Key Laboratory of Environmental Medicine Engineering of Ministry of Education, Medical School, Southeast University, Nanjing 210009, China.
College of Biology and Food Engineering, Chongqing Three Gorges University, Wanzhou 404100, China.
Chem Res Toxicol. 2021 May 17;34(5):1308-1318. doi: 10.1021/acs.chemrestox.0c00501. Epub 2021 Mar 2.
In this study, the association of expressional alterations in neuronal G protein-coupled receptors (GPCRs) with induction of protective response to polystyrene nanoparticles (PS-NPs) was investigated in . On the basis of both phenotypic analysis and expression levels, the alterations in expressions of NPR-1, NPR-4, NPR-8, NPR-9, NPR-12, DCAR-1, GTR-1, DOP-2, SER-4, and DAF-37 in neuronal cells mediated the protective response to PS-NPs exposure. In neuronal cells, NPR-9, NPR-12, DCAR-1, and GTR-1 controlled the PS-NPs toxicity by activating or inhibiting JNK-1/JNK MAPK signaling. Neuronal NPR-8, NPR-9, DCAR-1, DOP-2, and DAF-37 controlled the PS-NPs toxicity by activating or inhibiting MPK-1/ERK MAPK signaling. Neuronal NPR-4, NPR-8, NPR-9, NPR-12, GTR-1, DOP-2, and DAF-37 controlled the PS-NPs toxicity by activating or inhibiting DBL-1/TGF-β signaling. Neuronal NPR-1, NPR-4, NPR-12, and GTR-1 controlled the PS-NPs toxicity by activating or inhibiting DAF-7/TGF-β signaling. Our data provides an important neuronal basis for induction of protective response to PS-NPs in .
在这项研究中，我们研究了神经元 G 蛋白偶联受体 (GPCR) 表达变化与聚苯乙烯纳米颗粒 (PS-NPs) 诱导保护反应的关系。基于表型分析和表达水平，神经元细胞中 NPR-1、NPR-4、NPR-8、NPR-9、NPR-12、DCAR-1、GTR-1、DOP-2、SER-4 和 DAF-37 的表达变化介导了对 PS-NPs 暴露的保护反应。在神经元细胞中，NPR-9、NPR-12、DCAR-1 和 GTR-1 通过激活或抑制 JNK-1/JNK MAPK 信号来控制 PS-NPs 的毒性。神经元 NPR-8、NPR-9、DCAR-1、DOP-2 和 DAF-37 通过激活或抑制 MPK-1/ERK MAPK 信号来控制 PS-NPs 的毒性。神经元 NPR-4、NPR-8、NPR-9、NPR-12、GTR-1、DOP-2 和 DAF-37 通过激活或抑制 DBL-1/TGF-β 信号来控制 PS-NPs 的毒性。神经元 NPR-1、NPR-4、NPR-12 和 GTR-1 通过激活或抑制 DAF-7/TGF-β 信号来控制 PS-NPs 的毒性。我们的数据为 诱导对 PS-NPs 的保护反应提供了一个重要的神经元基础。
