2004Journal of Atherosclerosis and ThrombosisOpen access

Changes in the Expression of Leukocyte Adhesion Molecules Throughout the Acute Phase of Myocardial Infarction

Akira Kawamura, Shin‐ichiro Miura, Takahiro Murayama, Atsushi Iwata, Hiroaki Nishikawa, Yoshino Matsuo, Yoshihiro Tsuchiya, Kunihiro Matsuo, Emiko Tsuji, Keijiro Saku

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Abstract

Since increased leukocytes within days after the onset of acute myocardial infarction (AMI) may reflect an increased expression of the adhesion molecules necessary for effective endothelial transmigration, we evaluated the expression of adhesion molecules on leukocytes throughout the acute phase of MI. We measured the number of leukocytes and enzymes and the expression levels of CD11a, CD18, very-late-after-activation antigen-4 alpha, intracellular adhesion molecule-1 (ICAM-1) and L-selectin by flow cytometry before and after coronary intervention, and at 6, 12, 18, 48 and 72 hours of MI in 5 patients (AMI group). As controls, we measured these parameters in 5 patients who had been diagnosed with angina pectoris and underwent coronary intervention (AP group). In the AMI group the expression of monocyte CD11a was significantly increased after 6 hours, and CD18 and ICAM-1 expression were also significantly increased after 12 hours, whereas that of monocyte L-selectin was increased after 72 hours. In addition, the increased monocyte CD11a was accompanied by an increased number of monocytes and a greater expression of CD11a per cell in the AMI group. In conclusion, since CD11a and CD18 are expressed on the cell surface as a heterodimer and ICAM-1 is a ligand for CD11a/CD18, their increased expression may contribute to their adhesion to endothelium in ischemic regions and may lead to the formation of microaggregates.

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Since increased leukocytes within days after the onset of acute myocardial infarction (AMI) may reflect an increased expression of the adhesion molecules necessary for effective endothelial transmigration, we evaluated the expression of adhesion molecules on leukocytes throughout the acute phase of MI. We measured the number of leukocytes and enzymes and the expression levels of CD11a, CD18, very-late-after-activation antigen-4 alpha, intracellular adhesion molecule-1 (ICAM-1) and L-selectin by flow cytometry before and after coronary intervention, and at 6, 12, 18, 48 and 72 hours of MI in 5 patients (AMI group). As controls, we measured these parameters in 5 patients who had been diagnosed with angina pectoris and underwent coronary intervention (AP group). In the AMI group the expression of monocyte CD11a was significantly increased after 6 hours, and CD18 and ICAM-1 expression were also significantly increased after 12 hours, whereas that of monocyte L-selectin was increased after 72 hours. In addition, the increased monocyte CD11a was accompanied by an increased number of monocytes and a greater expression of CD11a per cell in the AMI group. In conclusion, since CD11a and CD18 are expressed on the cell surface as a heterodimer and ICAM-1 is a ligand for CD11a/CD18, their increased expression may contribute to their adhesion to endothelium in ischemic regions and may lead to the formation of microaggregates.

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Available abstract

Since increased leukocytes within days after the onset of acute myocardial infarction (AMI) may reflect an increased expression of the adhesion molecules necessary for effective endothelial transmigration, we evaluated the expression of adhesion molecules on leukocytes throughout the acute phase of MI. We measured the number of leukocytes and enzymes and the expression levels of CD11a, CD18, very-late-after-activation antigen-4 alpha, intracellular adhesion molecule-1 (ICAM-1) and L-selectin by flow cytometry before and after coronary intervention, and at 6, 12, 18, 48 and 72 hours of MI in 5 patients (AMI group). As controls, we measured these parameters in 5 patients who had been diagnosed with angina pectoris and underwent coronary intervention (AP group). In the AMI group the expression of monocyte CD11a was significantly increased after 6 hours, and CD18 and ICAM-1 expression were also significantly increased after 12 hours, whereas that of monocyte L-selectin was increased after 72 hours. In addition, the increased monocyte CD11a was accompanied by an increased number of monocytes and a greater expression of CD11a per cell in the AMI group. In conclusion, since CD11a and CD18 are expressed on the cell surface as a heterodimer and ICAM-1 is a ligand for CD11a/CD18, their increased expression may contribute to their adhesion to endothelium in ischemic regions and may lead to the formation of microaggregates.

Key concepts: CD11a, CD18, Cell adhesion molecule, Monocyte, Medicine, Myocardial infarction, Flow cytometry, Adhesion

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