Fig. 5: Hepatic PCK1 deficiency leads to HSC activation via PI3K/AKT pathway. | Nature Communications

Fig. 5: Hepatic PCK1 deficiency leads to HSC activation via PI3K/AKT pathway.

From: Deficiency of gluconeogenic enzyme PCK1 promotes metabolic-associated fatty liver disease through PI3K/AKT/PDGF axis activation in male mice

Fig. 5: Hepatic PCK1 deficiency leads to HSC activation via PI3K/AKT pathway.

a Pathway enrichment analysis of significantly upregulated genes in L-KO mice. b Gene Set Enrichment Analysis (GSEA) plot of enrichment in PI3K/AKT pathway. c–f Immunoblot analysis of AKT and p-AKT (S473 or T308) in mouse liver tissues (c), primary hepatocytes from HFCD-HF/G feeding mice (d), PCK1-OE (e), and PCK1-KO (f) MIHA cells with or without 0.2 mM palmitic acid (PA) treatment. The samples were derived from the same experiment and the blots were processed in parallel. g Schematic flow chart of co-culture models. h, i Quantitative PCR analysis of fibrosis-related genes in LX-2 cells co-cultured with PCK1-KO (h) or PCK1-OE (i) MIHA cells. j, k Western blotting of fibrosis-related protein in liver tissues (j) or primary HSCs from HFCD-HF/G feeding mice (k) (n = 3) l, m Relative mRNA expression (l) and immunofluorescence images (m) of ACTA2/α-SMA, COL1A1, and COL3A1 in LX-2 cells co-cultured with PCK1-KO MIHA cells treated with AKT inhibitor MK2206 (10 μM). Scale bars: 25 µm. Data are expressed as the mean ± SEM. p values obtained via two-tailed unpaired Student’s t tests or one-way ANOVA with Tukey’s post hoc test. Source data are provided as a Source Data file.

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