Prostacyclin (PGI2): a potential mediator of c-fos expression induced by hydrostatic pressure in osteoblastic cells

Eur J Clin Invest. 1996 Jul;26(7):544-8. doi: 10.1046/j.1365-2362.1996.165312.x.

Abstract

Application of compressive forces to osteoblastic cells is known to cause specific cellular responses. We report that hydrostatic pressure increased c-fos mRNA expression in MC3T3-E1 cells after 15, 30 and 60 min. This effect was absent when 5 x 10(-7) mol L-1 indomethacin, an inhibitor of prostaglandin synthesis, was present in the culture medium during pressurization. Using radioimmunoassay, a significant increase in the concentrations of 6-keto-PGF1 alpha, the stable conversion product of prostacyclin (PGI2), in the conditioned medium of pressurized cells, was measured after 60 min. In contrast, PGE2 levels were not significantly changed and we therefore assume that under these experimental conditions PGE2 is not responsible for the transduction of the hydrostatic force. However, we also found that PGE2 has the capacity to induce c-fos mRNA in MC3T3-E1 cells. Furthermore, we show for the first time that the stable prostacyclin analogue, Iloprost-Trometamol (Ilomedin), is a potent activator of c-fos gene transcription. Our data suggest that prostacyclin is a likely candidate in mediating the effect of hydrostatic compressive stress on bone cells by regulating the level of c-fos mRNA, a member of the activator protein (AP-1) complex and potent regulator of osteoblastic proliferation and differentiation.

MeSH terms

  • 3T3 Cells
  • 6-Ketoprostaglandin F1 alpha / metabolism
  • Animals
  • Biomechanical Phenomena
  • Dinoprostone / metabolism
  • Epoprostenol / metabolism*
  • Gene Expression
  • Genes, fos*
  • Hydrostatic Pressure
  • Mice
  • Osteoblasts / metabolism*
  • Osteoblasts / physiology
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Stress, Mechanical

Substances

  • RNA, Messenger
  • 6-Ketoprostaglandin F1 alpha
  • Epoprostenol
  • Dinoprostone