Prostaglandin F amplifies tumor necrosis factor-α promoter activity by the FPB prostanoid receptor

Hiromichi Fujino, John W. Regan

Research output: Contribution to journalArticlepeer-review

6 Scopus citations


This study examines the regulation of tumor necrosis factor-α (TNF-α) promoter activity by prostaglandin F (PGF ) in HEK cells stably expressing either the FPA or FPB prostanoid receptors. Cells were transiently transfected with a luciferase reporter plasmid under the control of a TNF-α promoter and luciferase activity was measured. In the absence of PGF basal TNF-α reporter gene activity is elevated in FPB cells as compared with FPA cells. This elevated basal activity is blocked by pretreatment with a Rho inhibitor, but not by pretreatment with an inhibitor of protein kinase C (PKC). TNF-α reporter activity in FPB cells is stimulated by PGF and this is decreased by pretreatment with a chelator of intracellular calcium or by a gap junction inhibitor. In FP B cells pretreatment with a Rho inhibitor combined with either a calcium chelator or a gap junction inhibitor decreases both basal and PGF stimulated TNF-α reporter activity. Interestingly post-treatment of FPB cells with an inhibitor of PKC decreased PGF stimulated TNF-α reporter gene activity even though pretreatment did not. It, therefore, appears that PGF stimulated TNF-α reporter activity in FPB cells is amplified by a Rho-dependent mechanism involving calcium, gap junctions, and PKC. These findings may help in understanding the function of the FPB isoform in the corpus luteum.

Original languageEnglish (US)
Pages (from-to)1114-1120
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number4
StatePublished - May 14 2004


  • FP receptors
  • Gap junctions
  • Luteolysis
  • PGF
  • PKC
  • Rho
  • TNF-α

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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