Zearalenone induces mitochondria-associated endoplasmic reticulum membranes dysfunction in piglet Sertoli cells based on endoplasmic reticulum stress
文献类型: 外文期刊
第一作者: Ma, Li
作者: Ma, Li;Hai, Sirao;Wang, Chenlong;Chen, Chuangjiang;Rahman, Sajid Ur;Zhao, Chang;Feng, Shibin;Wang, Xichun;Rahman, Sajid Ur;Rahman, Sajid Ur;Bazai, Mansoor Ahmed;Wang, Xichun
作者机构:
关键词: Zearalenone; Piglet sertoli cells; Mitochondria-associated endoplasmic; reticulum membranes; Endoplasmic reticulum stress
期刊名称:ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY ( 影响因子:6.8; 五年影响因子:6.9 )
ISSN: 0147-6513
年卷期: 2023 年 254 卷
页码:
收录情况: SCI
摘要: Zearalenone (ZEA) is an estrogen-like mycotoxin, which mainly led to reproductive toxicity. The study aimed to investigate the molecular mechanism of ZEA-induced dysfunction of mitochondria-associated endoplasmic re-ticulum membranes (MAM) in piglet Sertoli cells (SCs) via the endoplasmic reticulum stress (ERS) pathway. In this study, SCs were used as a research object that was exposed to ZEA, and ERS inhibitor 4-Phenylbutyrate acid (4-PBA) was used as a reference. The results showed that ZEA damaged cell viability and increased Ca2+ levels; damaged the structure of MAM; up-regulated the relative mRNA and protein expression of glucose-regulated protein 75 (Grp75) and mitochondrial Rho-GTPase 1 (Miro1), while inositol 1,4,5-trisphosphate receptor (IP3R), voltage-dependent anion channel 1 (VDAC1), mitofusin2 (Mfn2) and phosphofurin acidic cluster protein 2 (PACS2) were down-regulated. After a 3 h 4-PBA-pretreatment, ZEA was added for mixed culture. The results of 4-PBA pretreatment showed that inhibition of ERS reduced the cytotoxicity of ZEA against piglet SCs. Compared with the ZEA group, inhibition of ERS increased cell viability and decreased Ca2+ levels; restored the structural damage of MAM; down-regulated the relative mRNA and protein expression of Grp75 and Miro1; and up-regulated the relative mRNA and protein expression of IP3R, VDAC1, Mfn2, and PACS2. In conclusion, ZEA can induce MAM dysfunction in piglet SCs via the ERS pathway, whereas ER can regulate mitochondria through MAM.
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