 enhanced Wnt5a-induced inflammation and inhibited TCF4/LRP5 expression.

Conclusions:

  • SFRP5 enhances, rather than inhibits, Wnt5a's pro-inflammatory effects in RA FLS.
  • The interaction between Wnt5a and SFRP5 requires careful consideration for RA therapeutic development.