Zearalenone induces apoptosis and autophagy by regulating endoplasmic reticulum stress signalling in porcine trophectoderm cells
Zearalenone (ZEA), a mycotoxin produced mainly by fungi belonging to Fusarium species in foods and feeds, causes a serious hazard to humans and animals. Numerous studies have revealed that ingesting ZEA can disrupt the reproductive function and impair the reproductive process in animals. This experi...
| Main Authors: | , , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
KeAi Communications Co., Ltd.
2023-03-01
|
| Series: | Animal Nutrition |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2405654522001366 |
| _version_ | 1797860355149398016 |
|---|---|
| author | Jun Bai Jun Li Ning Liu Hai Jia Xuemeng Si Yusong Zhou Zhian Zhai Ying Yang Fazheng Ren Zhenlong Wu |
| author_facet | Jun Bai Jun Li Ning Liu Hai Jia Xuemeng Si Yusong Zhou Zhian Zhai Ying Yang Fazheng Ren Zhenlong Wu |
| author_sort | Jun Bai |
| collection | DOAJ |
| description | Zearalenone (ZEA), a mycotoxin produced mainly by fungi belonging to Fusarium species in foods and feeds, causes a serious hazard to humans and animals. Numerous studies have revealed that ingesting ZEA can disrupt the reproductive function and impair the reproductive process in animals. This experiment was to investigate the toxicological effect and the mechanism of ZEA exposure on reproduction in pigs during early stages of pregnancy. In the present study, we treated with 0 to 80 μmol/L ZEA for 12 or 24 h in trophoblast ectoderm (pTr) cells. The results showed that ZEA had significantly decreased cell proliferation (P < 0.05), which was accompanied by DNA damage-related cell cycle arrest at G2/M phase, activation of the apoptosis and endoplasmic reticulum (ER) stress, as well as impairment of barrier function (P < 0.05). Western blot analysis and transmission electron microscopy (TEM) showed that exposure to ZEA can activation of autophagy in pTr cells. Importantly, pretreatment with chloroquine (CQ) or 3-methyladenine (3-MA) led to increased apoptosis in pTr cells. Interestingly, pTr cells pretreated with 4-phenylbutyric acid (4-PBA), an inhibitor of ER stress, resulted in reduced cell death in pTr cells, indicating a critical role for ER stress in the activation of autophagy. In conclusion, these results reveal that ZEA-triggered ER stress is critical for the cell fate decision of pTr cells during early porcine embryonic development. Application of small molecules with ability of blocking ER stress might be therapeutic option to reduce the deleterious effect of ZEA in pregnant animals. |
| first_indexed | 2024-04-09T21:45:38Z |
| format | Article |
| id | doaj.art-6fba635394ae4c9aaf45cdd17228f67e |
| institution | Directory Open Access Journal |
| issn | 2405-6545 |
| language | English |
| last_indexed | 2024-04-09T21:45:38Z |
| publishDate | 2023-03-01 |
| publisher | KeAi Communications Co., Ltd. |
| record_format | Article |
| series | Animal Nutrition |
| spelling | doaj.art-6fba635394ae4c9aaf45cdd17228f67e2023-03-25T05:11:43ZengKeAi Communications Co., Ltd.Animal Nutrition2405-65452023-03-0112186199Zearalenone induces apoptosis and autophagy by regulating endoplasmic reticulum stress signalling in porcine trophectoderm cellsJun Bai0Jun Li1Ning Liu2Hai Jia3Xuemeng Si4Yusong Zhou5Zhian Zhai6Ying Yang7Fazheng Ren8Zhenlong Wu9State Key Laboratory of Animal Nutrition, Department of Companion Animal Science, China Agricultural University, Beijing, 100193, ChinaState Key Laboratory of Animal Nutrition, Department of Companion Animal Science, China Agricultural University, Beijing, 100193, ChinaState Key Laboratory of Animal Nutrition, Department of Companion Animal Science, China Agricultural University, Beijing, 100193, ChinaState Key Laboratory of Animal Nutrition, Department of Companion Animal Science, China Agricultural University, Beijing, 100193, ChinaState Key Laboratory of Animal Nutrition, Department of Companion Animal Science, China Agricultural University, Beijing, 100193, ChinaState Key Laboratory of Animal Nutrition, Department of Companion Animal Science, China Agricultural University, Beijing, 100193, ChinaState Key Laboratory of Animal Nutrition, Department of Companion Animal Science, China Agricultural University, Beijing, 100193, ChinaState Key Laboratory of Animal Nutrition, Department of Companion Animal Science, China Agricultural University, Beijing, 100193, ChinaBeijing Advanced Innovation Center for Food Nutrition and Human Health, China Agricultural University, Beijing, 100193, ChinaState Key Laboratory of Animal Nutrition, Department of Companion Animal Science, China