Ionizing Radiation Selectively Increases CXC Ligand 10 Level via the DNA-Damage-Induced p38 MAPK-STAT1 Pathway in Murine J774A.1 Macrophages

Author:

Seo You Na12ORCID,Baik Ji Sue13,Lee Song Mi4,Lee Ji Eun4,Ahn Hye Rim4,Lim Min Seo4,Park Moon-Taek1,Kim Sung Dae4

Affiliation:

1. Research Center, Dongnam Institute of Radiological & Medical Sciences, Busan 46033, Republic of Korea

2. Department of Microbiology and Immunology, College of Medicine, Inge University, Busan 47392, Republic of Korea

3. Department of Medicinal Biotechnology, College of Health Sciences, Dong-A University, Busan 49315, Republic of Korea

4. Department of Veterinary Medicine, College of Veterinary Medicine, Kyoung Pook National University, Daegu 41566, Republic of Korea

Abstract

Ionizing radiation (IR) is an important means of tumor treatment in addition to surgery and drugs. Attempts have been made to improve the efficiency of radiotherapy by identifying the various biological effects of IR on cells. Components of the tumor microenvironment, such as macrophages, fibroblasts, and vascular endothelial cells, influence cancer treatment outcomes through communication with tumor cells. In this study, we found that IR selectively increased the production of CXC motif chemokine ligand 10 (CXCL10), which is emerging as an important biomarker for determining the prognosis of anticancer treatments, without changing the levels of CXCL9 and CXCL11 in murine J774A.1 macrophages. Pretreatment with KU55933, an ataxia telangiectasia mutated (ATM) kinase inhibitor, significantly inhibited IR-induced CXCL10 production. In contrast, pretreatment with N-acetyl-cysteine or glutathione, a reactive oxygen species scavenger, did not inhibit IR-induced CXCL10 production. Further, we attempted to identify the intracellular molecular target associated with the IR-induced increase in CXCL10 secretion by J774A.1 macrophages. IR phosphorylated p38 mitogen-activated protein kinase (MAPK) and signal transducer and activator of transcription 1 (STAT1) in J774A.1 macrophages, and p38 MAPK and STAT1 were involved in CXCL10 via IR using pharmacological inhibitors (SB203580 and fludarabine, respectively) and the siRNA technique.

Funder

National Research Foundation of Korea

Dongnam Institute of Radiological & Medical Sciences

Publisher

MDPI AG

Subject

General Medicine

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