Zearalenone Exposure Induces the Apoptosis of Porcine Granulosa Cells and Changes Long Noncoding RNA Expression To Promote Antiapoptosis by Activating the JAK2-STAT3 Pathway.

Abstract

Zearalenone (ZEA), a pathogenic toxin produced by Fusarium, is widely detected in moldy feed materials. Previous studies have reported that ZEA exerts a harmful influence on animal reproductive systems; however, its effects on the changes of long noncoding RNAs (lncRNAs) remain unclear. Here, tackling this question, we performed RNA sequencing on porcine granulosa cells (GCs) after being exposed to 10 and 30 μM ZEA in vitro. The results showed that ZEA exposure observably changed the expression of lncRNAs in porcine GCs and increased the rate of apoptosis. Furthermore, Gene Ontology analysis showed that ZEA exposure induced variation of the Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 (STAT3) signaling pathway in porcine GCs. To verify our bioinformatics analysis, western blotting and immunofluorescence analysis were performed and the results demonstrated that porcine GCs after ZEA exposure increased the expression of key proteins in the JAK2-STAT3 signaling pathway. Further bioinformatics analysis found that MSTRG.22680 and MSTRG.23882 played a pivotal role in activating the JAK2-STAT3 signaling pathway. To summarize, our results throw light on the fact that ZEA exposure dramatically increases the apoptosis of porcine GCs and alters the expression of lncRNAs that play an antiapoptotic role in porcine GCs via activating the JAK2-STAT3 signaling pathway.