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. 2015 Mar 27;10(3):e0122258. doi: 10.1371/journal.pone.0122258

Fig 5. DT3 or anti-IL-1β antibody suppressed radiation-induced miR-30 expression in CD34+ cells.

Fig 5

(A) Vehicle, DT3, or neutralizing antibody for IL-1β activation were added into CD34+ cell culture before 2 Gy radiation, and miR-30b and miR-30c expression were examined 1 h after irradiation. RQ = relative quantitation; **p<0.01; mean ± SD, 0 Gy vs. 2 Gy. (B) IL-1β (10 ng/mL) was added to CD34+ culture with anti-IL-1β antibody or nonspecific IgG control, and miR-30b and miR-30c expression were tested at 15 min, 30 min, and 1 h after addition of IL-1β. IL-1β significantly induced both miR-30b and miR-30c expression in CD34+ cells at all-time points. **p<0.01; mean ± SD, IL-1β+IgG-treated or IL-1β+ anti-IL-1β vs. vehicle-treated control. (C) Vehicle or DT3 was added to CD34+ culture 22 h before IL-1β treatment, and miR-30 expression was examined at 24 h after DT3 addition and 1 h after IL-1β treatment. DT3 administration abolished IL-1β-induced miR-30 expression in CD34+ cells. **p<0.01; mean ± SD, DT3-treated vs. vehicle-treated controls. Results were from total three experiments.