Lipid metabolic response to polystyrene particles in nematode Caenorhabditis elegans.
Lipid metabolic response to polystyrene particles in nematode Caenorhabditis elegans.
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DOI：
10.1016/j.envpol.2019.113439
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发表时间：
2019-10
影响因子：
8.9
通讯作者：
Yunhan Yang;Huimin Shao;Qiuli Wu;Dayong Wang
中科院分区：
文献类型：
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作者：
Yunhan Yang;Huimin Shao;Qiuli Wu;Dayong Wang
纳米塑料可用于各种领域，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在很大程度上仍不清楚。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。100 nm纳米聚苯乙烯（≥1 μg/L）暴露（从L1-larave到成年第3天）可诱导严重的脂质蓄积和编码两种脂质代谢传感器的mdt-15和sbp-1表达增加。同时，我们发现SBP-1在对纳米聚苯乙烯反应的控制过程中作用于肠道MDT-15的下游。肠转录因子SBP-1激活两个下游靶点，脂肪酰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），以调节纳米聚苯乙烯毒性。MDT-15和SBP-1均参与了暴露于纳米聚苯乙烯的线虫中ER-UPR的激活。此外，SBP-1通过激活暴露于纳米聚苯乙烯的线虫中的FAT-6来调节先天免疫应答。在肠道中，MDT-15和SBP-1调节纳米聚苯乙烯毒性的功能受p38 MAPK信号通路上游信号级联（PMK-1-SKN-1）的控制。因此，我们的数据提出了一个重要的分子基础，在纳米聚苯乙烯暴露线虫的脂质代谢反应的潜在保护功能。
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. UsingCaenorhabditis elegansas 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 μg/L) induced severe lipid accumulation and increase in expressions ofmdt-15andsbp-1encoding 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.