Prostaglandin E2 suppresses beta1-integrin expression via E-prostanoid receptor in human monocytes/macrophages

Cell Immunol. 2010;263(2):161-5. doi: 10.1016/j.cellimm.2010.03.010. Epub 2010 Mar 29.

Abstract

Beta1-integrins mediate cell attachment to different extracellular matrix proteins, intracellular proteins, and intercellular adhesions. Recently, it has been reported that prostaglandin E2 (PGE2) has anti-inflammatory properties such as inhibition of the expression of adhesion molecules or production of chemokines. However, the effect of PGE2 on the expression of beta1-integrin remains unknown. In this study, we investigated the effects of PGE2 on the expression of beta1-integrin in the human monocytic cell line THP-1 and in CD14+ monocytes/macrophages in human peripheral blood. For this, we examined the role of four subtypes of PGE2 receptors and E-prostanoid (EP) receptors on PGE2-mediated inhibition. We found that PGE2 significantly inhibited the expression of beta1-integrin, mainly through EP4 receptors in THP-1 cells and CD14+ monocytes/macrophages in human peripheral blood. We suggest that PGE2 has anti-inflammatory effects, leading to the inhibited expression of beta1-integrin in human monocytes/macrophages, and that the EP4 receptor may play an important role in PGE2-mediated inhibition.

MeSH terms

  • Blotting, Western
  • Cell Line, Tumor
  • Dinoprostone / pharmacology*
  • Gene Expression Regulation / drug effects*
  • Humans
  • Integrin beta1 / metabolism*
  • Macrophages / drug effects
  • Macrophages / immunology*
  • Monocytes / drug effects
  • Monocytes / immunology*
  • RNA, Messenger / metabolism
  • Receptors, Prostaglandin E / antagonists & inhibitors
  • Receptors, Prostaglandin E / metabolism*
  • Reverse Transcriptase Polymerase Chain Reaction

Substances

  • Integrin beta1
  • RNA, Messenger
  • Receptors, Prostaglandin E
  • Dinoprostone