ArticleMolecular biology reports2024
Possible involvement of DExD/H box helicase 60 in synovial inflammation of rheumatoid arthritis: role of toll-like receptor 3 signaling.
Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 2 citations in OpenAlex.
- Rheumatoid arthritis and gout: a rare combination or overlooked coexistence?Arthritis research & therapy · 2026Article
- Deciphering the relevance of dead box RNA helicases in gliomagenesis and autophagy.Human cell · 2025Review
- Tripartite Motif-containing 22 Is Involved in TLR3-mediated Inflammatory Pathway in Rheumatoid Fibroblast-like Synoviocytes.In vivo (Athens, Greece)Article
- Negative Regulator of Interferon Response Promotes Toll-like Receptor 3-induced Interleukin 6 in Rheumatoid Synoviocyte.In vivo (Athens, Greece)Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInnate immunity is known to be implicated in the etiology of synovitis in rheumatoid arthritis (RA). However, details of the molecular mechanisms have not been fully clarified. DExD/H-box helicase 60 (DDX60), a putative RNA helicase, is of consequence in anti-viral innate immune reactions followed by inflammation. Although DDX60 is involved in the pathogenesis of autoimmune diseases such as systemic lupus nephritis, the role of DDX60 in RA has not been elucidated. The objective of this study was to examine the expression and the role of DDX60 in RA synovial inflammation. METHODS AND
resultsDDX60 protein expression was investigated by immunohistochemistry in synovial tissues resected from 4 RA and 4 osteoarthritis (OA) patients. We found that synovial DDX60 expression was more intense in RA than in OA. Treatment of human rheumatoid fibroblast-like synoviocytes in culture with polyinosinic-polycytidylic acid, a Toll-like receptor 3 (TLR3) ligand, increased DDX60 protein and mRNA expression. A knockdown experiment of DDX60 using RNA interference revealed a decrease in the expression of poly IC-induced C-X-C motif chemokine ligand 10 (CXCL10) which induces lymphocyte chemotaxis.
conclusionsThe synovial DDX60 was more expressed in RA patients than in OA. In human RFLS, DDX60 stimulated by TLR3 signaling affected CXCL10 expression. DDX60 may contribute to synovial inflammation in RA.
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