[The role of intercellular adhesion molecule-1 in binding of acute myeloid leukemic blasts cells to human umbilical vein endothelial cells].

Objective: To evaluate the adhesion of acute myeloid leukemia (AML) blasts to human umbilical vein endothelial cells (HUVECs) and the roles of intercellular adhesion molecule-1 (ICAM-1) and its ligand lymphocyte function associated antigen-1 (LFA-1) in binding of leukemic blasts to HUVECs.
Methods: AML blasts attachment to unactivated or tumor necrosis factor alpha (TNF alpha) activated-endothelial cell monolayers was investigate in vitro; The adhesion of leukemic blasts co cultured with unactivated endothelial cells under static conditions at 37 degrees C for 24 hours was observed;The binding of neutrophils and unactivated endothelial cell monolayers exposed to supernatant of blasts were tested. ICAM-1 on endothelial cell surface and sICAM-1 of endothelial cell supernatant were determined by flow cytometry and ELISA detection. We also observed the adhesion of leukemic blasts in the presence of the adhesion blocking mAbs anti-ICAM-1 and anti-LFA-1.
Results: This study has shown that the blast cells attached to unactivated endothelium was little (24.33 +/- 2.87)% and increased after exposure of endothelium to TNF alpha (81.87 +/- 4.08)% (n = 21, P < 0.001); The binding of blasts to endothelium also increased significantly after 24 hours co cultured with unactivated HUVEC (82.06 +/- 7.05)%, (n = 21, P < 0.001); The adhesion of neutrophils and unactivated endothelial cell monolayers exposed to supernatant of blasts was increased significantly (83.99 +/- 3.86)%, (n = 21, P < 0.001). Lower levels of ICAM-1 and sICAM-1 expression was detected on unactivated HUVECs (55.81 +/- 4.11)%, (0.839 +/- 0.236) microg/L respectively. Treatment of HUVECs with AML blasts supernatant for 24 hours increased the expression of ICAM-1 (65.36 +/- 5.97)%, (1.424 +/- 0.469) microg/L respectively (n = 21, P < 0.05) and anti-ICAM-1 and anti-LFA-1 significantly inhibited the adhesion of AML blasts attachment to TNF alpha activated-endothelial cell monolayers (20.12 +/- 1.73)%, (n = 10, P < 0.001).
Conclusion: Our results indicate that leukemic blasts have the ability to generate some factors that stimulate endothelial cell to secrete ICAM-1 ane to promote their own adhesion to vascular endothelium, interaction of ICAM-1 and its ligand LFA-1 has a key role in adhesion of leukemic blasts and HUVECs.