Retinoic acid regulates differentially the expression of IL-1 beta and IL-1 receptor antagonist (IL-1ra) in PMA-activated human monocytes

Biochem Biophys Res Commun. 1996 Jul 16;224(2):574-8. doi: 10.1006/bbrc.1996.1066.

Abstract

Retinoic acid (RA) is a well-known immunological modulator. Although it has been shown that RA stimulates IL-1 expression in monocytes, it is of interest for understanding of the regulatory role of RA in inflammation to examine whether RA also modulates the expression of the IL-1 receptor antagonist (IL-1ra), which is reported to reduce IL-1 beta-mediated inflammation. In this study, we examined the effect of RA on expression of IL-1 beta and IL-ra in phorbol-myristate-acetate (PMA)-activated human monocytes. RA enhanced gene expression and production of IL-1 beta in PMA-activated monocytes. However, interestingly, gene expression and production of IL-1ra in the cells were markedly inhibited by RA. These results show that RA differentially regulates IL-1 beta and IL-ra expression in PMA-activated human monocytes and suggest that RA may promote IL-1-mediated inflammation.

Publication types

  • Comparative Study

MeSH terms

  • Blotting, Northern
  • Cells, Cultured
  • Gene Expression Regulation / drug effects*
  • Humans
  • Interleukin 1 Receptor Antagonist Protein
  • Interleukin-1 / biosynthesis*
  • Interleukin-1 / blood
  • Kinetics
  • Monocytes / drug effects
  • Monocytes / immunology*
  • Sialoglycoproteins / biosynthesis*
  • Sialoglycoproteins / blood
  • Tetradecanoylphorbol Acetate / pharmacology*
  • Time Factors
  • Transcription, Genetic / drug effects*
  • Tretinoin / pharmacology*

Substances

  • IL1RN protein, human
  • Interleukin 1 Receptor Antagonist Protein
  • Interleukin-1
  • Sialoglycoproteins
  • Tretinoin
  • Tetradecanoylphorbol Acetate