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. 2020 Nov 3;32(5):829–843.e9. doi: 10.1016/j.cmet.2020.09.001

Figure 5.

Figure 5

BMSC-Dependent GSH-Related Pathways Protect AML Cells from Chemotherapy

(A) Reduced glutathione (GSH) measured by mBCI staining in AML blasts and BMSCs cultured alone or together for 24 h in presence of AraC.

(B) Frequency of AraC-treated GSHlo/hi AML cells monocultured (upper bar) or cocultured with BMSCs (middle and lower bar), separating leukemic blasts, which contain mitochondria derived from previously labeled BMSCs (lower bar) from those containing only blasts’ mitochondria (middle and upper bars); n = 4–5.

(C) mRNA expression of Gpx1 and Gpx3 in AML blasts and BMSCs cultured alone or together for 24 h in presence of AraC.

(D) GSH measured by mBCI staining in LKlo WT or iMLL-AF9 cells from mice with/without nestin+ cell depletion (Nes-creERT2;iDTA and control littermates) treated as in Figure S3H. Mice were treated with standard chemotherapy (AraC+) or vehicle (AraC−). (A, C, and D) Each dot represents a biological replicate. Data represent mean ± SEM. p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001. Unpaired two-tailed t test. (B and D) One-way ANOVA followed by pairwise Bonferroni comparisons.