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A Flow Adhesion Assay to Study Leucocyte Recruitment to Human Hepatic Sinusoidal Endothelium Under Conditions of Shear Stress
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Vascular adhesion protein-1, intercellular adhesion molecule-1 and P-selectin mediate leukocyte binding to ischemic

K Jaakkola1, S Jalkanen, K Kaunismäki

  • 1National Public Health Institute and MediCity Research Laboratory, University of Turku, Finland.

Journal of the American College of Cardiology
|July 18, 2000
PubMed

Insights

In acute myocardial infarction (AMI), P-selectin, ICAM-1, and VAP-1 are key adhesion molecules mediating granulocyte binding to heart blood vessels. Targeting these molecules may prevent tissue damage after ischemia.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Pathophysiology

Background:

  • Leukocyte extravasation via adhesion molecules worsens tissue injury after reperfusion.
  • Blocking adhesion molecules can reduce experimental myocardial reperfusion injury.
  • Key molecules in human acute myocardial infarction (AMI) remain poorly understood.

Purpose of the Study:

  • To investigate endothelial adhesion molecule expression in human AMI.
  • To determine the role of these molecules in leukocyte adhesion to myocardial vasculature.

Main Methods:

  • Semiquantitative immunohistochemistry and in vitro adhesion assays were employed.
  • Expression and granulocyte binding of endothelial adhesion molecules were assessed.
  • Vascular adhesion protein-1 (VAP-1) modifications were analyzed via immunoblotting.

Main Results:

  • ICAM-1 and P-selectin were upregulated in infarcted hearts; ICAM-2, CD31, and CD73 showed homogeneous expression.
  • E-selectin and peripheral lymph node addressin were absent.
  • P-selectin, ICAM-1, and VAP-1 mediated granulocyte binding in ischemic human hearts.

Conclusions:

  • Human P-selectin, ICAM-1, and VAP-1 are critical mediators of leukocyte adhesion in AMI.
  • These molecules represent promising targets for antiadhesive therapies to prevent leukocyte-mediated tissue destruction post-myocardial ischemia.
Abstract

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