title: Increased levels of p53 and PARP-1 in EL-4 cells probably related with the immune adaptive response induced by low dose ionizing radiation in vitro.
abstract: OBJECTIVE
  This paper is to explore the DNA repair mechanism of immune adaptive response (AR) induced by low dose radiation (LDR), the changes of mRNA levels and protein expressions of p53, ATM, DNA-PK catalytic subunit (DNA-PKcs) and PARP-1 genes in the LDR-induced AR in EL-4 cells.
  
  
  METHODS
  The apoptosis and cell cycle progression of EL-4 cells were detected by flow cytometry in 12 h after the cells received the pre-exposure of 0.075 Gy X-rays (inductive dose, D1) and the succeeding high dose irradiation (challenge dose, D2; 1.0, 1.5, and 2.0 Gy X-rays, respectively) with or without wortmannin (inhibitor of ATM and DNA-PK) and 3-aminobenzamid (inhibitor of PARP-1). And the protein expressions and mRNA levels related to these genes were detected with flow cytometry and reverse transcription-polymerase chain reaction in 12 h after irradiation with D2.
  
  
  RESULTS
  The mRNA and protein expressions of p53 and PARP-1 in EL-4 cells in the D1 + D2 groups were much lower than those in the D2 groups, and those of PARP-1 in the 3-AB + D2 and the 3-AB + D1 + D2 groups were much lower than those in the D2 and the D1 + D2 groups. The percentage of apoptotic EL-4 cells in the 3-AB + D1 + D2 groups was much higher than that in the D1 + D2 groups, that in the G₀/G₁ and the G₂ + M phases was much higher, and that in the S phase were much lower. Although the ATM and DNA-PKcs mRNA and protein expressions in wortmannin + D1 + D2 groups were much lower than those in the D1 + D2 groups, there were no significant changes in the apoptosis and cell cycle progression between the wortmannin + D1 + D2 and the D1 + D2 groups.
  
  
  CONCLUSIONS
  PARP-1 and p53 might play important roles in AR induced by LDR.
authors.affiliation: Department of Radiotherapy, China-Japan Union Hospital, Jilin University, Changchun 130033, Jilin, China.
authors.forename: Guang-Hui
authors.initials: GH
authors.lastname: Cheng
authors.forename: Ning
authors.initials: N
authors.lastname: Wu
authors.forename: De-Fu
authors.initials: DF
authors.lastname: Jiang
authors.forename: Hong-Guang
authors.initials: HG
authors.lastname: Zhao
authors.forename: Qian
authors.initials: Q
authors.lastname: Zhang
authors.forename: Jian-Feng
authors.initials: JF
authors.lastname: Wang
authors.forename: Shou-Liang
authors.initials: SL
authors.lastname: Gong
mesh_terms: D000730:Androstadienes; D000818:Animals; D017209:Apoptosis; D002453:Cell Cycle; D045744:Cell Line, Tumor; D004260:DNA Repair; D004307:Dose-Response Relationship, Radiation; D005786:Gene Expression Regulation / Q000528:radiation effects*; D051379:Mice; D000071137:Poly (ADP-Ribose) Polymerase-1; D011065:Poly(ADP-ribose) Polymerases / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011839:Radiation, Ionizing; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*; D000077191:Wortmannin
chemical_list: D000730:Androstadienes; D012333:RNA, Messenger; D016159:Tumor Suppressor Protein p53; C499321:Parp1 protein, mouse; D000071137:Poly (ADP-Ribose) Polymerase-1; D011065:Poly(ADP-ribose) Polymerases; D000077191:Wortmannin