Fig. 3.

Similarity of transcriptional responses in cultivated hepatocytes and diseased or damaged livers. a Analysis of cultivated primary mouse hepatocytes (M _c, M _s, S), mouse liver tissue 24 h after intraperitoneal injection of LPS, hepatocellular carcinoma induced by a single diethylnitrosamine injection followed by chronic CCl₄ intoxication (HCC, n = 3), steatosis in obese mice induced by leptin deficiency (ob/ob) and freshly isolated hepatocytes from healthy mice (FH). Principal components (PC1 and PC2) represent 66.2 % of the variance. b Analysis of human hepatocytes, liver tissue of patients with cirrhosis (n = 15), hepatocellular carcinoma (HCC, n = 15), non-alcoholic fatty liver disease (NAFLD) stages 0–1 (n = 40) and stages 3–4 (n = 32), and hepatitis B infection (n = 2). The graph shows the top two principal components (PC1 and PC2) representing 63.9 % of the variance. c, d Transcriptomic alterations in cultivated mouse hepatocytes compared to time course analysis of mouse liver tissue after acute liver damage by a single intoxication with CCl₄ (c) and after 2/3 partial hepatectomy (d). The dashed arrows indicate the trend of gene expression changes in time, on cultivated hepatocytes and in liver tissue after CCl₄ intoxication or partial hepatectomy. The top two principal components (in c, d) represent 65.9 and 78.5 % of the variance, respectively. All PCA graphs are based on the 1000 genes with highest variance