School of Bioengineering, Huainan Normal University, Huainan, 232038, China; Key Laboratory of Bioresource and Environmental Biotechnology of Anhui Higher Education Institutes, Huainan Normal University, Huainan, 232038, China.
School of Bioengineering, Huainan Normal University, Huainan, 232038, China; Key Laboratory of Bioresource and Environmental Biotechnology of Anhui Higher Education Institutes, Huainan Normal University, Huainan, 232038, China.
Environ Pollut. 2020 Jun;261:114081. doi: 10.1016/j.envpol.2020.114081. Epub 2020 Feb 5.
Cadmium (Cd) exposure poses a serious environmental problem due to the metal's bioaccumulation and difficult to eliminate from body. Understanding the mechanisms of Cd detoxification and resistance can provide insights into methods to protect against the damaging effects of the heavy metal. In the present study, we found that heat shock (HS) pretreatment increased Cd resistance of the nematode Caenorhabditis elegans by reducing the bagging phenotype and protecting the integrity of the intestinal barrier. HS pretreatment increased the expression of heat shock protein-16.2 (HSP-16.2) prior to Cd exposure, and HS-induced Cd resistance was absent in worms with hsp-16.2 loss-of-function mutation. Worm strain with daf-2(e1370) mutation presented enhanced HS-induced Cd resistance, which was eliminated in worm strains of daf-16(mu86) and hsf-1(sy441). HS pretreatment increased DAF-16 nuclear localization and HSF-1 granule formation prior to Cd exposure. DAF-16 and HSF-1 was essential in reducing bagging formation and protecting the integrity of intestinal barrier after HS pretreatment. In conclusion, the present study demonstrated that HS-induced Cd resistance in C. elegans is regulated by the DAF-16/FOXO and HSF-1 pathways through regulation of HSP-16.2 expression.
镉（Cd）暴露是一个严重的环境问题，因为金属的生物积累和难以从体内消除。了解 Cd 解毒和抗性的机制可以为保护重金属的破坏性影响提供方法。在本研究中，我们发现热休克（HS）预处理通过减少包裹表型和保护肠屏障的完整性来增加线虫秀丽隐杆线虫的 Cd 抗性。HS 预处理在暴露于 Cd 之前增加了热休克蛋白-16.2（HSP-16.2）的表达，并且在 hsp-16.2 功能丧失突变的蠕虫中不存在 HS 诱导的 Cd 抗性。daf-2(e1370)突变的蠕虫菌株表现出增强的 HS 诱导的 Cd 抗性，而在 daf-16(mu86)和 hsf-1(sy441)的蠕虫菌株中则消除了这种抗性。HS 预处理增加了 DAF-16 的核定位和 HSF-1 颗粒形成，然后再暴露于 Cd。DAF-16 和 HSF-1 在 HS 预处理后减少包裹形成和保护肠屏障的完整性方面是必不可少的。总之，本研究表明，HS 诱导的 C. elegans 中的 Cd 抗性是通过调节 HSP-16.2 的表达由 DAF-16/FOXO 和 HSF-1 途径调节的。
