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Lysophosphatidylcholine transduces Ca2+ signaling via the platelet-activating factor receptor in macrophages

T Ogita1, Y Tanaka, T Nakaoka

  • 1Fourth Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.

The American Journal of Physiology
|January 1, 1997
PubMed

Insights

Lysophosphatidylcholine (LPC) triggers calcium signaling in macrophages via the platelet-activating factor (PAF) receptor. This signaling pathway, distinct from cell lysis, is crucial for understanding atherosclerosis development.

Area of Science:

  • Molecular Biology
  • Cell Signaling
  • Immunology

Background:

  • Lysophosphatidylcholine (LPC) is implicated in cellular signaling pathways.
  • The precise molecular mechanisms of LPC signaling require further elucidation.

Purpose of the Study:

  • To investigate the effect of LPC on intracellular calcium concentration ([Ca2+]i) in macrophages.
  • To determine the specific receptor and pathway involved in LPC-mediated calcium signaling.

Main Methods:

  • Murine peritoneal macrophages were used to study LPC's effect on [Ca2+]i.
  • Experiments involved LPC with and without cholesterol, and the use of WEB-2086, a PAF receptor antagonist.
  • Cloned PAF receptors in Chinese hamster ovary cells were utilized to confirm the signaling pathway.

Main Results:

  • LPC alone induced a biphasic elevation of [Ca2+]i (rapid increase followed by sustained elevation).
  • Cholesterol co-administration abolished the sustained [Ca2+]i elevation, and the rapid increase was blocked by WEB-2086.
  • LPC-induced [Ca2+]i elevation was dependent on PAF receptor expression and blocked by WEB-2086.

Conclusions:

  • LPC transduces calcium signaling specifically through the platelet-activating factor (PAF) receptor.
  • LPC activation of the PAF receptor represents a novel mechanism potentially involved in atherosclerosis pathogenesis.

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