Ongoing DNA damage, induction of cellular senescence, and acquisition of the senescence-associated secretory phenotype 12 mo after 56Fe radiation. Ongoing.

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Ongoing DNA damage, induction of cellular senescence, and acquisition of the senescence-associated secretory phenotype 12 mo after 56Fe radiation. Ongoing DNA damage, induction of cellular senescence, and acquisition of the senescence-associated secretory phenotype 12 mo after 56Fe radiation. (A and B) γH2AX foci counts are graphically plotted demonstrating long-term persistence of DNA damage after 56Fe relative to γ-rays and control. Representative images from 12-mo samples showing increased DNA double-strand breakage after 56Fe radiation. HPF, high-power field. (Scale bars, 5 μm.) (C and D) Numbers of SA-β-gal–positive cells are plotted graphically showing persistently higher senescence induction after 56Fe radiation. (Scale bars, 10 μm.) (E) Quantitative RT-PCR results show increased expression of p16 and p21 after 56Fe radiation. (F) Representative costaining images showing Glb1+IL8–positive cells (white arrowheads) in 56Fe samples. (Scale bars, 5 μm.) (G) Quantification of Glb1+IL8 cells per 20× field is presented graphically showing higher numbers in 56Fe relative to control and γ-rays. (H) Quantitative RT-PCR results showing increased expression of IL6, Ptges, Faim2, and Opg after 56Fe radiation; *, significant relative to control; **, significant relative to γ-rays. Statistical significance is set at P < 0.05 and error bars represent mean ± SEM. Santosh Kumar et al. PNAS 2018;115:42:E9832-E9841 ©2018 by National Academy of Sciences