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. 2016 Nov 25;6:37827. doi: 10.1038/srep37827

Figure 3. Defects in CXCR4−/− HSPC function are counteracted by the antioxidant NAC.

Figure 3

(a–d) DCF MFIs of donor-derived BM subsets of CXCR4+/+ and CXCR4−/− chimeras treated with NAC or vehicle. Mean ± SEM from 6 mice per group pooled from three independent experiments. (e–g) Phospho-p38 MFIs in different BM subsets. Mean ± SEM from 6 mice per group pooled from 3 independent experiments. (h,i) Percentages of Annexin-V+ cells in BM LSK and LK cells. Mean ± SEM from 8 mice per group pooled from 2 independent experiments. (j) Representative γH2AX staining (red) in BM LSK cells of CXCR4+/+ and CXCR4−/− chimeras. Nuclei were stained with DAPI (blue). (k) Frequencies of γH2AX-positive BM LSK cells. More than 100 cells were counted per group in 3 independent experiments. Mean ± SEM from 3 independent experiments with 3 to 5 mice per group.