Subject	Pharmacology, Toxicology and Pharmaceutical Science: Toxicology; Medicine and Dentistry: Hepatology
Specific subject area	Cholestatic liver injury
Type of data	Raw data
How data were acquired	Affymetrix GeneChip Human Genome U133 plus 2.0 array (ThermoFisher, Belgium) Affymetrix GeneChip Mouse Genome 430 2.0 array (ThermoFisher, Belgium) Ingenuity Pathway Analysis (IPA) (Qiagen, Belgium) Transcriptome Analysis Console (TAC) (ThermoFisher, Belgium)
Data format	Raw (.CEL), normalized and analyzed
Parameters for data collection	Male 8-weeks-old Sv129 mice (Harlan, The Netherlands) were housed in the animal facility of the Faculty of Medicine and Health Sciences (Ghent University, Belgium). Mice were allowed to acclimatize for at least 1 weekprior to experiments. Care was given in accordance with the Federation for Laboratory Animal Science Associations guidelines and the national guidelines for animal protection. The animal protocols used in this study were evaluated and approved by the Ethical Committee of Experimental Animals at the Faculty of Medicine and Health Sciences, Ghent University, Belgium (ECD 15/36). Cholestasis was induced by performing bile duct ligation (BDL) surgery as previously described [1]. Control mice were sham operated, whereby the common bile duct was isolated, but not ligated. Liver samples were collected 6 weeks post-surgery. Cryopreserved differentiated HepaRG cells (Biopredic International, France) were cultured following manufacturer's instructions (Biopredic International, France). Hereafter, HepaRG cells were exposed to 60 µM atazanavir, 20 µM cyclosporin A and 30 µM nefazodone. A 50 times concentrated mixture of 5 bile acids (i.e. 66 µM glycochenodeoxycholic acid, 20 µM deoxycholic acid, 19.5 µM chenodeoxycholic acid, 19 µM glycodeoxycholic acid, and 17.5 µM glycocholic acid) was included in the cell culture medium of HepaRG cells from day 7 after seeding in combination with the drug. Incubations with drugs were routinely carried out for 72 h with daily renewal of cell culture media, including a 50 times concentrated bile acid mixture and drugs. Dimethyl sulfoxide (DMSO) treated HepaRG cells served as control. All conditions contained a final DMSO concentration of 0.25%. All compounds were purchased from Sigma Aldrich, Belgium.
Description of data collection	Total RNA was extracted from HepaRG cell culture samples that were treated with atazanavir, cyclosporin A and nefazodone in the absence or presence of a 50 times concentrated mixture of bile acids (i.e. ATA 60 µM, ATA + BA 60 µM, CsA 20 µM, CsA + BA 20 µM, NEFA 30 µM and NEFA + BA 30 µM), as well as from controls solely exposed to the 50 times concentrated bile acid mixture of bile acids and/or identical DMSO concentration (i.e. BA and CTL, respectively). For each condition samples were collected from 3 separate HepaRG batches (n = 3). Similarly, total RNA was extracted from liver samples of mice that underwent bile duct ligation (i.e. BDL) and sham surgery (i.e. CTL). Liver samples were collected from 6 BDL mice and 6 CTL mice (n = 6). Quantification and purity of the isolated RNA were determined via spectrophotometric analysis with a Nanodrop spectrophotometer (ThermoFisher Scientific, Belgium). Whole genome expression analysis was performed using microarray technologies (Affymetrix, Germany).
Data source location	Department of In Vitro Toxicology and Dermato-Cosmetology, Vrije Universiteit Brussel, Jette, Belgium.
Data accessibility	Raw data is available at the Gene Expression Omnibus (GEO) from The National Center for Biotechnology Information (NCBI) with access number GSE152494. https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE152494
Related research article	E. Gijbels, V. Vilas‐Boas, P. Annaert, T. Vanhaecke, L. Devisscher, M. Vinken, Robustness testing and optimization of an adverse outcome pathway on cholestatic liver injury. Arch Toxicol 94 (4): 1151–1172 (2020). 10.1007/s00204–020–02691–9[3]