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Tetrachlorobenzoquinone-InducednNrf2 Confers Neuron-likenPC12 Cells Resistance to Endoplasmic Reticulum Stress via RegulatingnGlutathione Synthesis and Protein Thiol Homeostasis 四氯苯醌诱导的nNrf2通过调节谷胱甘肽合成和蛋白硫醇稳态，赋予神经元样nPC12细胞对内质网应激的抗性

Figshare Pub Date : 2018-11-02 DOI: 10.1021/acs.chemrestox.8b00209.s001

Zixuan Liu (475331), Wenjing Dong (117921), Bingwei Yang (5657015), Lu Peng (769036), Xiaomin Xia (484046), Lanxiang Pu (5924435), Na Zhang (333280), Erqun Song (629771), Yang Song (88132)

{"title":"Tetrachlorobenzoquinone-InducednNrf2 Confers Neuron-likenPC12 Cells Resistance to Endoplasmic Reticulum Stress via RegulatingnGlutathione Synthesis and Protein Thiol Homeostasis","authors":"Zixuan Liu (475331), Wenjing Dong (117921), Bingwei Yang (5657015), Lu Peng (769036), Xiaomin Xia (484046), Lanxiang Pu (5924435), Na Zhang (333280), Erqun Song (629771), Yang Song (88132)","doi":"10.1021/acs.chemrestox.8b00209.s001","DOIUrl":"https://doi.org/10.1021/acs.chemrestox.8b00209.s001","url":null,"abstract":"Ournprevious studies demonstrated that tetrachlorobenzoquinonen(TCBQ) is toxic to neuron-like cells, which is related to endoplasmicnreticulum (ER) stress-induced apoptosis. However, it remains unclearnwhether TCBQ causes the opening of cellular defense responses. Herenwe found that activation of nuclear factor erythroid-derived 2-liken2 (Nrf2) triggered an adaptive response against the neurotoxicityninduced by TCBQ through the upregulation of intracellular glutathionen(GSH) levels in rat pheochromocytoma PC12 cells. TCBQnupregulated the levels of GSH mainly by the following two ways: (i)nNrf2 activation induced the expression of cystine/glutamate antiporternsolute carrier family 7 member 11 (SLC7A11, also called xCT); (ii)nNrf2 activation resulted in increased the expression of glutamylcysteinenligase. GSH is involved in cell antioxidant ability and protein thiolnhomeostasis, especially in the ER. Therefore, GSH has the abilitynto inhibit ER stress and promote cell survival. Our data showed thatndecreasing GSH levels exacerbated TCBQ-induced depletion of protein-SH,nparticularly in the ER. Conversely, increasing GSH levels attenuatednTCBQ-induced protein damage, degree of ER stress, and cell death.nThese findings demonstrated that GSH-inhibited cells were vulnerablento TCBQ-induced ER stress and apoptosis. Overall, our results analyzednthe relationships between Nrf2 and ER stress in response to TCBQ andnshowed that activation of Nrf2-GSH played a protective role againstnTCBQ-induced ER stress-associated neurotoxicity via regulatingnGSH synthesis and protein thiol homeostasis.","PeriodicalId":522235,"journal":{"name":"Figshare","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147893830","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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