Dexamethasone fails to inhibit the induction of cytosolic phospholipase A2 expression by interleukin-1β in cultured primary human amnion fibroblasts

K. Sun, X. Qu, L. Gao, L. Myatt

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Objective: To investigate the interaction of dexamethasone and interleukin-1β (IL-1β) on the expression of cytosolic phospholipase A2 (cPLA2), the enzyme catalyzing the first reaction in the formation of prostaglandins, in cultured primary human amnion fibroblasts. Design and methods: Human amnion fibroblasts were prepared from fetal amnion collected at term and were treated with dexamethasone with or without interleukin-1β for 24 h. Prostaglandin E2 (PGE2) output and cPLA2 expression in cultured amnion fibroblasts were measured with radioimmunoassay, quantitative real-time polymerase chain reaction, Western blotting and cPLA2 promoter-driven luciferase reporter gene activity. Results: Both dexamethasone and IL-1β caused a significant increase in prostaglandin E2 output, cPLA2 mRNA and protein expression in cultured human amnion fibroblasts. Both dexamethasone and IL-1β stimulated cPLA2 promoter-driven luciferase reporter gene activity. There was no obvious antagonistic or synergistic effect of combined treatment of dexamethasone and IL-1β on PGE2 output, cPLA2 expression or cPLA2 promoter-driven luciferase reporter gene activity in cultured human amnion fibroblasts. Conclusion: The above findings suggest that paradoxically dexamethasone is a stimulator for both prostaglandin synthesis and cPLA2 expression in human amnion fibroblasts. The interaction between dexamethasone and IL-1β on prostaglandin synthesis and cPLA2 expression is neither synergistic nor conventionally antagonistic.

Original languageEnglish (US)
Pages (from-to)164-170
Number of pages7
JournalPlacenta
Volume27
Issue number2-3
DOIs
StatePublished - Feb 2006
Externally publishedYes

Fingerprint

Cytosolic Phospholipases A2
Amnion
Interleukin-1
Dexamethasone
Fibroblasts
Luciferases
Reporter Genes
Dinoprostone
Prostaglandins
Radioimmunoassay
Real-Time Polymerase Chain Reaction
Western Blotting

Keywords

  • Amnion
  • Glucocorticoids
  • Parturition
  • Proinflammatory cytokines
  • Prostaglandins

ASJC Scopus subject areas

  • Obstetrics and Gynecology

Cite this

Dexamethasone fails to inhibit the induction of cytosolic phospholipase A2 expression by interleukin-1β in cultured primary human amnion fibroblasts. / Sun, K.; Qu, X.; Gao, L.; Myatt, L.

In: Placenta, Vol. 27, No. 2-3, 02.2006, p. 164-170.

Research output: Contribution to journalArticle

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N2 - Objective: To investigate the interaction of dexamethasone and interleukin-1β (IL-1β) on the expression of cytosolic phospholipase A2 (cPLA2), the enzyme catalyzing the first reaction in the formation of prostaglandins, in cultured primary human amnion fibroblasts. Design and methods: Human amnion fibroblasts were prepared from fetal amnion collected at term and were treated with dexamethasone with or without interleukin-1β for 24 h. Prostaglandin E2 (PGE2) output and cPLA2 expression in cultured amnion fibroblasts were measured with radioimmunoassay, quantitative real-time polymerase chain reaction, Western blotting and cPLA2 promoter-driven luciferase reporter gene activity. Results: Both dexamethasone and IL-1β caused a significant increase in prostaglandin E2 output, cPLA2 mRNA and protein expression in cultured human amnion fibroblasts. Both dexamethasone and IL-1β stimulated cPLA2 promoter-driven luciferase reporter gene activity. There was no obvious antagonistic or synergistic effect of combined treatment of dexamethasone and IL-1β on PGE2 output, cPLA2 expression or cPLA2 promoter-driven luciferase reporter gene activity in cultured human amnion fibroblasts. Conclusion: The above findings suggest that paradoxically dexamethasone is a stimulator for both prostaglandin synthesis and cPLA2 expression in human amnion fibroblasts. The interaction between dexamethasone and IL-1β on prostaglandin synthesis and cPLA2 expression is neither synergistic nor conventionally antagonistic.

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