Figure 3.
Effects of IFN-α treatment on accumulation of DNA damage and ROS and on cell division in HSPCs. (A) Accumulation of ROS and presence of γH2AX in lin–/Sca1+/Kit+ (LSK) cells from BM and spleen of recipient mice. GFP chimerism in LSK cells, gating strategy, and detection of DNA damage by anti-γH2AX antibody and ROS by staining with CellRox (left). Quantification of γH2AX and ROS in 9 mice per group (right). (B) Analysis of cell division (Ki67-positive cells) and DNA damage within the mutant (GFP-positive) LT-HSCs; LT-HSC chimerism and gating strategy (left); and the results obtained from 9 mice per group (right). (C) Analysis of ROS levels in GFP-positive LT-HSCs. These data were obtained from mice described in supplemental Figure 13. All data are presented as mean ± standard error of the mean. ANOVA with subsequent Tukey posttest was used. ∗∗P < .01; ∗∗∗P < .001; ∗∗∗∗P < .0001.

Effects of IFN-α treatment on accumulation of DNA damage and ROS and on cell division in HSPCs. (A) Accumulation of ROS and presence of γH2AX in lin–/Sca1+/Kit+ (LSK) cells from BM and spleen of recipient mice. GFP chimerism in LSK cells, gating strategy, and detection of DNA damage by anti-γH2AX antibody and ROS by staining with CellRox (left). Quantification of γH2AX and ROS in 9 mice per group (right). (B) Analysis of cell division (Ki67-positive cells) and DNA damage within the mutant (GFP-positive) LT-HSCs; LT-HSC chimerism and gating strategy (left); and the results obtained from 9 mice per group (right). (C) Analysis of ROS levels in GFP-positive LT-HSCs. These data were obtained from mice described in supplemental Figure 13. All data are presented as mean ± standard error of the mean. ANOVA with subsequent Tukey posttest was used. ∗∗P < .01; ∗∗∗P < .001; ∗∗∗∗P < .0001.

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