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. Author manuscript; available in PMC: 2020 Sep 5.
Published in final edited form as: Cell Stem Cell. 2019 Jun 20;25(3):357–372.e7. doi: 10.1016/j.stem.2019.05.019

Figure 5. Necroptosis-mediated elimination of NF-κB-deactivated HSCs.

Figure 5.

(A–C) Engraftment potential of BM HSCs ± TNFα (n=5–16 mice/group from 3 independent experiments): (A) experimental design, (B) donor-derived chimerism in PB and (C) absolute numbers of donor-derived BM HSCs at 4 months post-transplantation; mo, months.

(D-E) NF-κB-deactivation following TNFα treatment: (D) representative images and (E) quantification of nuclear p65 in BM HSCs ± TNFα (n = 3–9 biological replicates/group from 8 independent experiments); scale bar, 5 μm.

(F) Experimental design and changes in absolute numbers of the indicated BM populations ± TNFα (n = 4–11 mice/group from 5 independent experiments; * vs. WT).

(G–J) Necroptosis inhibition due to Ripk3 deficiency (Ripk3−/− mice, top) and Mlkl deficiency (Mlkl−/− mice, bottom) on the functionality of 48h TNFα-exposed BM HSCs: (G) experimental design, (H) expansion after 72h culture (n = 7–9 pools of 300 cells/group from 3 independent experiments; results are expressed as fold expansion compared to the number of plated cells/condition), and (I) donor chimerism in PB and (J) absolute number of donor-derived BM HSCs at 4 months post-transplantation (n = 6–25 mice/group from 4–5 independent experiments).

Data are mean ± SEM, *P < 0.05, **P < 0.01, ***P < 0.001.

See also Figures S4 and S5.