Phorbol esters inhibit low density lipoprotein processing by cultured human fibroblasts

FEBS Lett. 1986 Jan 20;195(1-2):135-9. doi: 10.1016/0014-5793(86)80147-8.

Abstract

A 24 h pretreatment of MRC5 fibroblasts with the protein kinase C activator 12-O-tetradecanoylphorbol 13-acetate (TPA) induced a marked decrease in low density lipoprotein (LDL) internalization and degradation; the maximal effect (about 55% decrease) was observed for 10(-7) M TPA. LDL binding was reduced about 35-40%. A significant decrease (about 25%) in LDL internalization was observed after a 2 h incubation of cells with the drug, but longer incubation times (4-6 h) led to a greater effect. Another tumor promoter, phorbol 12,13-dibutyrate decreased LDL internalization by about 35%, whereas the non-tumor promoting 4 alpha-phorbol 12,13-didecanoate had no effect. The protein kinase C inhibitor alpha-cobrotoxin partially antagonized the inhibitory effect of TPA on LDL internalization. The non-phorbol tumor promoter mezerein, another protein kinase C activator, decreased LDL uptake by about 50%. Finally, it was found that TPA had no significant effect on the affinity of the receptor for the LDL. These results suggest a role for protein kinase C in the LDL pathway in cultured human fibroblasts.

MeSH terms

  • Cell Line
  • Cobra Neurotoxin Proteins / pharmacology
  • Diterpenes*
  • Endocytosis / drug effects
  • Fibroblasts / metabolism
  • Humans
  • Lipoproteins, LDL / metabolism*
  • Phorbol Esters / pharmacology*
  • Receptors, LDL / drug effects
  • Receptors, LDL / metabolism
  • Terpenes / pharmacology

Substances

  • Cobra Neurotoxin Proteins
  • Diterpenes
  • Lipoproteins, LDL
  • Phorbol Esters
  • Receptors, LDL
  • Terpenes
  • mezerein