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26 November 2012 The Role of ROS in Ionizing Radiation-Induced VLA-4 Mediated Adhesion of RAW264.7 Cells to VCAM-1 Under Flow Conditions
Ye Yuan, Shin Hee Lee, Shiyong Wu
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Abstract

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 H2O2 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.

Ye Yuan, Shin Hee Lee, and Shiyong Wu "The Role of ROS in Ionizing Radiation-Induced VLA-4 Mediated Adhesion of RAW264.7 Cells to VCAM-1 Under Flow Conditions," Radiation Research 179(1), 62-68, (26 November 2012). https://doi.org/10.1667/RR3119.1
Received: 7 July 2012; Accepted: 1 August 2012; Published: 26 November 2012
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