The idiosyncratic drug-induced gene expression changes in HepG2 cells

• DOI: 10.1016/j.dib.2017.07.074
• Publication Date: 2017-07-30T00:15:30Z
• Authors: J. Jiang; K. Mathijs; L. Timmermans; S.M. Claessen; A. Hecka; J. Weusten; R. Peters; J.H. van Delft; J.C.S. Kleinjans; D.G.J. Jennen; T.M. de Kok
• Keywords: 0403 veterinary science; Q1-390; 03 medical and health sciences; Science (General); 0302 clinical medicine; Computer applications to medicine. Medical informatics; Journal Article; R858-859.7; 04 agricultural and veterinary sciences; Pharmacology, Toxicology and Pharmaceutical Science; 3. Good health

The inflammatory stress has been associated with an increase in susceptibility to idiosyncratic drug-induced liver injury (DILI). However, the molecular mechanisms of this inflammation-associated idiosyncratic drug hepatotoxicity remain unknown. We exposed HepG2 cells with high and low doses of three idiosyncratic (I) and three non-idiosyncratic (N) compounds, in the presence (I+ and N+) or absence (I- and N-) of a cytokine mix for 6, 12 and 24 h. To investigate the genome-wide expression patterns, microarray was performed using the Agilent 4×44K Whole Human Genome chips. The data presented in this DIB include the expression of genes participating in the ceramide metabolism, ER stress, apoptosis and cell survival pathways. The functions of these genes were illustrated in our associated article (Jiang et al., 2017) [1]. Raw and normalized gene expression data are available through NCBI GEO (accession number GSE102006).