ArticleAnnals of the rheumatic diseases1998
Effects of induced mast cell activation on prostaglandin E and metalloproteinase production by rheumatoid synovial tissue in vitro.
Article in Annals of the rheumatic diseases, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 38 citations in OpenAlex.
- Roles of mast cells in rheumatoid arthritis.The Korean journal of internal medicine · 2020Review
- Vascular Contributions to Migraine: Time to Revisit?Frontiers in cellular neuroscience · 2018Article
- Simulated airplane headache: a proxy towards identification of underlying mechanisms.The journal of headache and pain · 2017Article
- Mast cells as early responders in the regulation of acute blood-brain barrier changes after cerebral ischemia and hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2010Review
- A role for type 1alpha corticotropin-releasing hormone receptors in mediating local changes in chronically inflamed tissue.The American journal of pathology · 2007Article
- Revisiting immunosurveillance and immunostimulation: Implications for cancer immunotherapy.Journal of translational medicine · 2005Article
- Mast cell activation and its relation to proinflammatory cytokine production in the rheumatoid lesion.Arthritis research · 2000Article
- Mast cells as a target in the treatment of rheumatoid arthritis.Inflammopharmacology · 1999Article
- The effects of 1 alpha,25-dihydroxyvitamin D(3) on matrix metalloproteinase and prostaglandin E(2) production by cells of the rheumatoid lesion.Arthritis research · 1999Article
- Synovial mast cell responses during clinical improvement in early rheumatoid arthritis.Annals of the rheumatic diseases · 1998Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo determine whether induced mast cell activation/degranulation in rheumatoid synovial explants modulates the production of prostaglandin E (PGE2), and the matrix metalloproteinases (MMPs) collagenase 1, gelatinase A, and stromelysin 1.
methodsSynovial explant cultures were treated either with rabbit IgG anti-human IgE as a mast cell (MC) secretagogue or with non-immune rabbit IgG as controls. After 20 hours conditioned medium was assayed for the release of MC tryptase, PGE2, collagenase 1, gelatinase A, and stromelysin 1 using radioimmunoassay, enzyme linked immunosorbent assay, western blot, and zymogram techniques; tissue explants were examined immunohistologically for the relative distributions of MC tryptase, collagenase 1, and stromelysin 1.
resultsOver a 20 hour incubation period the MC secretagogue treated explants showed a significant increase in the quantities of released tryptase and PGE2 compared with controls. By contrast, the three MMPs showed variable values between experiments in response to MC activation; no reproducible trend of either an increased or decreased production of each MMP over control values was evident. Each MMP initially appeared as an inactive precursor form; collagenase 1 and stromelysin 1 were more effectively processed to active forms in the MC activated cultures. Immunolocalisation studies of MC activated explants showed that areas of extracellular tryptase were commonly associated with the local production of both collagenase 1 and stromelysin 1.
conclusionMC degranulation induced artificially in rheumatoid synovial explant cultures consistently resulted in an increased production of PGE2 but had variable effects on the quantification of released collagenase 1, gelatinase A, and stromelysin 1. Such observations support the concept that activated synovial MCs within their native environment stimulate the production of non-MC derived PGE2 and may contribute to the regulation and processing of specific MMPs; both aspects represent important components of the inflammatory and degradative processes of the rheumatoid lesion.
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