PDF(Pubmed)
Abstract：
Earthworms are affected by physical stress, like injury, and by exposure to xenobiotics, such as the toxic metal cadmium (Cd), which enters the environment mainly through industry and agriculture. The stress response to the single and the combination of both stressors was examined in regenerative and unharmed tissue of Lumbricus terrestris to reveal if the stress response to a natural insult like injury (amputation) interferes with Cd detoxification mechanisms. We characterized the roles of metallothionein 1 (MT1) and MT2 isoforms, heat shock protein 70 as well as immune biomarkers such as the toll-like receptors (TLR) single cysteine cluster TLR and multiple cysteine cluster TLR. The role of the activated transcription factors (ATFs) ATF2, ATF7, and the cAMP responsive element binding protein as putative regulatory intersection as well as a stress-dependent change of the essential trace elements zinc and calcium was analyzed. Phosphorylated AMP activated protein kinase, the cellular energy sensor, was measured to explore the energy demand, while the energy status was determined by detecting carbohydrate and protein levels. Taken together, we were able to show that injury rather than Cd is the driving force that separates the four treatment groups - Control, Cd exposure, Injury, Cd exposure and injury. Interestingly, we found that gene expression differed regarding the tissue section that was analyzed and we hypothesize that this is due to the migration of coelomocytes, earthworm immune cells, that take over a key role in protecting the organism from a variety of environmental challenges. Surprisingly, we discovered a role for MT1 in the response to multiple stressors and an isoform-specific function for the two newly characterized TLRs. In conclusion, we gathered novel information on the relation of innate immunity, wound healing, and Cd detoxification mechanisms in earthworms.
摘要：
蚯蚓受到身体压力的影响，比如受伤，通过暴露于外源性物质，如有毒的金属镉（Cd），主要通过工业和农业进入环境。在Lumbricusterridis的再生和未受伤害组织中检查了对单一和两种应激源组合的应激反应，以揭示对自然损伤样损伤（截肢）的应激反应是否会干扰Cd解毒机制。我们表征了金属硫蛋白1（MT1）和MT2亚型的作用，热休克蛋白70以及免疫生物标志物如toll样受体(TLR)单半胱氨酸簇TLR和多半胱氨酸簇TLR。分析了激活的转录因子（ATF）ATF2，ATF7和cAMP响应元件结合蛋白作为推定的调节交集以及必需微量元素锌和钙的应激依赖性变化的作用。磷酸化AMP活化蛋白激酶,细胞能量传感器，被测量以探索能源需求，而能量状态是通过检测碳水化合物和蛋白质水平来确定的。一起来看,我们能够证明损伤而不是Cd是将四个治疗组分开的驱动力-对照组，Cd暴露,伤害,Cd暴露与伤害。有趣的是,我们发现所分析的组织切片的基因表达不同，我们假设这是由于腔体细胞的迁移，蚯蚓免疫细胞,在保护生物体免受各种环境挑战方面发挥着关键作用。令人惊讶的是,我们发现了MT1在对多种应激源的反应中的作用以及两种新表征的TLR的同工型特异性功能.总之,我们收集了关于先天免疫关系的新信息，伤口愈合，蚯蚓的Cd解毒机制。
