神经PRDX-2-介导的ROS信号调节通过外围UPRmt激活调节食物消化
Yating Liu1, Qian Li1, Guojing Tian1
1Southwest United Graduate School, Yunnan Key Laboratory of Cell Metabolism and Diseases, State Key Laboratory of Conservation and Utilization of Bio-resources in Yunnan Center for Life Sciences, School of Life Sciences, Yunnan University, Kunming, China.
Nature communications
|December 5, 2024
概括
涉及神经元活性氧物种 (ROS) 的脑肠信号抑制了消化. 这条由PRDX-2和神经NLP-1介导的途径突出显示了自由基.
科学领域:
- 神经生物学 神经生物学 神经生物学
- 胃肠病学 胃肠病学
- 细胞应激反应的应激反应
背景情况:
- 生物的生存取决于有效的食物消化.
- 大脑-肠轴在调节消化过程中起着至关重要的作用.
- 连接神经元信号与肠道消化过程的机制仍然不完全理解.
研究的目的:
- 为了阐明大脑-肠道信号通路,以响应神经元信号来调节消化.
- 研究反应性氧物种 (ROS) 在调节消化功能中的作用.
- 为了确定这个大脑-肠沟通的关键分子媒介.
主要方法:
- 使用C. elegans模型研究消化过程.
- 进行基因查以确定参与ROS平衡和消化中的基因.
- 研究了基因淘汰 (PRDX-2),神经操纵 (NLP-1) 和神经元剥离 (AWC) 对消化能力和细胞应激反应的影响.
主要成果:
- 维持ROS平衡的基因减少导致自由基增加和消化减弱.
- 嗅觉神经元 (AWC) 中的PRDX-2淘汰会增加ROS,通过神经NLP-1降低消化能力,并在肠道中激活线粒体未折叠蛋白反应 (UPRmt).
- 对nlp-1的过度表达或AWC神经元的切除诱导了UPRmt和抑制了消化.
结论:
- 发现了一种新的脑肠道通路,其中神经元的ROS信号抑制了消化.
- 神经PRDX-2-介导的ROS通过NLP-1和UPRmt作用,抑制肠道消化.
- 这突出了自由基在关闭消化过程中发挥的关键作用,以减轻压力和减少食物摄入量.
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