Fig. 2: CTX specifically induced the decline of EZH2 and H3K27me3 in GCs. | Cell Death Discovery

Fig. 2: CTX specifically induced the decline of EZH2 and H3K27me3 in GCs.

From: The EZH2-H3K27me3 axis modulates aberrant transcription and apoptosis in cyclophosphamide-induced ovarian granulosa cell injury

Fig. 2

A Western blot results of the H3K27me3, H2AK119ub1, H3K9me3, H3K4me3, EZH2, and SUZ12 levels in the PBS and CTX groups. H3, GAPDH, and β-tubulin were blotted as loading controls. N = 6 mice per time point for each group. B–D Immunofluorescence staining of the ovaries collected 6 and 24 h after the i.p. injection of PBS or CTX. Rabbit monoclonal antibodies H3K27me3 (B), H3K9me3 (C), and EZH2 (D) were detected using anti-rabbit IgG (red). TUNEL was probed with Alexa Fluor 488 (green). Cell nuclei were labeled with DAPI (blue). Scale bar, 100 μm. N = 6 ovaries from different mice per time point for each group. E Western blot results for EZH2, H3K27me3, and γH2AX levels in the negative control (NC) and 4-HC treatment groups. β-actin and H3 were blotted as loading controls. F Quantitative expression of Ezh2 in the siNC and siEzh2-1 + 2 + 3 groups. G Western blot results of EZH2, H3K27me3, and γH2AX levels in the siNC and siEzh2-1 + 2 + 3 groups. β-actin and H3 were blotted as loading controls. Data are the mean ± SD of at least three independent experiments. Statistical analyses were carried out using a two-tailed Student’s t-test; ***P < 0.001.

Back to article page