Agricultural University, Beijing, 100193, China; Beijing Advanced Innovation Center for Food Nutrition and Human Health, China Agricultural University, Beijing, 100193, China; Corresponding author.Zearalenone (ZEA), a mycotoxin produced mainly by fungi belonging to Fusarium species in foods and feeds, causes a serious hazard to humans and animals. Numerous studies have revealed that ingesting ZEA can disrupt the reproductive function and impair the reproductive process in animals. This experiment was to investigate the toxicological effect and the mechanism of ZEA exposure on reproduction in pigs during early stages of pregnancy. In the present study, we treated with 0 to 80 μmol/L ZEA for 12 or 24 h in trophoblast ectoderm (pTr) cells. The results showed that ZEA had significantly decreased cell proliferation (P < 0.05), which was accompanied by DNA damage-related cell cycle arrest at G2/M phase, activation of the apoptosis and endoplasmic reticulum (ER) stress, as well as impairment of barrier function (P < 0.05). Western blot analysis and transmission electron microscopy (TEM) showed that exposure to ZEA can activation of autophagy in pTr cells. Importantly, pretreatment with chloroquine (CQ) or 3-methyladenine (3-MA) led to increased apoptosis in pTr cells. Interestingly, pTr cells pretreated with 4-phenylbutyric acid (4-PBA), an inhibitor of ER stress, resulted in reduced cell death in pTr cells, indicating a critical role for ER stress in the activation of autophagy. In conclusion, these results reveal that ZEA-triggered ER stress is critical for the cell fate decision of pTr cells during early porcine embryonic development. Application of small molecules with ability of blocking ER stress might be therapeutic option to reduce the deleterious effect of ZEA in pregnant animals.http://www.sciencedirect.com/science/article/pii/S2405654522001366ZearalenonePorcine trophectodermApoptosisEndoplasmic reticulum stressAutophagy |
| spellingShingle | Jun Bai Jun Li Ning Liu Hai Jia Xuemeng Si Yusong Zhou Zhian Zhai Ying Yang Fazheng Ren Zhenlong Wu Zearalenone induces apoptosis and autophagy by regulating endoplasmic reticulum stress signalling in porcine trophectoderm cells Animal Nutrition Zearalenone Porcine trophectoderm Apoptosis Endoplasmic reticulum stress Autophagy |
| title | Zearalenone induces apoptosis and autophagy by regulating endoplasmic reticulum stress signalling in porcine trophectoderm cells |
| title_full | Zearalenone induces apoptosis and autophagy by regulating endoplasmic reticulum stress signalling in porcine trophectoderm cells |
| title_fullStr | Zearalenone induces apoptosis and autophagy by regulating endoplasmic reticulum stress signalling in porcine trophectoderm cells |
| title_full_unstemmed | Zearalenone induces apoptosis and autophagy by regulating endoplasmic reticulum stress signalling in porcine trophectoderm cells |
| title_short | Zearalenone induces apoptosis and autophagy by regulating endoplasmic reticulum stress signalling in porcine trophectoderm cells |
| title_sort | zearalenone induces apoptosis and autophagy by regulating endoplasmic reticulum stress signalling in porcine trophectoderm cells |
| topic | Zearalenone Porcine trophectoderm Apoptosis Endoplasmic reticulum stress Autophagy |
| url | http://www.sciencedirect.com/science/article/pii/S2405654522001366 |
| work_keys_str_mv | AT junbai zearalenoneinducesapoptosisandautophagybyregulatingendoplasmicreticulumstresssignallinginporcinetrophectodermcells AT junli zearalenoneinducesapoptosisandautophagybyregulatingendoplasmicreticulumstresssignallinginporcinetrophectodermcells AT ningliu zearalenoneinducesapoptosisandautophagybyregulatingendoplasmicreticulumstresssignallinginporcinetrophectodermcells AT haijia zearalenoneinducesapoptosisandautophagybyregulatingendoplasmicreticulumstresssignallinginporcinetrophectodermcells AT xuemengsi zearalenoneinducesapoptosisandautophagybyregulatingendoplasmicreticulumstresssignallinginporcinetrophectodermcells AT yusongzhou zearalenoneinducesapoptosisandautophagybyregulatingendoplasmicreticulumstresssignallinginporcinetrophectodermcells AT zhianzhai zearalenoneinducesapoptosisandautophagybyregulatingendoplasmicreticulumstresssignallinginporcinetrophectodermcells AT yingyang zearalenoneinducesapoptosisandautophagybyregulatingendoplasmicreticulumstresssignallinginporcinetrophectodermcells AT fazhengren zearalenoneinducesapoptosisandautophagybyregulatingendoplasmicreticulumstresssignallinginporcinetrophectodermcells AT zhenlongwu zearalenoneinducesapoptosisandautophagybyregulatingendoplasmicreticulumstresssignallinginporcinetrophectodermcells |