在缺血性中风中,FTO/miR-503-5p/USP10轴调节神经元内质网膜中压力介导的亡
Qiang Peng1, Shiyao Wang1, Shi Huang1
1Department of Neurology, Nanjing First Hospital, Nanjing Medical University, Nanjing 210006 China.
International immunopharmacology
|February 4, 2025
概括
在急性缺血性中风 (AIS) 中,MicroRNA-503-5p通过降低USP10.10的调节加剧了脑损伤. 脂肪质量和与肥胖相关的蛋白质 (FTO) 通过调节miR-503-5p成熟来防止这种损伤.
科学领域:
- 神经科学是一个神经科学.
- 分子生物学分子生物学
- 遗传学 遗传学 是一个
背景情况:
- 微RNA-503-5p (miR-503-5p) 与缺血性疾病有关.
- 它在急性缺血性中风 (AIS) 中的具体作用和调节是未知的.
研究的目的:
- 研究miR-503-5p在AIS中的功能和调节机制.
- 在AIS中探索miR-503-5p/USP10轴和FTO的治疗潜力.
主要方法:
- 使用中脑动脉封闭/再输 (MCAO/R) 和氧-葡萄糖剥夺/氧化 (OGD/R) 模型.
- 分析了miR-503-5p,USP10,细胞内膜网膜应激 (ERS) 生物标志物 (GRP78,CHOP) 和亡.
- 通过m6A修饰研究了FTO在miR-503-5p成熟中的作用.
主要成果:
- 在MCAO/R小鼠中,MiR-503-5p增加了脑梗塞量,神经元损伤和神经行为缺陷.
- MiR-503-5p降低了USP10,提高了ERS生物标志物,并在OGD/R神经元中加剧了亡.
- 通过调节miR-503-5p/USP10轴,FTO抑制了ERS介导的亡.
结论:
- MiR-503-5p通过准USP10并诱导ERS介导的亡来加剧AIS.
- 在AIS中,FTO通过抑制miR-503-5p成熟而表现出神经保护作用.
- miR-503-5p/USP10轴代表了AIS的一个潜在的治疗目标.
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