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Apolipoprotein CIII-induced THP-1 cell adhesion to endothelial cells involves pertussis toxin-sensitive G protein-

Akio Kawakami1, Masanori Aikawa, Noriko Nitta

  • 1Department of Nutrition, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115, USA.

Arteriosclerosis, Thrombosis, and Vascular Biology
|October 14, 2006
PubMed

Insights

Plasma apolipoprotein CIII (apoCIII) activates protein kinase C alpha (PKC alpha) in monocytes, leading to NF-kappaB activation and increased cell adhesion. This pathway contributes to inflammatory responses in atherosclerosis.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Cellular Signaling

Background:

  • Plasma apolipoprotein CIII (apoCIII) is an independent predictor of coronary heart disease (CHD).
  • Previous research indicated apoCIII enhances monocyte adhesion to endothelial cells (ECs) via protein kinase C alpha (PKC alpha) activation.

Purpose of the Study:

  • To investigate the hypothesis that apoCIII activates PKC alpha in human monocytic THP-1 cells.
  • To determine if this activation leads to nuclear factor-kappaB (NF-kappaB) activation.

Main Methods:

  • Utilized phosphatidylcholine-specific phospholipase C (PC-PLC) inhibitor D609 and pertussis toxin (PTX) to assess signaling pathways.
  • Measured PKC alpha activation, PC-PLC activity, NF-kappaB activation, and beta1-integrin expression in THP-1 cells.
  • Exposed cells to apoCIII and apoCIII-rich very-low-density lipoprotein (VLDL).

Main Results:

  • ApoCIII increased PC-PLC activity, leading to PKC alpha activation in THP-1 cells.
  • PTX-sensitive G protein pathways were implicated in apoCIII-induced PC-PLC and PKC alpha activation.
  • ApoCIII activated NF-kappaB through PKC alpha, augmenting beta1-integrin expression and enhancing THP-1 cell adhesion to ECs.

Conclusions:

  • A PTX-sensitive G protein pathway is critical for apoCIII-mediated PKC alpha stimulation in monocytes.
  • This pathway activates NF-kappaB and increases beta1-integrin, promoting monocyte adhesion to ECs.
  • ApoCIII may drive diverse inflammatory responses in atherogenesis through monocyte activation.
Abstract

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