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• W2321839890 endingPage "e0153142" @default.
• W2321839890 startingPage "e0153142" @default.
• W2321839890 abstract "The Toll-like receptor (TLR) signaling pathway is activated in synovial fibroblast cells in patients with rheumatoid arthritis (RA). The receptor activator of nuclear factor-κB (RANK) and its ligand, RANKL, are key molecules involved in the differentiation of osteoclasts and joint destruction in RA. Hyaluronan (HA) is a major extracellular component and an important immune regulator. In this study, we show that lipopolysaccharide (LPS) stimulation significantly increases RANKL expression via a TLR-4 signaling pathway. We also demonstrate that HA suppresses LPS-induced RANKL expression, which is dependent on CD44, but not intercellular adhesion molecule-1 (ICAM-1). Our study provides evidence for HA-mediated suppression of TLR-4-dependent RANKL expression. This could present an alternative target for the treatment of destructed joint bones and cartilages in RA." @default.
• W2321839890 created "2016-06-24" @default.
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• W2321839890 date "2016-04-07" @default.
• W2321839890 modified "2023-09-28" @default.
• W2321839890 title "Hyaluronan Inhibits Tlr-4-Dependent RANKL Expression in Human Rheumatoid Arthritis Synovial Fibroblasts" @default.
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• W2321839890 doi "https://doi.org/10.1371/journal.pone.0153142" @default.
• W2321839890 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4824426" @default.
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• W2321839890 hasPublicationYear "2016" @default.
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