ArticleArthritis research & therapy2017
Effect of tryptase inhibition on joint inflammation: a pharmacological and lentivirus-mediated gene transfer study.
Article in Arthritis research & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- SPAG11B, a potential biomarker for rheumatoid arthritis: a two-sample bidirectional Mendelian randomization analysis.BMC rheumatology · 2025Article
- Tryptase β regulation of joint lubrication and inflammation via proteoglycan-4 in osteoarthritis.Nature communications · 2023Article
- Sperm Associated Antigens: Vigorous Influencers in Life.Cell journal · 2021Review
- Regulation of osteoclastogenesis by mast cell in rheumatoid arthritis.Arthritis research & therapy · 2021Article
- Article
- Roles of mast cells in rheumatoid arthritis.The Korean journal of internal medicine · 2020Review
- When alpha meets beta, mast cells get hyper.The Journal of experimental medicine · 2019Article
- Serine proteinases in the turnover of the cartilage extracellular matrix in the joint: implications for therapeutics.British journal of pharmacology · 2019Review
- Proteases: Pivot Points in Functional Proteomics.Methods in molecular biology (Clifton, N.J.) · 2019Review
- 5-oxoETE triggers nociception in constipation-predominant irritable bowel syndrome through MAS-related G protein-coupled receptor D.Science signaling · 2018Article
- Target-Directed Self-Assembly of Homodimeric Drugs Against β-Tryptase.ACS medicinal chemistry letters · 2018Article
- Potential Role of Cytochrome c and Tryptase in Psoriasis and Psoriatic Arthritis Pathogenesis: Focus on Resistance to Apoptosis and Oxidative Stress.Frontiers in immunology · 2018Review
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9 authors at 6 institutions in 3 countries.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundIncreasing evidences indicate that an unbalance between tryptases and their endogenous inhibitors, leading to an increased proteolytic activity, is implicated in the pathophysiology of rheumatoid arthritis. The aim of the present study was to evaluate the impact of tryptase inhibition on experimental arthritis.
methodsAnalysis of gene expression and regulation in the mouse knee joint was performed by RT-qPCR and in situ hybridization. Arthritis was induced in male C57BL/6 mice with mBSA/IL-1β. Tryptase was inhibited by two approaches: a lentivirus-mediated heterologous expression of the human endogenous tryptase inhibitor, sperm-associated antigen 11B isoform C (hSPAG11B/C), or a chronic treatment with the synthetic tryptase inhibitor APC366. Several inflammatory parameters were evaluated, such as oedema formation, histopathology, production of IL-1β, -6, -17A and CXCL1/KC, myeloperoxidase and tryptase-like activities.
resultsSpag11c was constitutively expressed in chondrocytes and cells from the synovial membrane in mice, but its expression did not change 7 days after the induction of arthritis, while tryptase expression and activity were upregulated. The intra-articular transduction of animals with the lentivirus phSPAG11B/C or the treatment with APC366 inhibited the increase of tryptase-like activity, the late phase of oedema formation, the production of IL-6 and CXCL1/KC. In contrast, neutrophil infiltration, degeneration of hyaline cartilage and erosion of subchondral bone were not affected.
conclusionsTryptase inhibition was effective in inhibiting some inflammatory parameters associated to mBSA/IL-1β-induced arthritis, notably late phase oedema formation and IL-6 production, but not neutrophil infiltration and joint degeneration. These results suggest that the therapeutic application of tryptase inhibitors to rheumatoid arthritis would be restrained to palliative care, but not as disease-modifying drugs. Finally, this study highlighted lentivirus-based gene delivery as an instrumental tool to study the relevance of target genes in synovial joint physiology and disease.
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