Regulation of interleukin-1 and tumor necrosis factor-alpha induced granulocyte-macrophage colony-stimulating factor gene expression: potential involvement of arachidonic acid metabolism

Exp Hematol. 1994 Jan;22(1):87-94.

Abstract

Signal transduction pathways evoked by interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha) to stimulate expression of other cytokines in mesenchymal cells are not clearly understood. Stimulation of the murine bone marrow stromal cell line +/(+)-1.LDA 11 with IL-1 (500 U/ml) in combination with TNF-alpha (500 U/ml) (IL-1 plus TNF-alpha) induced expression of c-jun mRNA as well as granulocyte-macrophage colony stimulating factor (GM-CSF) mRNA. We investigated the possibility that arachidonic acid metabolites, acting through protein kinase C (PKC) and perhaps also through the PKC-responsive transcription factor c-jun/AP-1, may be responsible for regulating GM-CSF transcription in these stromal cells. Expression of GM-CSF mRNA was preceded by IL-1 plus TNF-alpha induced arachidonate release (assayed using the 3H-derivative). Pretreatment of cells with the phospholipase A2 inhibitor quinacrine (20 microM) inhibited accumulation of both c-jun and GM-CSF mRNA but had no influence on expression of other genes induced by IL-1 and TNF-alpha, including leukemia inhibitory factor (LIF). In addition, quinacrine partially blocked IL-1 plus TNF-alpha induced 3H-arachidonic acid release from prelabeled stromal cells. Furthermore, exogenous arachidonate (10 to 50 microM) induced expression of c-jun. To investigate the role of arachidonate in GM-CSF transcription, we used a reporter vector consisting of the murine GM-CSF promoter linked to firefly luciferase. Transfection efficiency was monitored by assessing expression of a constitutively active gene, RSV-beta galactosidase. In this system, quinacrine significantly inhibited IL-1 plus TNF-alpha induced GM-CSF transcription assayed with the reporter construct. Exogenous arachidonic acid alone (10 microM) increased activity of GM-CSF reporter vector 1.5-fold over control. These results are consistent with the hypothesis that arachidonate metabolites are involved in the signaling pathway that leads to IL-1 plus TNF-alpha induced GM-CSF gene expression. Thus, transcriptional activation of GM-CSF gene is mediated, in part, by the arachidonate cascade.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Arachidonic Acids / metabolism*
  • Arachidonic Acids / physiology
  • Blotting, Northern
  • Bone Marrow / drug effects
  • Bone Marrow / metabolism
  • Bone Marrow Cells
  • Cell Line
  • Dose-Response Relationship, Drug
  • Gene Expression Regulation / genetics*
  • Gene Expression Regulation / physiology*
  • Genetic Vectors
  • Granulocyte-Macrophage Colony-Stimulating Factor / genetics*
  • Granulocyte-Macrophage Colony-Stimulating Factor / metabolism
  • Humans
  • Interleukin-1 / pharmacology*
  • Mice
  • Protein Kinase C / metabolism
  • Proto-Oncogene Proteins c-jun / analysis
  • Proto-Oncogene Proteins c-jun / genetics
  • Proto-Oncogene Proteins c-jun / metabolism
  • Quinacrine / pharmacology
  • RNA, Messenger / analysis
  • RNA, Messenger / genetics
  • Signal Transduction / physiology
  • Transcription, Genetic
  • Transfection
  • Tritium
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Arachidonic Acids
  • Interleukin-1
  • Proto-Oncogene Proteins c-jun
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Tritium
  • Granulocyte-Macrophage Colony-Stimulating Factor
  • Protein Kinase C
  • Quinacrine