Peripheral blood mononuclear cells stimulate prostacyclin levels of human synovial fibroblast-like cells

Fibroblast-like synovial cells, isolated from intact joints of non-arthritic human donors and from explants of rheumatoid and non-rheumatoid synovial tissue, released prostacyclin (PGI2) when incubated in conditioned medium from human peripheral blood mononuclear cells (MCCM). The effect of MCCM on...

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Bibliographic Details
Published in:Rheumatology international 1985-01, Vol.5 (3), p.121-125
Main Authors: Hamilton, J A, Clarris, B J, Fraser, J R, Niall, M C
Format: Article
Language:English
Subjects:
6-Ketoprostaglandin F1 alpha - analysis
Arthritis, Rheumatoid - metabolism
Cell Line
Culture Media
Cycloheximide - pharmacology
Dactinomycin - pharmacology
Dexamethasone - pharmacology
Dinoprostone
Epoprostenol - biosynthesis
Humans
Kinetics
Leukocytes - physiology
Prostaglandins E - biosynthesis
Radioimmunoassay
Synovial Membrane - cytology
Synovial Membrane - metabolism
Tretinoin - pharmacology
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Summary:Fibroblast-like synovial cells, isolated from intact joints of non-arthritic human donors and from explants of rheumatoid and non-rheumatoid synovial tissue, released prostacyclin (PGI2) when incubated in conditioned medium from human peripheral blood mononuclear cells (MCCM). The effect of MCCM on the rate of PGI2 synthesis (measured by radioimmunoassay as the stable product, 6-keto-PGF1 alpha) was clearly established within 2 h and appeared to require RNA and protein synthesis as judged by inhibition with actinomycin D and cycloheximide, respectively. Low concentrations of dexamethasone suppressed the increase in PGI2 levels. Prostaglandin E2 (PGE2) levels were also raised by the MCCM and reduced by dexamethasone. All-trans retinoic acid did not stimulate the levels of either prostanoid. These findings offer an explanation for some of the inflammatory events occurring in rheumatoid lesions.
ISSN:0172-8172
1437-160X
DOI:10.1007/BF00541331