Fig. 2: CKI-based analysis of mouse hepatocyte maturation. | Nature Communications

Fig. 2: CKI-based analysis of mouse hepatocyte maturation.

From: PIM1 promotes hepatic conversion by suppressing reprogramming-induced ferroptosis and cell cycle arrest

Fig. 2

a Experimental design of the trans-omics-based analysis of immature hepatocytes generated from liver progenitor cells (CLiP-Hep) and mature hepatocytes (MH) isolated from mouse liver. Representative image of bile duct structure (b) and CK19 immunofluorescence staining (c) of biliary epithelial cells induced from liver progenitor cells (CLiP-BEC). Scale bars = 100 μm. n = 4 biological replicates. d Immunofluorescence staining of ALBUMIN in hepatocytes generated from CLiPs (CLiP-Hep). Scale bars = 100 μm. n = 3 biological replicates. e Gene expression analysis by RT-qPCR demonstrated significant differences of hepatic and biliary marker genes between CLiP-BEC and CLiP-Hep cells for Aat (p = 0.0067), Alb (p = 0.0007), Ae2 (p = 0.0065), Aqp1 (p = 0.0109), Cftr (p = 0.0002), Ck19 (p = 0.0065), n = 3 biological samples. Data are shown as the mean + SD. *p < 0.05, **p < 0.01, ***p < 0.001 (unpaired two-sided Student’s t-test). f Number of raw and clean reads sequenced from MH and CLiP-Hep samples (n = 3 biological samples). Box and whisker plots present the means (lines inside the boxes), the 1st and 3rd quartiles (bottom and top bounds of the boxes), and the extents of the data (whiskers). g Number of mapped mRNAs in mouse cell samples (n = 3). h Number of up- and down-regulated DEMs in CLiP-Hep compared to MH. i Number of potentially central PKs predicted from different data types for CLiP-Hep vs. MH. j Comparison of central PKs predicted with CKI, KSEA15, 16, and the individual datasets comprising CKI. k Expression levels of liver metabolic genes in CLiP-Hep cells overexpressing individual candidate central PK as quantified by qRT-PCR (n = 3). Source data are provided as a Source Data file.

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