Fig. 2: DNA-PK is activated in the nucleus of reserve oocytes following cyclophosphamide treatment. | Cell Death & Disease

Fig. 2: DNA-PK is activated in the nucleus of reserve oocytes following cyclophosphamide treatment.

From: Kinase-independent inhibition of cyclophosphamide-induced pathways protects the ovarian reserve and prolongs fertility

Fig. 2

P7 mice were injected with vehicle (PBS) or increasing concentrations of cyclophosphamide (75, 100, and 200 mg/kg) and sacrificed within 16 h after injection. DNAPK activation was evaluated with IF assay using a phospho-specific antibody (green) and Msy2 (red), a cytoplasmic antigen of germ cells (a). Blue arrows at the bottom indicate the oocytes positive for p-DNAPK and γH2AX. Quantification was performed by counting several (6 < x < 8) middle ovarian sections derived from distinct ovaries. b Confocal images of middle ovarian sections from cyclophosphamide-injected mice indicated that the oocytes with high expression of p-DNAPK or γH2AX showed reduced expression of TAp63. c Western blot analysis of ovarian lysates for female pups injected with 100 mg/kg of cyclophosphamide or PBS. Cyclophosphamide treatment induced a mobility shift of TAp63 (indicated with an asterisk [*]) that was absent in the control. Scale bar magnification, 25 μm for IF assay and 7 μm for confocal images. a Bar column represents mean ± s.d.; statistical significance was determined using one-way analysis of variance (ANOVA) (*P < 0.5; **P < 0.01; ***P < 0.001 as compared with PBS-treated group)

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