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一个与自相关的MITF-GAS5-miR-23循环减轻了败血症中的血管氧化和炎症损伤

Junning Cheng^1,2, Chang Ding^2,3, Huying Tang^2,4

¹Department of Vascular Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China.

|July 29, 2023

概括

败血症通过氧化应激升级血管中的GAS5. GAS5通过调节抗氧化剂和自途径来预防败血症,最终减少肺损伤.

科学领域:

分子生物学分子生物学
细胞生物学细胞生物学
病理生理学病理生理学

背景情况:

已知败血症会增加血管内皮中的GAS5表达.
驱动这种增加的精确分子机制和GAS5在败血症中的功能作用在很大程度上是未知的.

研究的目的:

阐明毒症在血管内皮中诱导GAS5表达的分子机制.
研究GAS5在败血症引起的血管功能障碍和器官损伤中的作用.

主要方法:

利用败血症小鼠模型观察GAS5表达.
采用染色体免疫沉,其次是PCR (ChIP-PCR) 和电泳运动移位试验 (EMSA) 来确认转录因子结合.
对内皮细胞 (ECs) 进行了体外研究,并对小鼠进行了体内实验.
进行 luciferase 报告员测试以调查调控相互作用.

主要成果:

在败血症期间,GAS5表达在内皮中显著上调.
氧化应激激活的MiT-TFE转录因子 (MITF,TFE3,TFEB) 中介于GAS5转录.
在EC中GAS5的过度表达减少了氧化应激和炎症,保持了线粒体的完整性.
在体内,GAS5通过减少ROS减轻败血症引起的肺损伤,保持血管屏障功能.
确定了涉及MITF,GAS5和miR-23的积极反循环,其中GAS5保护MITF免受降解.
通过转录和后转录机制,MITF通过Nrf2进行升级调节,Nrf2相互转录MITF.

结论:

由ROS激活的MITF-GAS5-miR-23循环集成了抗氧化剂和自系统在败血症.
这个循环动态调节自,并调解抗氧化和抗炎作用.
这些发现揭示了一种新的调节网络,对于减轻败血症引起的血管损伤至关重要.

关键词:

转录因子 MiTTFE 的转录因子自自是自的过程.这是一种炎症炎症炎症炎症.氧化应激是一种氧化应激.这是一种血症.

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