Expression of G2A, a receptor for lysophosphatidylcholine, by macrophages in murine, rabbit, and human atherosclerotic plaques

Arterioscler Thromb Vasc Biol. 2002 Dec 1;22(12):2049-53. doi: 10.1161/01.atv.0000040598.18570.54.

Abstract

Objective: Lysophosphatidylcholine (LPC), a major phospholipid component of oxidized low density lipoprotein, has been demonstrated to induce multiple functional alterations of vasculature that are potentially involved in atherosclerosis. Recently, an orphan G-protein-coupled receptor, G2A, has been identified as a high-affinity receptor for LPC. Although it has been demonstrated that G2A is expressed predominantly in lymphoid tissues and lymphocytes, there are no reports to determine whether G2A is expressed in atherosclerotic lesions and cardiovascular cells.

Methods and results: Immunohistochemistry with an anti-G2A antibody revealed that G2A was expressed predominantly by macrophages within atherosclerotic lesions at the aortic root of apolipoprotein E-deficient mice and the thoracic aortas of Watanabe heritable hyperlipidemic rabbits. In atherosclerotic plaques of human coronary arterial specimens, G2A was expressed by macrophages within the lipid-rich plaques, whereas no immunoreactivity of G2A was observed in fibrous plaques where macrophages did not exist. Reverse transcription-polymerase chain reaction analysis demonstrated that G2A mRNA was highly expressed in human and murine monocytes/macrophages. The expression of G2A protein was detected in human and murine monocytes/macrophages by immunoblotting.

Conclusions: These findings demonstrate that monocytes/macrophages abundantly express G2A and suggest that G2A may play a role in the formation and progression of atherosclerotic lesions.

MeSH terms

  • Animals
  • Aorta, Thoracic / chemistry
  • Aorta, Thoracic / metabolism
  • Apolipoproteins E / deficiency
  • Cardiovascular System / metabolism
  • Cardiovascular System / pathology
  • Cell Cycle Proteins / biosynthesis*
  • Cell Cycle Proteins / immunology
  • Cell Cycle Proteins / metabolism*
  • Cells, Cultured
  • Coronary Artery Disease / metabolism*
  • Coronary Artery Disease / pathology
  • Coronary Vessels / chemistry
  • Coronary Vessels / metabolism
  • Coronary Vessels / pathology
  • Endothelium, Vascular / chemistry
  • Endothelium, Vascular / cytology
  • Endothelium, Vascular / pathology
  • Humans
  • Jurkat Cells / chemistry
  • Jurkat Cells / metabolism
  • Lysophosphatidylcholines / metabolism*
  • Macrophages / chemistry
  • Macrophages / metabolism*
  • Macrophages / pathology
  • Macrophages, Peritoneal / chemistry
  • Macrophages, Peritoneal / metabolism
  • Macrophages, Peritoneal / pathology
  • Mice
  • Mice, Knockout
  • Monocytes / chemistry
  • Monocytes / metabolism
  • Muscle, Smooth, Vascular / chemistry
  • Muscle, Smooth, Vascular / metabolism
  • Muscle, Smooth, Vascular / pathology
  • Rabbits
  • Receptors, Cell Surface / biosynthesis*
  • Receptors, Cell Surface / immunology
  • Receptors, Cell Surface / metabolism*
  • Receptors, G-Protein-Coupled*
  • Tumor Cells, Cultured
  • Umbilical Veins / chemistry
  • Umbilical Veins / metabolism
  • Umbilical Veins / pathology

Substances

  • Apolipoproteins E
  • Cell Cycle Proteins
  • G2A receptor
  • Lysophosphatidylcholines
  • Receptors, Cell Surface
  • Receptors, G-Protein-Coupled