Alteration of adhesion molecule expression on endothelial cells has a direct connection with ionizing radiation-induced
atherosclerosis, which is an adverse effect observed after
radiotherapy. However, minimal attention has been given to monocytes/macrophages role in
atherosclerosis development, which are exposed to the radiation at the same time. Under flow conditions using a parallel plate flow chamber to mimic physiological shear stress, we demonstrate here that the avidity between
very late antigen-4 (VLA-4) of RAW264.7 cells and its
ligand vascular cell adhesion molecule-1 (VCAM-1), was increased after low dose (0.5 Gy) irradiation, but was reduced after higher dose (5 Gy) treatment of ionizing radiation despite the fact that the surface expression of
VLA-4 was up-regulated at 5 Gy of ionizing radiation. Treating the cells with
free radical scavenger N-acetylcysteine had no effect on
VLA-4 expression, but did reduce the avidity between RAW264.7 cells and
VCAM-1 to a similar level, independent of ionizing radiation dose. The effect of H(2)O(2) treatment (from 1-100 μM) on RAW264.7 cell adhesion to
VCAM-1 generated a similar bell-shaped graph as ionizing radiation. These results suggest that ionizing radiation regulates adhesive interactions between
VLA-4 and
VCAM-1, and that
reactive oxygen species might function as a regulator, for this increased adhesiveness but with altered expression of
integrin not play a major role.