Radiation-induced ICAM-1 expression via TGF-β1 pathway onhuman umbilical vein endothelial cells; comparisonbetween X-ray and carbon-ion beam irradiation

Adhesion of inflammatory cells to endothelial cells is considered to be involved in the process of radiation-induced damage and fibrosis. intercellular adhesion molecule-1 (icam-1) and transforming growth factor-beta1 (tgf-β1) are thought to play important roles in this process. in this study,radiation-induced icam-1 expression on endothelial cells was investigated with the use of an inhibitor of tgf-β1 receptor kinase (sb431542) and the effects of x-ray and carbon-ion beam were compared. cell cultures of human umbilical vein endothelial cells (huve cells) were incubated with tgf-β1 and irradiated with 140 kv x-ray. next,huve cells were irradiated with x-ray and 220 mev carbon-ion beam with or without sb431542. immunofluorescence analysis was used to quantify icam-1 expression. the expression of icam-1 on huve cells was significantly increased by the stimulation with tgf-β1. expression of icam-1 was increased by x-ray and carbon-ion beam irradiation and decreased significantly with sb431542 after both irradiations. the expression of icam-1 by 2 gy of carbon-ion beam irradiation was 6.7 fold higher than that of non-irradiated cells,while 5 gy of x-ray irradiation increased the expression of icam-1 by 2.5 fold. according to icam-1 expression,the effect of carbon-ion beam irradiation was about 2.2,4.4 and 5.0 times greater than that of the same doses of x-ray irradiation (1,2 and 5 gy,respectively). the present results suggested that radiation-induced icam-1 expression on huve cells was,at least partially,regulated by tgf-β1. carbon-ion beam induced significantly higher icam-1 expression than x-ray.