Two intracellular signaling pathways for activation of protein kinase C are involved in oxidized low-density lipoprotein-induced macrophage growth

Arterioscler Thromb Vasc Biol. 1997 Nov;17(11):3013-20. doi: 10.1161/01.atv.17.11.3013.

Abstract

Recent studies demonstrated that oxidized LDL (Ox-LDL) induces macrophage growth in vitro. The present study was undertaken to elucidate the intracellular signaling pathways for macrophage growth. Ox-LDL initiated a rapid and transient rise in intracellular free calcium ion and induced activation of membrane protein kinase C (PKC). Pertussis toxin completely inhibited the Ox-LDL-induced rise in free calcium ion and significantly inhibited macrophage growth by 50%. Moreover, PKC inhibitors calphostin C and H-7 significantly inhibited Ox-LDL-induced macrophage growth by 80%. On the other hand, phospholipase A2-treated acetylated LDL did not induce a rise in calcium but significantly activated PKC and led to significant macrophage growth that was significantly inhibited by calphostin C by 90%. These results suggest the presence of two intracellular signaling pathways for activation of PKC, a rise in calcium that was mediated by pertussis toxin-sensitive G protein and the internalization of lysophosphatidylcholine through the scavenger receptors. These two pathways may play an important role in Ox-LDL-induced macrophage growth.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / pharmacology
  • Animals
  • Calcium / physiology
  • Cell Division / drug effects
  • DNA Replication / drug effects
  • Enzyme Activation / drug effects
  • Enzyme Inhibitors / pharmacology
  • GTP-Binding Proteins / antagonists & inhibitors
  • GTP-Binding Proteins / physiology
  • Lipids / analysis
  • Lipoproteins, LDL / chemistry
  • Lipoproteins, LDL / drug effects
  • Lipoproteins, LDL / pharmacology*
  • Macrophages, Peritoneal / drug effects*
  • Macrophages, Peritoneal / enzymology
  • Male
  • Mice
  • Mice, Inbred C3H
  • Naphthalenes / pharmacology
  • Pertussis Toxin
  • Phospholipases A / pharmacology
  • Phospholipases A2
  • Protein Kinase C / metabolism*
  • Signal Transduction / physiology*
  • Virulence Factors, Bordetella / pharmacology

Substances

  • Enzyme Inhibitors
  • Lipids
  • Lipoproteins, LDL
  • Naphthalenes
  • Virulence Factors, Bordetella
  • acetyl-LDL
  • oxidized low density lipoprotein
  • 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
  • Pertussis Toxin
  • Protein Kinase C
  • Phospholipases A
  • Phospholipases A2
  • GTP-Binding Proteins
  • calphostin C
  • Calcium