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ICAM-3 activation modulates cell-cell contacts of human bone marrow endothelial cells

J D van Buul1, F P J Mul, C E van der Schoot

  • 1Department of Experimental Immunohematology, Sanquin Research at CLB and the Landsteiner Laboratorium, University of Amsterdam, Amsterdam, The Netherlands.

Journal of Vascular Research
|January 17, 2004
PubMed

Insights

Intercellular Adhesion Molecule 3 (ICAM-3) is expressed on human bone marrow endothelial cells. Its activation disrupts endothelial cell-cell contacts through reactive oxygen species (ROS), impacting vascular integrity.

Area of Science:

  • Immunology
  • Cell Biology
  • Vascular Biology

Background:

  • Intercellular Adhesion Molecule 3 (ICAM-3) is primarily found on leukocytes, mediating cell-cell interactions.
  • ICAM-3 expression is noted on endothelium in certain diseases and tumors, but its role in endothelial cells is unclear.

Purpose of the Study:

  • To investigate the expression and function of ICAM-3 on human endothelial cells.
  • To elucidate the molecular mechanisms underlying ICAM-3's effect on endothelial cell integrity.

Main Methods:

  • Detection of ICAM-3 expression on primary and immortalized human endothelial cells (ECs) from bone marrow and cord blood.
  • Functional assays involving ICAM-3 crosslinking to assess effects on endothelial monolayer electrical resistance and cell-cell contacts.
  • Biochemical analysis to identify associated proteins (moesin, ezrin) and reactive oxygen species (ROS) production.

Main Results:

  • ICAM-3 was detected on various human endothelial cell types, including bone marrow-derived ECs.
  • Crosslinking ICAM-3 led to decreased electrical resistance and loss of cell-cell contacts in bone marrow EC monolayers.
  • ICAM-3 crosslinking was associated with moesin/ezrin recruitment and induced ROS production.

Conclusions:

  • ICAM-3 is expressed on human bone marrow endothelial cells.
  • ICAM-3 activation negatively regulates endothelial integrity through a ROS-dependent pathway.
  • ICAM-3 plays a novel role in controlling endothelial cell-cell contacts and vascular integrity.

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