Elsevier

Metabolism

Volume 45, Issue 5, May 1996, Pages 559-564
Metabolism

Lysophosphatidylcholine stimulates the expression and production of MCP-1 by human vascular endothelial cells

https://doi.org/10.1016/S0026-0495(96)90024-4Get rights and content

Abstract

Lysophosphatidylcholine (LPC) increased monocyte chemoattractant protein-1 (MCP-1) messenger RNA concentrations in human umbilical vein endothelial cells (HUVECs). A time-course study showed that the increase in MCP-1 mRNA levels peaked at 6 hours after treatment with LPC. The effect of LPC on the accumulation of MCP-1 mRNA levels in HUVECs depended on LPC concentration, and the maximal effect was obtained at 50 μmol/L LPC, which induced a sixfold increase in MCP-1 mRNA levels. The amount of MCP-1 released from HUVECs measured using an enzyme-linked immunosorbent assay (ELISA) showed a 38% increase in the presence of 50 μmol/L LPC, but not in the presence of phosphatidylcholine or lysophosphatidylethanolamine. Coincubation with staurosporine, a potent inhibitor of protein kinase C (PKC) activity, attenuated the LPC-induced increase in MCP-1 mRNA levels by 53%. These results indicate that LPC can induce an increase in MCP-1 mRNA concentrations and stimulate the release of MCP-1 protein from HUVECs, and that the effect of LPC on the MCP-1 gene may be mediated through activation of the PKC pathway.

References (31)

  • RG Gerrity

    The role of the monocyte in atherogenesis. I. Transition of blood-borne monocyte into foam cells in fatty lesions

    Am J Pathol

    (1981)
  • BJ Rollins et al.

    Cytokine-activated human endothelial cells synthesize and secrete a monocyte chemoattractant, MCP-1/JE

    Am J Pathol

    (1990)
  • NA Nelken et al.

    Monocyte chemoattractant protein-1 in human atheromatous plaques

    J Clin Invest

    (1991)
  • X Yu et al.

    Elevated expression of monocyte chemoattractant protein 1 by vascular smooth muscle cells in hypercholesterolemic primates

  • D Steinberg et al.

    Modifications of low-density lipoprotein that increase its atherogenicity

    N Engl J Med

    (1989)
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