Roles of selenoprotein S in reactive oxygen species-dependent neutrophil extracellular trap formation induced by selenium-deficient arteritis

Chi, Qianru; Zhang, Qing; Lu, Yanxia; Zhang, Yiming; Xu, Shiwen

doi:10.1016/j.redox.2021.102003

Cited by 86 publications

(30 citation statements)

References 55 publications

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“…For SelK knockdown in vitro, C2C12 myoblasts were cultured in 6-well plates containing growth medium until the confluency reached 60–70%. Subsequently, cells were transfected with siRNAs using Lipofectamine RNAi MAX transfection reagent (Invitrogen) according to the method described by Chi et al [ 33 ]. Cells transfected with stealth RNAi Negative Control (siNC) were used as controls.…”

Section: Methodsmentioning

confidence: 99%

Selenoprotein K protects skeletal muscle from damage and is required for satellite cells-mediated myogenic differentiation

et al. 2022

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Section: Methodsmentioning

confidence: 99%

Selenoprotein K protects skeletal muscle from damage and is required for satellite cells-mediated myogenic differentiation

et al. 2022

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“…Oxidative stress, defined as excess production of reactive oxygen species (ROS) relative to antioxidant defense, has been shown to play an important role in the pathophysiology of atherosclerosis, ischemia, reperfusion, and cardiac hypertrophy. 41,42 The research suggested that TMT caused oxidative stress through increasing hydrogen peroxide, hydroxyl radicals and superoxide anions in the pathological response of different tissues induced by TMT. 43 TMT exposure decreased the activities of SOD, CAT, and GPX enzymes in the brain of Sprague Dawley rats.…”

Section: Discussionmentioning

confidence: 99%

Melatonin ameliorates trimethyltin chloride‐induced cardiotoxicity: The role of nuclear xenobiotic metabolism and Keap1‐Nrf2/ARE axis‐mediated pyroptosis

et al. 2021

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Trimethyltin chloride (TMT) is a stabilizer for polyvinyl chloride plastics that causes serious health hazards in nontarget organisms. Melatonin (MT) exhibits powerful protective effects in cardiac diseases. As a new environmental pollutant, TMT‐induced cardiotoxicity and the protective effects of MT remain unclear. To explore this, the mice were treated with TMT (2.8 mg/kg) and/or MT (10 mg/kg) for 7 days. Firstly, the histopathological and ultrastructural evaluation showed that TMT induced cardiac damage, tumescent rupture and nuclear pyknosis. Moreover, TMT elevated the expressions of pyroptosis genes NLRP3, ASC and Cas1 and inflammation factors IL‐6, IL‐17 and TNFα. Secondly, TMT reduced antioxidant enzymes (GSH, CAT and T‐AOC) via decreasing the expression of genes associated with the Keap1‐Nrf2/ARE pathway to increase oxidative stress. Thirdly, TMT decreased the expression of genes associated with the ARE‐driven drug metabolizing enzymes (DMEs), including Akr7a3, Akr1b8, and Akr1b10. Besides, TMT upregulated the mRNA expression of nuclear Xenobiotic metabolism on cytochrome P450s enzymes via increasing the expression of CAR, PXP, and AHR genes. Furthermore, MT treatment mitigated the aforementioned adverse changes induced by TMT. Overall, these results demonstrated that TMT caused pyroptosis and inflammation to aggravate cardiac damage via inducing excessive oxidative stress, imbalance of DMEs homeostasis, and nuclear Xenobiotic metabolism disorder, which could be alleviated by MT.

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“…Sec is mainly located in the redox catalytic site and has a higher redox potential ( 25 ). Selenoproteins exist primarily in the form of redox enzymes and carry out very diverse functions such as regulation of cellular oxidative stress, immune function, ER stress, and autophagy, which are integrally related to the development of diverse tumors ( 26 , 27 ). As mentioned, autophagy is activated under oxidative stress situations.…”

Section: Introductionmentioning

confidence: 99%

Schisandrin B Induced ROS-Mediated Autophagy and Th1/Th2 Imbalance via Selenoproteins in Hepa1-6 Cells

et al. 2022

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Schisandrin B (Sch B) is well-known for its antitumor effect; however, its underlying mechanism remains confusing. Our study aimed to investigate the role of selenoproteins in Sch B-induced autophagy and Th1/Th2 imbalance in Hepa1-6 cells. Hepa1-6 cells were chosen to explore the antitumor mechanism and were treated with 0, 25, 50, and 100 μM of Sch B for 24 h, respectively. We detected the inhibition rate of proliferation, transmission electron microscopy (TEM), monodansylcadaverine (MDC) staining, reactive oxygen species (ROS) level and oxidative stress-related indicators, autophagy-related genes, related Th1/Th2 cytokines, and selenoprotein mRNA expression. Moreover, the heat map, principal component analysis (PCA), and correlation analysis were used for further bioinformatics analysis. The results revealed that Sch B exhibited well-inhibited effects on Hepa1-6 cells. Subsequently, under Sch B treatment, typical autophagy characteristics were increasingly apparent, and the level of punctate MDC staining enhanced and regulated the autophagy-related genes. Overall, Sch B induced autophagy in Hepa1-6 cells. In addition, Sch B-promoted ROS accumulation eventually triggered autophagy initiation. Results of Th1 and Th2 cytokine mRNA expression indicated that Th1/Th2 immune imbalance was observed by Sch B treatment in Hepa1-6 cells. Intriguingly, Sch B downregulated the majority of selenoprotein expression. Also, the heat map results observed significant variation of autophagy-related genes, related Th1/Th2 cytokines, and selenoprotein expression in response to Sch B treatment. PCA outcome suggested the key role of Txnrd1, Txnrd3, Selp, GPX2, Dio3, and Selr with its potential interactions in ROS-mediated autophagy and Th1/Th2 imbalance of Hepa1-6 cells. In conclusion, Sch B induced ROS-mediated autophagy and Th1/Th2 imbalance in Hepa1-6 cells. More importantly, the majority of selenoproteins were intimately involved in the process of autophagy and Th1/Th2 imbalance, Txnrd3, Selp, GPX2, Dio3, and Selr had considerable impacts on the process.

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Roles of selenoprotein S in reactive oxygen species-dependent neutrophil extracellular trap formation induced by selenium-deficient arteritis

Cited by 86 publications

References 55 publications

Selenoprotein K protects skeletal muscle from damage and is required for satellite cells-mediated myogenic differentiation

Selenoprotein K protects skeletal muscle from damage and is required for satellite cells-mediated myogenic differentiation

Melatonin ameliorates trimethyltin chloride‐induced cardiotoxicity: The role of nuclear xenobiotic metabolism and Keap1‐Nrf2/ARE axis‐mediated pyroptosis

Schisandrin B Induced ROS-Mediated Autophagy and Th1/Th2 Imbalance via Selenoproteins in Hepa1-6 Cells

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