Differential expression of thymic DNA repair genes in low-dose-rate irradiated AKR/J mice.
10.4142/jvs.2013.14.3.271
- Author:
Jin Jong BONG
1
;
Yu Mi KANG
;
Suk Chul SHIN
;
Seung Jin CHOI
;
Kyung Mi LEE
;
Hee Sun KIM
Author Information
1. Radiation Health Research Institute, Korea Hydro and Nuclear Power, Seoul 132-703, Korea. hskimdvm@khnp.co.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
AKR/J mice;
DNA repair genes;
low-dose-rate radiation;
thymic lymphoma
- MeSH:
Animals;
DNA Repair/*radiation effects;
Dose-Response Relationship, Radiation;
Female;
Gene Expression Regulation/*radiation effects;
Gene Regulatory Networks/radiation effects;
Lymphoma/etiology/*genetics;
Mice;
Mice, Inbred AKR;
Oligonucleotide Array Sequence Analysis;
*Radiation, Ionizing;
Reverse Transcriptase Polymerase Chain Reaction;
Thymus Gland/*radiation effects;
Thymus Neoplasms/etiology/*genetics
- From:Journal of Veterinary Science
2013;14(3):271-279
- CountryRepublic of Korea
- Language:English
-
Abstract:
We previously determined that AKR/J mice housed in a low-dose-rate (LDR) (137Cs, 0.7 mGy/h, 2.1 Gy) gamma-irradiation facility developed less spontaneous thymic lymphoma and survived longer than those receiving sham or high-dose-rate (HDR) (137Cs, 0.8 Gy/min, 4.5 Gy) radiation. Interestingly, histopathological analysis showed a mild lymphomagenesis in the thymus of LDR-irradiated mice. Therefore, in this study, we investigated whether LDR irradiation could trigger the expression of thymic genes involved in the DNA repair process of AKR/J mice. The enrichment analysis of Gene Ontology terms and Kyoto Encyclopedia of Genes and Genomes pathways showed immune response, nucleosome organization, and the peroxisome proliferator-activated receptors signaling pathway in LDR-irradiated mice. Our microarray analysis and quantitative polymerase chain reaction data demonstrated that mRNA levels of Lig4 and RRM2 were specifically elevated in AKR/J mice at 130 days after the start of LDR irradiation. Furthermore, transcriptional levels of H2AX and ATM, proteins known to recruit DNA repair factors, were also shown to be upregulated. These data suggest that LDR irradiation could trigger specific induction of DNA repair-associated genes in an attempt to repair damaged DNA during tumor progression, which in turn contributed to the decreased incidence of lymphoma and increased survival. Overall, we identified specific DNA repair genes in LDR-irradiated AKR/J mice.
