chi‐miR‐130b‐3p regulates the ZEA‐induced oxidative stress damage through the KEAP1/NRF2 signaling pathway by targeting SESN2 in goat GCs

Abstract

AbstractAs a dominant mycotoxin, zearalenone (ZEA) has attracted extensive attention due to its estrogen‐like effect and oxidative stress damage in cells. In order to find a way to relieve cell oxidative stress damage caused by ZEA, we treated goat granulosa cells (GCs) with ZEA and did a whole transcriptome sequencing. The results showed that the expression level of Sesterin2 (SESN2) was promoted extremely significantly in the ZEA group (p < .01). In addition, our research demonstrated that SESN2 could regulate oxidative stress level in GCs through Recombinant Kelch Like ECH Associated Protein 1 (KEAP1)/Nuclear factor erythroid 2‐related factor 2 (NRF2) signaling pathway. The overexpression of SESN2 could reduce the oxidative damage, whereas knockdown of SESN2 would aggravate the oxidative damage caused by ZEA. What's more, microRNA (miRNA) chi‐miR‐130b‐3p can bind to SESN2 3′‐untranslated region (3′UTR) to regulate the expression of SESN2. The mimics/inhibition of chi‐miR‐130b‐3p would have an effect on oxidative damage triggered by ZEA in GCs as well. In summary, these results elucidate a new pathway by which chi‐miR‐130b‐3p affects the KEAP1/NRF2 pathway in GCs by modulating SESN2 expression in response to ZEA‐induced oxidative stress damage.