Fig. 4: Hepatic deletion of Mettl3 in mice induces fibrosis and activation of hepatic progenitors. | Nature Communications

Fig. 4: Hepatic deletion of Mettl3 in mice induces fibrosis and activation of hepatic progenitors.

From: Mettl3-mediated mRNA m6A modification controls postnatal liver development by modulating the transcription factor Hnf4a

Fig. 4: Hepatic deletion of Mettl3 in mice induces fibrosis and activation of hepatic progenitors.The alternative text for this image may have been generated using AI.

a Representative Masson’s trichrome staining and αSMA immunohistochemistry staining photographs of liver sections from Control and Mettl3 cKO mice at 4 weeks after birth (10 experiments were repeated independently with similar results). Scale bar = 50 μm. b Quantification of the αSMA positive area (n = 8 for each group). c Quantification of the Masson’s trichrome staining positive area (n = 8 for cKO group; n = 12 for Control group). d CK19 and Sox9 immunohistochemistry staining of liver sections from Control and Mettl3 cKO mice at 4 weeks after birth (6 experiments were repeated independently with similar results). Scale bar = 50 μm. e RT-qPCR analysis of hepatocyte markers, hepatic progenitor markers, and fibrosis markers for liver tissues from Control and Mettl3 cKO mice at different time points postnatally (n = 3 for 1 day Control group, 3 weeks cKO group, and 5 weeks groups; n = 5 for 3 weeks Control group; n = 4 for other groups). f Western blot for Albumin, Sox9, and αSMA of Control and Mettl3 cKO mouse liver tissues at 4 weeks after birth (3 experiments were repeated independently with similar results). Data in b, c, and e were shown as mean ± SEM with the indicated significance (*P < 0.05, **P < 0.01, ***P < 0.001; two-tailed student’s t-test). Source data are provided as a Source Data file.

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