Endogenous Galectin-9 Suppresses Apoptosis in Human Rheumatoid Arthritis Synovial Fibroblasts

Mark J. Pearson, Magdalena A. Bik, Caroline Ospelt, Amy J. Naylor, Corinna Wehmeyer, Simon W. Jones, Christopher D. Buckley, Steffen Gay, Andrew Filer, Janet M. Lord

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Galectin-9 (Gal9) has been postulated to have anti-infammatory properties based on the ability of
exogenous Gal9 to induce apoptosis in synovial fbroblasts in animal models of rheumatoid arthritis
(RA). Here we aimed to assess the potential role of endogenous Galectins, including Gal9, in the
infammatory pathology of the RA synovium in humans. Firstly expression of Galectins 1–9 was
determined in synovial fbroblasts (RASF) and dermal fbroblasts (DF) isolated from RA patients, the
latter representing a non-infamed site. We then further challenged the cells with pro-infammatory
TLR agonists and cytokines and assessed Galectin expression. Gal9 was found to be diferentially and
abundantly expressed in RASF compared to DF. Agonists of TLR3 and TLR4, along with IFNgamma were
also found to induce Gal9 expression in RASF. siRNA was then used to knock-down Gal9 expression
in RASF and the efects of this on apoptosis and cell viability were assessed. Increased apoptosis was
observed in RASF following Gal9 knock-down. We conclude that, unlike exogenous Gal9, endogenous
Gal9 is protective against apoptosis and enhances synovial fbroblast viability suggesting that its role in
RA is both pathogenic and pro-infammatory.
Original languageEnglish
Article number12887
JournalScientific Reports
Issue number1
Publication statusPublished - 27 Aug 2018

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