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Lipid metabolic response to polystyrene particles in nematode Caenorhabditis elegans

机译:线虫秀丽隐杆线虫对聚苯乙烯颗粒的脂质代谢反应

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Nanoplastics can be used in various fields, such as personal care products. Nevertheless, the effect of nanoplastic exposure on metabolism and its association with stress response remain largely unclear. Using Caenorhabditis elegans as an animal model, we determined the effect of nanopolystyrene exposure on lipid metabolism and its association with the response to nanopolystyrene. Exposure (from L1-larave to adult day-3) to 100 nm nanopolystyrene (>= 1 mu g/L) induced severe lipid accumulation and increase in expressions of mdt-15 and sbp-1 encoding two lipid metabolic sensors. Meanwhile, we found that SBP-1 acted downstream of intestinal MDT-15 during the control of response to nanopolystyrene. Intestinal transcriptional factor SBP-1 activated two downstream targets, fatty acyl CoA desaturase FAT-6 and heat-shock protein HSP-4 (a marker of endoplasmic reticulum unfolded protein response (ER UPR)) to regulate nanopolystyrene toxicity. Both MDT-15 and SBP-1 were involved in the activation of ER-UPR in nanopolystyrene exposed nematodes. Moreover, SBP-1 regulated the innate immune response by activating FAT-6 in nanopolystyrene exposed nematodes. In the intestine, function of MDT-15 and SBP-1 in regulating nanopolystyrene toxicity was under the control of upstream signaling cascade (PMK-1-SKN-1) in p38 MAPK signaling pathway. Therefore, our data raised an important molecular basis for potential protective function of lipid metabolic response in nanopolystyrene exposed nematodes. (C) 2019 Elsevier Ltd. All rights reserved.
机译:纳米塑料可用于各种领域,例如个人护理产品。然而,纳米塑料暴露对代谢的影响及其与应激反应的关系仍然不清楚。使用秀丽隐杆线虫作为动物模型,我们确定了纳米聚苯乙烯暴露对脂质代谢的影响及其与纳米聚苯乙烯反应的关系。暴露(从L1幼虫到成年第3天)暴露于100 nm纳米聚苯乙烯(> = 1μg / L)会引起严重的脂质蓄积,并增加编码两个脂质代谢传感器的mdt-15和sbp-1的表达。同时,我们发现在对纳米聚苯乙烯的反应控制过程中,SBP-1在肠道MDT-15的下游起作用。肠转录因子SBP-1激活两个下游靶标,脂肪酰基CoA去饱和酶FAT-6和热休克蛋白HSP-4(内质网未折叠蛋白反应(ER UPR)的标志物)来调节纳米聚苯乙烯的毒性。 MDT-15和SBP-1均参与了纳米聚苯乙烯暴露的线虫中ER-UPR的活化。此外,SBP-1通过激活纳米聚苯乙烯暴露的线虫中的FAT-6来调节先天免疫应答。在肠道中,MDT-15和SBP-1在调节纳米聚苯乙烯毒性中的功能受p38 MAPK信号传导途径中上游信号传导级联(PMK-1-SKN-1)的控制。因此,我们的数据为暴露于纳米聚苯乙烯的线虫中脂质代谢反应的潜在保护功能提供了重要的分子基础。 (C)2019 Elsevier Ltd.保留所有权利。

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