한빛사논문
- 조회244
Na Yeon Kim1, Myoung Ok Kim1,2, Sangsu Shin1,2, Woo‑Sung Kwon1,2, Bomi Kim3, Joon Yeop Lee3 and Sang In Lee1,2*
1Department of Animal Science and Biotechnology, Kyungpook National University, Sangju, Gyeong‑sangbuk‑do, 37224, Republic of Korea
2Research Institute for Innovative Animal Science, Kyungpook National University, Sangju, Gyeongsangbuk‑do 37224, Republic of Korea
3National Institute for Korean Medicine Development, Gyeongsan 38540, Republic of Korea
*Correspondence: Sang In Lee
Abstract
Background: The intestinal epithelium performs essential physiological functions, such as nutrient absorption, and acts as a barrier to prevent the entry of harmful substances. Mycotoxins are prevalent contaminants found in animal feed that exert harmful effects on the health of livestock. Zearalenone (ZEA) is produced by the Fusarium genus and induces gastrointestinal dysfunction and disrupts the health and immune system of animals. Here, we evaluated the molecular mechanisms that regulate the effects of ZEA on the porcine intestinal epithelium.
Results: Treatment of IPEC-J2 cells with ZEA decreased the expression of E-cadherin and increased the expression of Snai1 and Vimentin, which induced Snail1-mediated epithelial-to-mesenchymal transition (EMT). In addition, ZEA induces Snail-mediated EMT through the activation of TGF-β signaling. The treatment of IPEC-J2 cells with atractylenolide III, which were exposed to ZEA, alleviated EMT.
Conclusions: Our findings provide insights into the molecular mechanisms of ZEA toxicity in porcine intestinal epithelial cells and ways to mitigate it.
논문정보
- Research article
- 2024년 06월 (BRIC 등록일 2024-06-11)
- 국내 연구진
- 생명과학 > 동물자원학
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