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. 2022 Nov 19;13(11):976. doi: 10.1038/s41419-022-05413-4

Fig. 2. BNIP3-dependent mitophagy protects ESC from oxidative stress-induced DNA damage.

Fig. 2

A Western blot of γH2AX and 53BP1 in bnip3−/− ESCs and rescued ESCs with actin as the loading control. B Increased cellular 8-OHdG in bnip3−/− ESCs was rescued by gain of expression of wild-type but not ∆LIR Bnip3. Data shown are the mean ± SD, n = 3; *, P < 0.05; **, P < 0.01; Student’s t-test. C NAC treatment (100 μM for 12 h) suppressed elevated oxidative stress in bnip3−/− ESCs. Data shown are the mean ± SD, n = 3; *, P < 0.05; **, P < 0.01; NS no significant difference, Student’s t-test. D NAC treatment antagonized increased DNA damage in bnip3−/− ESCs. Data shown are the mean ± SD, n = 3; *, P < 0.05; NS no significant difference, Student’s t-test. E Compromised pluripotency gene expression and enhanced DNA damage in bnip3−/− ESCs can be rescued by NAC treatment. Actin served as the loading control. F Deteriorated self-renewal of bnip3−/− ESCs can be restored by NAC treatment. Data shown are the mean ± SD, n = 3; *, P < 0.05; **, P < 0.01; NS no significant difference, Student’s t-test. G Activation of ATM and p53 in bnip3−/− ESCs can be rescued by wild-type but not ∆LIR Bnip3. Actin served as the loading control. H Decreased expression of pluripotency genes in bnip3−/− ESCs can be rescued by knockout of either ATM or p53. Actin served as the loading control. I Compromised self-renewal in bnip3−/− ESCs can be rescued by knockout of either ATM or p53. Data shown are the mean ± SD, n = 3; P < 0.01; Student’s t-test.