Effect of bradykinin on loss of density-dependent growth inhibition of normal rat kidney cells

Cell Mol Biol (Noisy-le-grand). 1994 Jul;40(5):717-21.

Abstract

Normal rat kidney fibroblasts, density-arrested in the presence of epidermal growth factor (EGF), can be restimulated to proliferate in a synchronous way and acquire a transformed phenotype following treatment with additional growth factors like retinoic acid (RA) and transforming growth factor (TGF)-beta. It was found that bradykinin has a strong inhibitory effect on growth stimulation induced by these factors, an effect which cannot be mimicked by PGF2 alpha. The growth-inhibiting effect can be blocked by inhibitors of cyclo-oxygenase activity, indicating that the relevant second messenger is most likely a prostaglandin. Externally added PGJ2, at a concentration of 10 microM, can mimic the inhibitory effect of bradykinin on the loss of density-arrest induced by RA suggesting that PGJ2 is a possible candidate for being the bradykinin induced growth-inhibiting prostaglandin.

MeSH terms

  • Animals
  • Bradykinin / pharmacology*
  • Cell Count
  • Cell Division / drug effects
  • Clone Cells
  • Cyclooxygenase Inhibitors / pharmacology
  • Dinoprost / pharmacology
  • Epidermal Growth Factor / pharmacology
  • Kidney / cytology
  • Kidney / drug effects*
  • Prostaglandin D2 / analogs & derivatives
  • Prostaglandin D2 / pharmacology
  • Prostaglandins / pharmacology
  • Rats
  • Receptors, Bradykinin / drug effects
  • Transforming Growth Factor beta / pharmacology
  • Tretinoin / pharmacology

Substances

  • Cyclooxygenase Inhibitors
  • Prostaglandins
  • Receptors, Bradykinin
  • Transforming Growth Factor beta
  • Tretinoin
  • 9-deoxy-delta-9-prostaglandin D2
  • Epidermal Growth Factor
  • Dinoprost
  • Prostaglandin D2
  • Bradykinin