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Nuclear factor E2-associated factor 2 and musculoaponeurotic fibrosarcoma K mediate regulation glutathione peroxidase of Cristaria plicata after microcystin-induced oxidative stress
Comparative Biochemistry and Physiology C: Toxicology & Pharmacology ( IF 3.9 ) Pub Date : 2023-09-07 , DOI: 10.1016/j.cbpc.2023.109742
Xinying Cao 1 , Jinhua An 1 , Shanshan Zhu 1 , Maolin Feng 1 , Yang Gang 1 , Chungen Wen 1 , Baoqing Hu 1
Affiliation  

Nuclear factor E2-associated factor 2 (Nrf2)/Antioxidant Response Element (ARE) signaling pathway is an endogenous antioxidant pathway that protects cells from oxidative damage. This pathway is triggered when aquatic organisms are exposed to environmental toxicants. In this study, CpMafK (musculoaponeurotic fibrosarcoma K of Cristaria plicata) mRNA expression in hepatopancreas and gills were up regulated after Cristaria plicata (C. plicata) was exposed to microcystin (MC), which showed that CpMafK protected C. plicata from MC. After MC treatment and CpNrf2 (Nrf2 of Cristaria plicata) knockdown, the mRNA expression of CpMafK was down regulated. After MC treatment and CpMafK knockdown, the mRNA expression of CpNrf2 was down regulated. Indicating that the expression of CpNrf2 was positively correlated with CpMafK. CpGPx (GPx of Cristaria plicata) mRNA was also down regulated with the down regulation of CpMafK and CpNrf2. CpGPx promoter contains a variety of transcription factor binding sites, including Nrf2, ARE elements, etc. Gel blocking experiments showed that CpNrf2/CpMafK heterodimers were bound to CpGPx promoters in vitro. Dual luciferase reporter assay showed that CpNrf2/CpMafK heterodimer negatively regulated CpGPx promoter in cells. In conclusion, Nrf2 and MafK mediate regulation of GPx play a crucial role in protecting bivalves from MC.



中文翻译:

核因子E2相关因子2和肌肉腱膜纤维肉瘤K在微囊藻毒素诱导的氧化应激后介导褶皱嵴谷胱甘肽过氧化物酶的调节

核因子 E2 相关因子 2 (Nrf2)/抗氧化反应元件 (ARE) 信号通路是一种内源性抗氧化通路,可保护细胞免受氧化损伤。当水生生物暴露于环境毒物时,就会触发该途径。在本研究中,CpMafK( C. plicata)暴露于微囊藻毒素(MC)后,肝胰腺和鳃中的CpMafK(肌筋膜纤维肉瘤K of Cristaria plicata)mRNA表达上调,这表明CpMafK可以保护C. plicata免受MC侵害。MC处理和CpNrf2( Cristaria plicata的Nrf2 )敲除后,CpMafK的mRNA表达下调。MC处理和CpMafK敲除后,CpNrf2的mRNA表达下调。说明CpNrf2的表达量与CpMafK呈正相关。CpGPx ( Cristaria plicata的 GPx ) mRNA 也随着 CpMafK 和 CpNrf2 的下调而下调。CpGPx启动子含有多种转录因子结合位点,包括Nrf2、ARE元件等。凝胶封闭实验表明,CpNrf2/CpMafK异二聚体在体外与CpGPx启动子结合。双荧光素酶报告基因检测显示,CpNrf2/CpMafK 异二聚体负向调节细胞中的 CpGPx 启动子。总之,Nrf2 和 MafK 介导的GPx 调节在保护双壳类免受 MC 侵害方面发挥着至关重要的作用。

更新日期:2023-09-07
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