Mounting evidence has shown that zearalenone (ZEA) can have toxic effects on the intestinal epithelial cells (IECs) of mammals and humans, but the mechanism of ZEA-induced toxicity on IECs is unclear. The aim of this study was to reveal the mechanism of action of ZEA on intestinal epithelial cells via RNA-seq technology. We measured the effects of ZEA on the viability and lactate dehydrogenase (LDH) activity of the pig intestinal epithelial cell line J2 (IPEC-J2). The results showed ZEA can decrease the IPEC-J2 cell viability and increase LDH activity. Appropriate treatment concentrations were determined (40 μM ZEA) to study the toxic effect of ZEA on IPEC-J2. The results showed that 40 μM ZEA significantly inhibited IPEC-J2 proliferation and arrested the cell cycle at the G2/M phase. A total of 783 differentially expressed genes (DEGs) were identified after ZEA treatment. KEGG pathway analysis revealed that PERK regulates gene expression, Toll-like receptor cascades signaling pathway, mitosis, mitotic metaphase and anaphase, DNA replication and G2/M checkpoints, were involved in the cell cycle pathway. Eleven key genes involved in G2/M checkpoints were validated by qPCR. Thus, these data highlighted that ZEA caused abnormalities in the G2/M transition in IPEC-J2 cells by altering the cell cycle signaling pathway, thereby inhibiting cell proliferation and inducing injury in IECs. And the study will contribute to get the molecular mechanisms of ZEA inhibition of IECs cell proliferation.
Keywords: Cell cycle; IPEC-J2 cells; RNA-Seq; Zearalenone.
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