Increased expression of monocyte CD11a and intracellular adhesion molecule-1 in patients with initial atherosclerotic coronary stenosis.

نویسندگان

  • Akira Kawamura
  • Shin-ichiro Miura
  • Takahiro Murayama
  • Atsushi Iwata
  • Bo Zhang
  • Hiroaki Nishikawa
  • Yoshihiro Tsuchiya
  • Kunihiro Matsuo
  • Emiko Tsuji
  • Keijiro Saku
چکیده

BACKGROUND Cell adhesion molecules have been implicated in the adhesion of leukocytes to endothelial cells and therefore play a role in atherosclerosis, which is a frequent cause of morbidity and mortality in patients with coronary artery disease (CAD) or undergoing hemodialysis (HD). The levels of expression of leukocyte adhesion molecules were evaluated in patients with CAD or HD. METHODS AND RESULTS The expression of leukocyte (ie, neutrophil, monocyte and lymphocyte) surface CD11a, CD18, intracellular adhesion molecule-1 (ICAM-1), very late antigen-4 alpha (VLA-4 alpha) and L-selectin was investigated by flow cytometry in 20 patients who were initially diagnosed with CAD (CAD group), 15 patients with coronary re-stenosed vessels (RESTE group), 20 undergoing HD (HD group) and 20 without CAD (CONT group). Monocyte surface expression of both CD11a and ICAM-1 in the CAD group was significantly higher than in the CONT group. Interestingly, when 15 patients with RESTE were analyzed, they showed monocyte CD11a and ICAM-1 expression levels comparable to those in the CONT group. On the other hand, there were no significant differences in the expression of CD11a, CD18, L-selectin or VLA-4 alpha between the HD group and CONT group, but monocyte L-selectin was increased in the CAD group compared with the CONT group. CONCLUSIONS Because CD11a and CD18 are expressed on the cell surface as a heterodimer and ICAM-1 is a ligand for CD11a/CD18, this increased expression of CD11a and ICAM-1 may affect the development of initial atherosclerotic coronary stenosis, but not re-stenosis.

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عنوان ژورنال:
  • Circulation journal : official journal of the Japanese Circulation Society

دوره 68 1  شماره 

صفحات  -

تاریخ انتشار 2004