Gamma-irradiation-induced Intercellular Adhesion Molecule-1 (ICAM-1) Expression is Associated with Catalase: Activation of Ap-1 and JNK

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Abstract
The ionizing radiation used in cancer therapy frequently produces damage to normal tissues and induces complex responses, including inflammation. The upregulation of the intercellular adhesion molecule-1 (ICAM-1) in response to numerous inducing factors is associated with inflammation. Therefore, this study examined the molecular mechanisms responsible for ICAM-1 expression induced by γ-irradiation (γIR). ICAM-1 mRNA and cell surface expression were induced in A549 human lung epithelial cells after exposing them to γIR. Catalase expression and activity were also increased in γIR-treated cells. Treatment of the γIR-treated cells with catalase resulted in a significant increase in the ICAM-1 cell surface expression level. The catalase inhibitor 3-amino-1,2,4-triazole (AT) reduced the level of ICAM-1. Electrophoretic mobility shift assay (EMSA) analysis showed that activating protein 1 (AP-1) was activated by γIR, whereas NF-κB was not. Specific Jun N-terminal kinase (JNK) inhibition attenuated the upregulation of γIR stimulated ICAM-1. Western blot analysis revealed a marked elevation in activation of JNK. In addition, pretreatment with AT resulted in a decrease in the level of JNK phosphorylation and AP-1 activation. Overall, data suggest that induction of ICAM-1 expression by γIR is associated with catalase. Furthermore, catalase, JNKs, and AP-1 activation induce ICAM-1 upregulation through a sequential process.

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