Differential effects of 1,25-(OH)2D3 on acyl hydrolase and cycloxygenase activities in interleukin 1β-stimulated human synovial fibroblast cultures

F. A. Meyer; I. Yaron; N. Kamin-Belsky; M. Yaron; A. Raz

doi:10.1016/S0952-3278(96)90097-6

Differential effects of 1,25-(OH)₂D₃ on acyl hydrolase and cycloxygenase activities in interleukin 1β-stimulated human synovial fibroblast cultures

F. A. Meyer, I. Yaron, N. Kamin-Belsky, M. Yaron^*, A. Raz

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

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Abstract

Effects of proinflammatory cytokines on synovial fibroblasts are considered to play a role in the accumulation of prostaglandin E₂ (PGE₂) in the inflamed joint in rheumatoid arthritis. We have previously shown that interleukin 1β (IL-1β) induces PGE₂ production in synovial fibroblast cultures and that this effect is suppressed by the active metabolite of vitamin D3, 1,25-(OH)₂D₃. To study the mechanism of the inhibitory action of 1,25-(OH)₂D₃, its effect on acyl hydrolase (arachidonic acid (AA) release) and cyclooxygenase (COX) activities were investigated. Our findings indicate that IL-1β caused an increase in AA release and COX activity and that in the presence of 1,25(OH)₂D₃ AA release, but not COX activity, is suppressed. In comparison, dexamethasone, which also inhibits IL-1β induction of PGE₂, had inhibitory effects on both parameters.

Original language	English
Pages (from-to)	191-194
Number of pages	4
Journal	Prostaglandins Leukotrienes and Essential Fatty Acids
Volume	55
Issue number	3
DOIs	https://doi.org/10.1016/S0952-3278(96)90097-6
State	Published - Sep 1996

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title = "Differential effects of 1,25-(OH)2D3 on acyl hydrolase and cycloxygenase activities in interleukin 1β-stimulated human synovial fibroblast cultures",

abstract = "Effects of proinflammatory cytokines on synovial fibroblasts are considered to play a role in the accumulation of prostaglandin E2 (PGE2) in the inflamed joint in rheumatoid arthritis. We have previously shown that interleukin 1β (IL-1β) induces PGE2 production in synovial fibroblast cultures and that this effect is suppressed by the active metabolite of vitamin D3, 1,25-(OH)2D3. To study the mechanism of the inhibitory action of 1,25-(OH)2D3, its effect on acyl hydrolase (arachidonic acid (AA) release) and cyclooxygenase (COX) activities were investigated. Our findings indicate that IL-1β caused an increase in AA release and COX activity and that in the presence of 1,25(OH)2D3 AA release, but not COX activity, is suppressed. In comparison, dexamethasone, which also inhibits IL-1β induction of PGE2, had inhibitory effects on both parameters.",

author = "Meyer, {F. A.} and I. Yaron and N. Kamin-Belsky and M. Yaron and A. Raz",

year = "1996",

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AU - Meyer, F. A.

AU - Yaron, I.

AU - Kamin-Belsky, N.

AU - Yaron, M.

AU - Raz, A.

PY - 1996/9

Y1 - 1996/9

N2 - Effects of proinflammatory cytokines on synovial fibroblasts are considered to play a role in the accumulation of prostaglandin E2 (PGE2) in the inflamed joint in rheumatoid arthritis. We have previously shown that interleukin 1β (IL-1β) induces PGE2 production in synovial fibroblast cultures and that this effect is suppressed by the active metabolite of vitamin D3, 1,25-(OH)2D3. To study the mechanism of the inhibitory action of 1,25-(OH)2D3, its effect on acyl hydrolase (arachidonic acid (AA) release) and cyclooxygenase (COX) activities were investigated. Our findings indicate that IL-1β caused an increase in AA release and COX activity and that in the presence of 1,25(OH)2D3 AA release, but not COX activity, is suppressed. In comparison, dexamethasone, which also inhibits IL-1β induction of PGE2, had inhibitory effects on both parameters.

AB - Effects of proinflammatory cytokines on synovial fibroblasts are considered to play a role in the accumulation of prostaglandin E2 (PGE2) in the inflamed joint in rheumatoid arthritis. We have previously shown that interleukin 1β (IL-1β) induces PGE2 production in synovial fibroblast cultures and that this effect is suppressed by the active metabolite of vitamin D3, 1,25-(OH)2D3. To study the mechanism of the inhibitory action of 1,25-(OH)2D3, its effect on acyl hydrolase (arachidonic acid (AA) release) and cyclooxygenase (COX) activities were investigated. Our findings indicate that IL-1β caused an increase in AA release and COX activity and that in the presence of 1,25(OH)2D3 AA release, but not COX activity, is suppressed. In comparison, dexamethasone, which also inhibits IL-1β induction of PGE2, had inhibitory effects on both parameters.

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Differential effects of 1,25-(OH)₂D₃ on acyl hydrolase and cycloxygenase activities in interleukin 1β-stimulated human synovial fibroblast cultures

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