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互补的转录基因和蛋白质基因分析阐明了肠直肌细胞中脱氧尼瓦伦醇诱导的收缩功能障碍的毒理学分子机制

Yu Qiao¹, Xu Ji², Huiduo Guo³

¹College of Animal Science and Technology, Nanjing Agricultural University, Nanjing, 210095, China; Anhui Province Key Laboratory of Livestock and Poultry Product Safety Engineering, Institute of Animal Science and Veterinary Medicine, Anhui Academy of Agricultural Sciences, Hefei, 230031, China.

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

|February 25, 2024

概括

脱氧尼瓦伦醇 (DON) 菌毒素通过破坏肠道光滑肌肉细胞来损害肠道运动能力. 这项研究揭示了DON破坏了细胞外矩阵-整合素-活性素通路,抑制肌肉收缩并导致体重减轻.

科学领域:

毒理学毒理学毒理学
细胞生物学细胞生物学
胃肠病学胃肠病学

背景情况:

脱氧尼瓦伦醇 (DON) 是一种普遍存在的菌菌毒素,具有重大公共卫生影响.
DON诱导的体重减轻与减少料摄入量和胃肠道 (GIT) 运动性的改变有关.
之前的研究表明,DON通过损害肠道光滑肌细胞 (SMC) 来损害肠道运动能力.

研究的目的:

阐明DON影响肠道SMC收缩性的分子机制.
调查细胞外矩阵 (ECM) 和整合素信号在DON毒性的作用.
探索DON对肠道SMC中的actin细胞骨架和收缩器官的影响.

主要方法:

使用猪肠滑肌细胞系 (PISMC) 作为实验模型.
采用转录组学和蛋白质组学来分析在DON暴露下细胞变化.
评估了ECM蛋白,整体蛋白,Rho GTPase激活蛋白,科菲林和收缩器官基因的表达水平.

主要成果:

在PISMC中,DON暴露降低了ECM蛋白和整合素子单元的表达.
DON抑制了ECM-整合素受体相互作用和下游信号通路.
DON治疗抑制了actin聚合和下调的收缩器官基因,由改变的Rho GTPase激活蛋白和cofilin水平表明.

结论:

通过破坏ECM-整合素-动氨酸聚合信号通路,DON抑制了肠道SMC收缩性.
这些发现为GIT中DON的毒理机制提供了新的见解.
了解这些途径对于解决DON对人类和动物的不良影响至关重要.

关键词:

动氨酸的聚合方式脱氧尼瓦伦 (deoxynivalenol) 是一种除氧化.ECM-受体相互作用的相互作用肠道平滑肌肉收缩性肠道平滑肌肉收缩性蛋白质基的蛋白质基体是什么文字转录文字转录文字转录

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