Fig. 4: High levels of ROS in the AIF−/Y HSC and progenitor cells provoked DNA damage and apoptosis | Cell Death & Differentiation

Fig. 4: High levels of ROS in the AIF−/Y HSC and progenitor cells provoked DNA damage and apoptosis

From: AIF loss deregulates hematopoiesis and reveals different adaptive metabolic responses in bone marrow cells and thymocytes

Fig. 4

a Left, ECAR of AIF+/Y and AIF−/Y HSC and progenitors cells measured in response to sequential addition of Glucose, Oligomycin, and 2-deoxyglucose (2-DG). Arrows indicate the time of the addition of each reagent. Right, ECAR of HSC and progenitor cells after Glucose treatment expressed as a histogram (n = 3 independent experiments). b–d Mitochondrial ROS generation (MitoSOX labeling) b, DNA damage (γH2AX levels) c, and cell death (Annexin-V/7AAD co-staining) d were evaluated in AIF+/Y and AIF−/Y LT-HSC, ST-HSC, MPP cells from 7-day-old mice. Data are the fold change recorded in the AIF−/Y cells relative to the basal levels of the AIF+/Y cells (n = 5 mice per group). e Mitochondrial ROS levels measured by flow cytometry in AIF+/Y and AIF−/Y BM cells in the presence or absence of NAC (n = 6 mice per group). f Colony counting of BM AIF+/Y or AIF−/Y cells plated in methylcellulose in the presence or absence of NAC (n = 5 independent experiments). Representative images of the morphology of the different colonies are shown. g Dams were supplied or not with NAC in drinking water and the number of LT-HSC, ST-HSC, and MPP cells from 21-day-old AIF+/Y and AIF−/Y newborn mice was counted (n = 7 mice per group). Statistical significance was calculated by Mann–Whitney (a–e and g or two-way ANOVA f tests. Bars represent mean ± SEM

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