Altered expression of microRNA-23a in psoriatic arthritis modulates synovial fibroblast pro-inflammatory mechanisms via phosphodiesterase 4B
Open accessAbstract
OBJECTIVES: To investigate the functional role of miR-23a in synovial fibroblasts (SFC) activation in psoriatic arthritis (PsA). METHODS: Differential expression of the miR-23a-27a-24-2 cluster was identified by real-time quantitative PCR in PsA synovial tissue and peripheral blood mononuclear cells (PBMC) compared to osteoarthritis (OA) and correlated with disease activity. For regulation experiments, PsA synovial fibroblasts (SFC) were cultured with Toll-like receptor (TLR) ligands and pro-inflammatory cytokines. PsA SFC were transfected with a miR-23a inhibitor to assess the functional effect on migration, invasion and expression of pro-inflammatory meditators. The direct interaction between miR-23a and predicted target mRNA, phosphodiesterase 4B (PDE4B), was examined by luciferase reporter gene assay, with the expression and regulation confirmed by RT-PCR and western blot. A PDE4 inhibitor was used to analyse the function of PDE4B signalling in both miR-23a and Poly(I:C)-induced PsA SFC activation. RESULTS: Synovial tissue expression of miR-23a was lower in PsA compared to OA and correlated inversely with disease activity and synovitis. TLR activation via Poly(I:C) and LPS, but not Pam3CSK4, significantly decreased miR-23a expression, with no significant effect observed in reponse to stimulation with pro-inflammatory cytokines. Decreased miR-23a expression enhanced PsA SFC migration, invasion and secretion of IL-6, IL-8, MCP-1, RANTES and VEGF. We identified PDE4B as a direct target of miR-23a and demonstrated enhanced mRNA and protein expression of PDE4B in anti-miR-23a transfected PsA SFC. Poly(I:C) and/or miR-23a-induced migration and enhanced cytokine expression was suppressed by the blockade of PDE4 signalling. CONCLUSIONS: In PsA, dysregulated miR-23a expression contributes to synovial inflammation through enhanced SFC activation, via PDE4B signalling, and identifies a novel anti-inflammatory mechanism of PDE4 blockade.
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Altered expression of miRNA-23a in synovial fibroblasts of psoriatic arthritis patients results in enhanced expression of pro-inflammatory mediators and matrix degrading enzymes, promoting joint degeneration and synovial inflammation.
“In addition, the altered expression of this miRNA in synovial fibroblasts of psoriatic arthritis patients, results in the enhanced expression of pro-inflammatory mediators and matrix degrading enzymes, further promoting joint degeneration and synovial inflammation [173].”
From Cellular and Molecular Mechanisms in the Pathogenesis of Classical, Vascular, and Hypermobile Ehlers‒Danlos Syndromes (2019) · cites this paper as [173]
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- Authors
- Wade, S. M., Trenkmann, M., McGarry, T., Canavan, M., Marzaioli, V., Wade, S. C., Veale, D. J., & Fearon, U.
- Affiliations
- University College Dublin (IE)
- Trinity College Dublin (IE)
- Corresponding author
- Fearon, Ursula
- ORCID
- Venue
- Journal of Autoimmunity
- Publisher
- Elsevier BV
- Published
- 2019-01
- Volume
- 96
- Pages
- 86-93
- ISSN
- 0896-8411 (ISSN-L)
- OpenAlex
- W2889011557
- Cited by
- 35
- References
- 43
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 4 · 2023: 4 · 2021: 7 · 2020: 10 · 2019: 5
- FWCI
- 4.68
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Autoimmunity (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- Irish Research Council
- Topics
- Health Sciences › Medicine › Rheumatology › Spondyloarthritis Studies and Treatments
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Health Sciences › Medicine › Rheumatology › Osteoarthritis Treatment and Mechanisms
- Keywords
- psoriatic arthritis, microRNA-23a, synovial fibroblasts, PDE4B, synovitis, Toll-like receptor activation, poly(I:C), inflammatory cytokines, PDE4 inhibition, osteoarthritis, disease activity
- MeSH terms
- Cell Movement, Cells, Cultured, Fibroblasts, Gene Expression Regulation, Humans, Inflammation, Lipopolysaccharides, Poly I-C, Synovial Membrane, Signal Transduction, Arthritis, Psoriatic, Cytokines, MicroRNAs, Cell Proliferation, Cyclic Nucleotide Phosphodiesterases, Type 4
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