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Differential regulation of transendothelial migration of THP-1 cells by ICAM-1/LFA-1 and VCAM-1/VLA-4

J A Ronald1, C V Ionescu, K A Rogers

  • 1Department of Anatomy and Cell Biology, The University of Western Ontario, London, Ontario, Canada.

Journal of Leukocyte Biology
|October 9, 2001
PubMed

Insights

Blocking vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) differentially impacts monocyte adhesion and migration in atherosclerosis models. Simultaneous blockade is crucial for reducing monocyte diapedesis.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Cellular Biology

Background:

  • Atherogenesis involves monocyte recruitment into lesions.
  • Intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) are implicated in monocyte adhesion.
  • Their precise roles in monocyte diapedesis remain unclear.

Purpose of the Study:

  • To elucidate the distinct functions of ICAM-1 and VCAM-1 in monocyte diapedesis.
  • To investigate the effects of blocking these molecules on monocyte morphology, motility, and transmigration.

Main Methods:

  • Utilized a human coronary artery endothelial cell and THP-1 cell co-culture model.
  • Employed function-blocking antibodies against ICAM-1 and VCAM-1.
  • Assessed THP-1 cell morphology, motility, and diapedesis.

Main Results:

  • VCAM-1 blockade alone or with ICAM-1 blockade reduced the number of motile THP-1 cells.
  • Simultaneous blockade of ICAM-1 and VCAM-1 was necessary to significantly reduce diapedesis.
  • Blocking either molecule inhibited pseudopodia formation; ICAM-1 blockade induced filopodia.

Conclusions:

  • Endothelial ICAM-1 and VCAM-1 differentially regulate monocyte diapedesis steps.
  • These molecules modulate small GTPase activity (Rho, Rac, Cdc42) affecting cell migration.
  • Findings provide insight into adhesion molecule function in atherogenesis.

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