HERP depletion inhibits zearalenone-induced apoptosis through autophagy activation in mouse ovarian granulosa cells

Chen, Fenglei; Wen, Xin; Lin, Peng; Chen, Huatao; Wang, Aihua; Jin, Yaping

doi:10.1016/j.toxlet.2018.10.026

Cited by 33 publications

(28 citation statements)

References 56 publications

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“…The adverse effects of ZEA have been widely investigated in humans, farm animals, poultry, birds and companion animals such as pig, sheep, bovine, horse, chicken, birds, dogs and cats [23,24,25,26,27,28]. ZEA and its derivatives affect the synthesis and secretion of steroid sex hormones through disturbing the cell function of Leydig cells in testis [29,30].…”

Section: Discussionmentioning

confidence: 99%

The Role of miRNAs in Zearalenone-Promotion of TM3 Cell Proliferation

Zheng

Fan

Feng

et al. 2019

IJERPH

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Zearalenone (ZEA) is a non-steroidal estrogen mycotoxin produced by several Gibberella and Fusarium species. Accumulating evidence has indicated that ZEA strongly stimulates cell proliferation. However the detailed molecular and cellular mechanisms of ZEA-mediated induction of cell proliferation have not yet been completely explained. The aim of this study was to detect the role of miRNAs in ZEA-mediated induction of cell proliferation. The effects of ZEA on cell proliferation were assessed using a cell counting kit assay and xCELLigence system. Micro-RNA sequencing was performed after treatment of TM3 cells with ZEA (0.01 μmol/L) for different time periods (0, 2, 6 and 18 h). Cell function and pathway analysis of the miRNA target genes were performed by Ingenuity Pathway Analysis (IPA). We found that ZEA promotes TM3 cell proliferation at low concentrations. miRNA sequenceing revealed 66 differentially expressed miRNAs in ZEA-treated cells in comparison to the untreated control ( p < 0.05). The miRNA sequencing indicated that compared to control group, there were 66 miRNAs significant change (p < 0.05) in ZEA-treated groups. IPA analysis showed that the predicated miRNAs target gene involved in cell Bio-functions including cell cycle, growth and proliferation, and in signaling pathways including MAPK and RAS-RAF-MEK-ERK pathways. Results from flow cytometry and Western Blot analysis validated the predictions that ZEA can affect cell cycle, and the MAPK signaling pathway. Taking these together, the cell proliferation induced ZEA is regulated by miRNAs. The results shed light on the molecular and cellular mechanisms for the mediation of ZEA to induce proliferation.

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Section: Discussionmentioning

confidence: 99%

The Role of miRNAs in Zearalenone-Promotion of TM3 Cell Proliferation

Zheng

Fan

Feng

et al. 2019

IJERPH

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“…No. AM5760, Life Technologies, Carlsbad, CA, United States) was amplified and cloned into pCD513B-1 (SBI, Mountain View, CA, United States), which contains a GFP expression construct, to generate a pCD513B-U6 lentiviral vector (Chen et al, 2019). Lentivirus vectors encoding the EIF2S1 shRNA (shEIF2S1) and non-silencing negative control (shNC) were constructed by our group.…”

Section: Transducing Short Hairpin Interfering Rnas (Shrnas) Via Lentmentioning

confidence: 99%

Prostaglandin F2α Induces Goat Corpus Luteum Regression via Endoplasmic Reticulum Stress and Autophagy

Wen

Liu

et al. 2020

Front. Physiol.

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Corpus luteum (CL) is a transient endocrine tissue that produces progesterone for maintaining pregnancy in mammals. In addition, the regression of CL is necessary for the initiation of the estrous cycle. Extensive research has shown that the prostaglandin F2α (PGF2α) induces the regression of CL in ruminants. However, the mechanisms of endoplasmic reticulum (ER) stress and autophagy in the regression of goat CL induced by PGF2α are still unclear. In this study, ovaries of dioestrus goats and goats that were 3 months pregnant were collected to detect the location of the ER stress-related protein GRP78. The relationship between the different stages of the luteal phase of goat CL during the estrous cycle and changes in the expression of ER stress-related proteins and autophagy-related proteins was confirmed by western blot analysis. The results showed that both ER stress and autophagy were activated in the late luteal phase of the goat CL. To reveal the function of ER stress and autophagy in the CL regression process induced by PGF2α, we used 4-phenyl butyric acid (4-PBA) and chloroquine (CQ) for inhibiting ER stress and autophagy, respectively. Through the apoptotic rate detected by the flow cytometry and the expression of ER stress-and autophagy-related proteins detected by western blotting, we demonstrated that ER stress promoted goat luteal cell apoptosis and autophagy, and that apoptosis can be enhanced by the inhibition of autophagy. In addition, knockdown of EIF2S1, which blocked the PERK pathway activation, promoted apoptosis by reducing autophagy in goat luteal cells treated with PGF2α. In conclusion, our study indicates that ER stress promotes goat luteal cell apoptosis to regulate the regression of CL and activates autophagy to inhibit the goat luteal cell apoptosis via PERK signaling pathway.

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“…ZEA inhibited the proliferation of GCs in a dose-dependent manner, induce apoptosis and necrosis of GCs through the mitochondrial apoptosis pathway 16 The ER stress and autophagy were also involved in the mechanism of the action of ZEA on GCs 17 . Therefore, inhibiting GCs apoptosis may alleviate the reproductive toxicity caused by ZEA.…”

Section: Introductionmentioning

confidence: 99%