Dysregulation of G protein-coupled receptors in the intestine by nanoplastic exposure in Caenorhabditis elegans,Environmental Science: Nano

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Dysregulation of G protein-coupled receptors in the intestine by nanoplastic exposure in Caenorhabditis elegans
Environmental Science: Nano ( IF 5.8 ) Pub Date : 2021-2-22 , DOI: 10.1039/d0en00991a
Yunhan Yang _{1,

2,

3,

4} , Qiuli Wu _{1,

2,

3,

4} , Dayong Wang _{1,

2,

3,

4,

5}

Affiliation

After their uptake, environmental toxicants may cause toxicity to organisms by activating or inhibiting certain G protein-coupled receptors (GPCRs). Nevertheless, the roles of GPCRs in mediating the response of organisms to nanoplastic exposure are still largely unclear. We here employed Caenorhabditis elegans as an animal model and focused on the identification of intestinal GPCRs required for control of the toxicity of nanopolystyrene (100 nm). Based on gene expression and functional analysis, we identified 13 GPCRs (PAQR-2, NPR-1, DOP-2, CED-1, NPR-9, FSHR-1, DCAR-1, NPR-12, NPR-4, SER-4, DAF-37, GTR-1, and NPR-8) involved in the control of nanopolystyrene toxicity. Moreover, among these identified GPCRs, only PAQR-2 and FSHR-1 acted in the intestine to regulate nanopolystyrene toxicity. PAQR-2 and FSHR-1 regulated nanopolystyrene toxicity in the intestine by at least modulating the activities of insulin, Wnt, p38 mitogen-activated protein kinase (MAPK), ELT-2, and/or mitochondrial unfolded protein response (mt UPR) signaling pathways. Therefore, our results provide a crucial basis for understanding the functions of GPCRs in the intestine to mediate the response to nanoplastic exposure in organisms.

中文翻译：

秀丽隐杆线虫的纳米塑料暴露肠道中G蛋白偶联受体的失调。

吸收后，环境有毒物质可能通过激活或抑制某些G蛋白偶联受体（GPCR）来对生物体产生毒性。尽管如此，GPCR在介导生物体对纳米塑料暴露的反应中的作用仍不清楚。我们在这里聘用秀丽隐杆线虫作为动物模型，重点研究了控制纳米聚苯乙烯（100 nm）毒性所需的肠道GPCR。根据基因表达和功能分析，我们鉴定出13个GPCR（PAQR-2，NPR-1，DOP-2，CED-1，NPR-9，FSHR-1，DCAR-1，NPR-12，NPR-4，SER -4，DAF-37，GTR-1和NPR-8）参与了纳米聚苯乙烯毒性的控制。此外，在这些已鉴定的GPCR中，只有PAQR-2和FSHR-1在肠中起作用以调节纳米聚苯乙烯的毒性。PAQR-2和FSHR-1通过至少调节胰岛素，Wnt，p38丝裂原活化蛋白激酶（MAPK），ELT-2和/或线粒体未折叠蛋白应答（mt UPR）信号传导的活性来调节肠道中的纳米聚苯乙烯毒性途径。所以，

更新日期：2021-03-05

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