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Genome‐wide binding and transcriptome analysis of human farnesoid X receptor in the liver

Farnesoid X receptor (FXR, NR1H4) is a ligand‐activated transcription factor, belonging to the nuclear receptor superfamily. FXR is highly expressed in the liver and functions as the bile acid sensor. FXR deficiency is implicated in numerous liver diseases, and modulation of FXR in mice has been used as animal models to study human liver physiology and pathology. By using chromatin immunoprecipitation followed by deep sequencing (ChIP‐seq), genome‐wide binding of FXR in mice indicates that FXR may be involved in regulating diverse pathways in the liver. However, limited information exists in terms of human FXR function and the suitability of using murine models to study it. To compare and contrast the genome‐wide FXR binding in the liver of mice and humans, ChIP‐seq were performed in frozen human livers of healthy male and female donors (FHLs) and livers of mice treated with FXR agonist (GW4064), as well as in primary human hepatocytes (PHHs) and a hepatoma cell line, HepG2 cells, with or without FXR activation. In addition, RNA‐seq was performed to determine the transcriptome with FXR activation in PHHs. The results showed similarities and differences of genome‐wide FXR binding in the liver between humans and mice in terms of motif analysis and pathway prediction. In addition, differences in FXR binding between male and female humans were not significant. In summary, we have established genome‐wide FXR binding and transcriptome in human livers. These results will aid in determining the human FXR functions, as well as judging the suitability of using mouse models to study human FXR function.