Antiproliferative action of protein kinase C in cultured rabbit aortic smooth muscle cells

Exp Cell Res. 1987 Dec;173(2):504-14. doi: 10.1016/0014-4827(87)90290-4.

Abstract

In rabbit aortic smooth muscle cells (SMC), protein kinase C-activating 12-O-tetradecanoylphorbol-13-acetate (TPA) inhibited the whole blood serum (WBS)-induced DNA synthesis. The inhibitory action of TPA was mimicked by another protein kinase C-activating phorbol ester, phorbol-12,13-dibutyrate (PDBu), but not by 4 alpha-phorbol-12,13- didecanoate known to be inactive for this enzyme. Prolonged treatment of the cells with PDBu caused the down-regulation of protein kinase C. In these cells, WBS still induced DNA synthesis but the inhibitory action of TPA was abolished. DNA synthesis started at 18 h and reached a maximal level 24 h after the addition of WBS. TPA inhibited the WBS-induced DNA synthesis even when added 12 h after the addition of WBS. These results suggest that protein kinase C has an antiproliferative action in rabbit aortic SMC and that this action is attributed to the inhibition of the progression from the late G1 into S phase of the cell cycle. TPA also inhibited the phospholipase C-mediated hydrolysis of phosphoinositides which was induced by WBS within several minutes, but the relevance of this effect on the antiproliferative action of TPA is uncertain.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Aorta, Thoracic
  • Cell Division / drug effects*
  • Cells, Cultured
  • Hydrolysis
  • Interphase / drug effects
  • Male
  • Muscle, Smooth / cytology*
  • Muscle, Smooth / drug effects
  • Muscle, Smooth / metabolism
  • Phosphatidylinositols / blood
  • Protein Kinase C / blood
  • Protein Kinase C / metabolism
  • Protein Kinase C / pharmacology*
  • Rabbits
  • Tetradecanoylphorbol Acetate / antagonists & inhibitors
  • Tetradecanoylphorbol Acetate / pharmacology

Substances

  • Phosphatidylinositols
  • Protein Kinase C
  • Tetradecanoylphorbol Acetate