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通过改善线粒体功能,NDUFA3的HDAC/H3K27ac介导的转录对高葡萄糖处理的人类细胞核脉细胞产生保护作用

Cheng Zheng^1,2, Dongshuai Guo¹, Tong Zhang¹

¹Department of Spinal and Spinal Surgery, Henan Key Laboratory for Intelligent Precision Orthopedic Medicine, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, No.7, Wei Wu Road, Jinshui District, Zhengzhou, 450003, China.

Scientific reports

|September 10, 2024

概括

糖尿病会导致椎间盘退化. NADH:乌比昆氧化降解酶亚单元A3 (NDUFA3) 过度表达保护人类核脉细胞免受高葡萄糖的影响,减轻细胞亡并改善线粒体功能.

科学领域:

生物医学科学生物医学科学
细胞生物学细胞生物学
分子医学是分子医学.

背景情况:

糖尿病 (DM) 是椎间盘退化 (IVDD) 的重要危险因素.
高血糖水平,DM的特征,诱导细胞损伤的人类细胞核质细胞 (HNPCs).
在DM诱导的IVDD背后的特定分子机制需要进一步阐明.

研究的目的:

为了研究NADH的作用和机制:在高葡萄糖条件下,在HNPC中 ubiquinone oxidoreductase亚单元A3 (NDUFA3).
探索NDUFA3作为糖尿病IVDD的治疗点的潜力.

主要方法:

在使用lentivirus转导的HNPC中过度表达NDUFA3.
暴露HNPCs高葡萄糖和轮 (线粒体综合体I抑制剂).
评估细胞活力,细胞亡,活性氧物种 (ROS),线粒体膜潜力 (MMP),氧消耗率 (OCR) 和线粒体复合体I活动.

主要成果:

高葡萄糖损害了HNPC活力,增加了细胞灭绝,增加了ROS,并减少了MMP和OCR.
轮激素加剧了高葡萄糖诱导的细胞损伤.
NDUFA3过度表达显著保护HNPCs免受高葡萄糖诱导的损伤.
NDUFA3的淘汰会使细胞损伤恶化,而N-乙半氨酸 (ROS清除剂) 可以缓解这种损伤.
鉴定出HDAC/H3K27ac通路是调节NDUFA3转录的.

结论:

在HNPC中,NDUFA3对高葡萄糖诱导的损伤起着保护作用.
NDUFA3减轻了亡,减少了ROS,并增强了线粒体功能和氧化酸化.
通过HDAC/H3K27ac介导的NDUFA3转录是保护糖尿病IVDD的关键机制.
NDUFA3代表了治疗糖尿病椎间盘退行症的潜在治疗标.

关键词:

椎间盘退化椎间盘退化线粒体复合体I 线粒体复合体I 线粒体功能线粒体功能氧化酸化是一种氧化酸化.这就是ROSOS ROS.

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