细胞内膜网膜应激驱动单细胞细胞中的VEGF基因表达
Fatemah Bahman1, Taha Nadeem2, Abdulrahman Alayyaf3
1Immunology and Microbiology Department, Dasman Diabetes Institute, Dasman 15462, Kuwait.
Current issues in molecular biology
|October 28, 2025
概括
在新陈代谢应激过程中,内质网膜 (ER) 应激会在单细胞细胞中放大血管内皮生长因子 (VEGF). 这通过活性氧物种 (ROS) 发生,将肥胖,炎症和血管生成联系起来.
科学领域:
- 生物化学 生物化学
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
背景情况:
- 肥胖与慢性炎症和氧化压力有关,破坏新陈代谢平衡并增加血管内皮生长因子 (VEGF).
- 虽然缺氧和脂肪酸通过氧化应激诱导VEGF,但在单细胞中,内细胞网膜 (ER) 应激的作用尚未完全理解.
研究的目的:
- 研究ER应激如何与代谢应激相互作用,以调节THP-1单细胞中VEGF表达的过程.
- 阐明参与这种相互作用的机制,包括反应性氧物种 (ROS) 生产.
主要方法:
- 使用棕酸 (PA) 的THP-1单细胞受到代谢应激,使用thapsigargin (TG) 的ER应激.
- 测量了VEGF mRNA和蛋白质水平,ROS产生,ER压力标志物 (CHOP,ATF6,IRE1) 和抗氧化剂防御基因 (SOD2,NRF2).
- 评估了抗氧化剂黄素对VEGF表达和ROS的影响.
主要成果:
- 与PA和TG同时治疗与单独使用PA相比,显著增加了VEGF表达.
- 这种增加与ROS产量增加和ER压力标志物升高有关.
- 黄素治疗降低了VEGF表达和ROS水平,证实了ROS依赖的途径.
- 抗氧化剂防御基因表达 (SOD2,NRF2) 被上调,表明细胞对氧化应激的反应.
结论:
- 在脂质毒性条件下,ER压力加剧了单细胞中VEGF诱导.
- 这种放大通过ROS介导的途径发生.
- 这些发现表明,在与肥胖相关的疾病中,代谢压力,炎症和血管生成之间存在联系的机制.
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