过多的铜会损害肝细胞内流通和蛋白P的分泌
Maria Schwarz1,2, Caroline E Meyer1,2, Alina Löser1,2
1Department of Nutritional Physiology, Institute of Nutritional Sciences, Friedrich Schiller University Jena, Dornburger Str. 24, 07743, Jena, Germany.
Nature communications
|June 13, 2023
概括
高水平的铜会破坏肝脏的功能.
科学领域:
- 生物化学 生物化学
- 细胞生物学 细胞生物学
- 营养科学 营养科学
背景情况:
- 的稳态依赖于肝脏产生的蛋白P (SELENOP) 来运输到像大脑这样的器官.
- 肝功能包括保持铜恒温,在和铜代谢之间观察到逆调节.
- 血铜升高和水平降低与衰老和炎症有关.
研究的目的:
- 研究铜对运输和肝细胞中SELENOP代谢的影响.
- 阐明铜影响细胞内SELENOP水平及其从肝脏释放的机制.
主要方法:
- 肝细胞用铜处理,观察细胞内和细胞外SELENOP的变化.
- 在威尔逊病患者和肝脏铜积累的老鼠中分析了血清SELENOP水平.
- 针对戈尔吉复杂蛋白质运输的药物剂被用于模仿铜诱导的效应.
主要成果:
- 铜治疗增加了肝细胞内的细胞内和SELENOP,同时减少了细胞外的SELENOP.
- 威尔逊病患者和老鼠的血清SELENOP水平较低,与肝脏铜积累相关.
- 戈尔吉运输的抑制模仿了铜的作用,这表明铜破坏了细胞内SELENOP运输,并导致戈尔吉晚期的积累.
结论:
- 肝脏中的铜水平极大地调节了SELENOP从肝脏中的释放.
- 过多的铜会干扰细胞内SELENOP的运输,影响到外围组织的输送,包括大脑.
- 了解这种相互作用对于和铜的平衡至关重要,特别是在像威尔逊病这样的疾病中.
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