Abstract
Purpose: To identify new ionizing radiation (IR)-sensitive genes and observe the dose-effect of gene expression alteration (GEA) induced by IR.
Materials and methods: Microarray was used to screen the differentially expressed genes in human lymphoblastoid cells (AHH-1) using three doses of 60Co γ-rays (0.5–8 Gy at 1 Gy/min). Given that p53-inducible gene 3 (PIG3) was consistently upregulated, the GEA of PIG3 in AHH-1 cells and human peripheral blood lymphocytes (HPBL) induced by γ-rays (1 Gy/min) was measured at messenger RNA (mRNA) and protein levels. The GEA of PIG3 in AHH-1 cells exposed to neutron radiation (californium-252, 0.073 Gy/min) was also quantified.
Results: PIG3 was one of the seven differentially expressed genes found in the microarray analysis. The PIG3 mRNA and protein levels in AHH-1 cells were significantly increased from 1–10 Gy of γ-rays 8–72 h or 8–168 h after exposure, respectively. The enhancement was also observed in AHH-1 cells from 0.4–1.6 Gy of neutrons 48 h post-irradiation. The PIG3 mRNA levels (mRNA copy numbers) in HPBL were significantly increased from 1–8 Gy of γ-rays within 4–24 h post-irradiation, but the highest increase in signal-to-noise responsiveness is approximately two-fold, which was less than that of AHH-1 (approximately 20-fold).
Conclusions: IR can upregulate the PIG3 gene expression in AHH-1 and HPBL in the early phase after exposure; however, the IR induced expression levels of PIG3 are greater in AHH-1 than HPBL.
Acknowledgements
The authors are thankful to Mrs Renee Zhao from IDP Beijing who provided linguistic support. We also thank Drs Xiang-Yan Zhou, Hui-Min Lv and Wei Zhang for helpful review of original study protocols.
Declaration of interest
The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
This work was supported in part by the grants from National Natural Science Foundation of China (grant nos. 30570551, 81172593] and Young Scholar Scientific Foundation of China CDC (grant no. 2011A202).