LncRNA TUG1通过调节葡萄糖代谢重编程来调节微质炎症激活
Chunxiang He1,2, Ze Li1,2, Wenjing Yu1,2
1School of Integrated Chinese and Western Medicine, Hunan University of Chinese Medicine, Changsha, 410208, Hunan, China.
Scientific reports
|May 27, 2024
概括
长非编码RNA TUG1通过增强糖解促进微质炎症. 下调TUG1将新陈代谢转移到氧化酸化,减少炎症并促进微质中的抗炎性表型.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 代谢过程中的代谢.
背景情况:
- 中枢神经系统的免疫细胞微细胞在激活时表现出代谢重编程.
- 葡萄糖代谢的改变对微质激活和功能至关重要.
研究的目的:
- 研究长非编码RNA牛上调基因1 (TUG1) 在调节微质葡萄糖代谢和激活中的作用.
- 确定TUG1如何影响微质细胞的代谢概况和炎症反应.
主要方法:
- 建立了一个微质激活模型,使用用脂聚糖 (LPS) /干扰素-γ (IFN-γ) 治疗的BV2细胞.
- 使用了TUG1沉默 (siRNA) 和淘汰 (CRISPR/Cas9) 技术.
- 通过RT-qPCR和西式涂抹评估代谢酶和细胞因子的基因和蛋白质表达.
- 使用Seahorse测量糖分分解率,并通过代谢学分析代谢物.
主要成果:
- TUG1表达在激活的微质细胞中升高,与炎症因素相关.
- TUG1淘汰赛 (TUG1KO) 抑制了葡萄糖分解,促进了氧化酸化,并减少了炎症性细胞因子表达.
- TUG1KO将微质代谢从糖解转移到氧化酸化,恢复三碳酸循环.
- 低调TUG1具有抗炎作用,促进抗炎微质表型.
结论:
- 在激活过程中,TUG1在重编程微质葡萄糖代谢以向糖解方面发挥着至关重要的作用.
- 下调TUG1抑制微质糖解,将新陈代谢转移到氧化酸化,并赋予抗炎性质.
- 向TUG1代表了神经炎症疾病的潜在治疗策略.
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