Fig. 6: STAT1 was involved in HDAC9-mediated G2/M arrest. | Nature Communications

Fig. 6: STAT1 was involved in HDAC9-mediated G2/M arrest.

From: HDAC9-mediated epithelial cell cycle arrest in G2/M contributes to kidney fibrosis in male mice

Fig. 6: STAT1 was involved in HDAC9-mediated G2/M arrest.The alternative text for this image may have been generated using AI.

a–c Photomicrographs and quantifications showing that overexpression of STAT1 counteracted the effect of HDAC9 knockdown in HK-2 by increasing the level of p-H3, cyclin B1 and p21. Scale bar: white = 20 μm. (n = 6 biologically independent experiments). d Cell cycle analysis by flow cytometry for HK-2 in different groups. (n = 6 biologically independent experiments). e Representative Western blot gel documents and summarized data showing the relative protein levels of TGF-β1 in HK-2 with different treatments. (n = 6 biologically independent experiments). f Photomicrographs and quantifications showing the relative protein levels of α-SMA, Vimentin and PCNA in fibroblasts treated with conditioned medium from HK-2 cells with different treatments. Scale bar: white = 25 μm. (n = 6 biologically independent experiments). HK-2 cells were stimulated with AA (5 μg/ml) for 48 h. Data are expressed as mean ± SEM (a–f). Two-way ANOVA followed by Tukey’s post-test (a–f). Source data are provided as a Source Data file.

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