DPPC regulates COX-2 expression in monocytes via phosphorylation of CREB.

R. H.K. Morris*, AJ Tonks, K. P. Jones, M. K. Ahluwalia, A. W. Thomas, A Tonks, S. K. Jackson

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

The major phospholipid in pulmonary surfactant dipalmitoyl phosphatidylcholine (DPPC) has been shown to modulate inflammatory responses. Using human monocytes, this study demonstrates that DPPC significantly increased PGE(2) (P<0.05) production by 2.5-fold when compared to untreated monocyte controls. Mechanistically, this effect was concomitant with an increase in COX-2 expression which was abrogated in the presence of a COX-2 inhibitor. The regulation of COX-2 expression was independent of NF-kappaB activity. Further, DPPC increased the phosphorylation of the cyclic AMP response element binding protein (CREB; an important nuclear transcription factor important in regulating COX-2 expression). In addition, we also show that changing the fatty acid groups of PC (e.g. using l-alpha-phosphatidylcholine beta-arachidonoyl-gamma-palmitoyl (PAPC)) has a profound effect on the regulation of COX-2 expression and CREB activation. This study provides new evidence for the anti-inflammatory activity of DPPC and that this activity is at least in part mediated via CREB activation of COX-2.
Original languageEnglish
Pages (from-to)174-178
Number of pages0
JournalBiochem Biophys Res Commun
Volume370
Issue number1
DOIs
Publication statusPublished - 23 May 2008

Keywords

  • 1
  • 2-Dipalmitoylphosphatidylcholine
  • Cells
  • Cultured
  • Cyclic AMP Response Element-Binding Protein
  • Cyclooxygenase 2
  • Dinoprostone
  • Humans
  • Monocytes
  • Phosphorylation
  • Pulmonary Surfactants

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