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The role of junctional adhesion molecule-C (JAM-C) in oxidized LDL-mediated leukocyte recruitment

Tanja Keiper1, Nadia Al-Fakhri, Emmanouil Chavakis

  • 1Experimental Immunology Branch, NCI, NIH, Bethesda, Maryland 20892, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|October 1, 2005
PubMed

Insights

Junctional adhesion molecule-C (JAM-C) increases with oxidized LDL, promoting leukocyte adhesion and migration in atherosclerosis. Targeting JAM-C may offer a new therapeutic strategy for vascular inflammation.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Cell Biology

Background:

  • Junctional adhesion molecule-C (JAM-C) acts as a counter receptor for leukocyte Mac-1, mediating vascular cell interactions.
  • Inflammatory cell recruitment is crucial in atherosclerosis development.
  • The role of JAM-C in oxidized low-density lipoprotein (oxLDL)-induced leukocyte recruitment remains to be fully elucidated.

Purpose of the Study:

  • To investigate the role of JAM-C in oxLDL-mediated leukocyte recruitment in atherosclerosis.
  • To determine how oxLDL affects JAM-C expression and localization in vascular cells.

Main Methods:

  • Immunostaining of atherosclerotic human arteries and mouse lesions.
  • In vitro studies using cultured human arterial smooth muscle cells (HASMC) and endothelial cells.
  • Treatment with oxLDL and enzymatically modified LDL (eLDL).
  • Analysis of JAM-C localization and function in leukocyte adhesion and transmigration.

Main Results:

  • JAM-C expression is elevated in atherosclerotic vessels and early lesions in ApoE-/- mice.
  • OxLDL and eLDL up-regulate JAM-C expression in HASMC and endothelial cells in a time- and dose-dependent manner.
  • OxLDL treatment disrupts JAM-C localization at endothelial cell-cell junctions.
  • Endothelial JAM-C mediates both leukocyte adhesion and transmigration upon oxLDL stimulation.

Conclusions:

  • JAM-C is up-regulated by oxLDL, contributing to increased inflammatory cell recruitment in atherosclerosis.
  • Endothelial JAM-C acts as both an adhesion and transmigration receptor for leukocytes following oxLDL stimulation.
  • JAM-C represents a potential molecular target for therapeutic intervention in atherosclerosis.

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