米R-204-5p通过准P4HBp来调节HUVEC细胞炎症和亡
Jun Chen1, Kaixin Zhang2, Yi Yang3
1Department of Vascular Surgery, Suqian Hospital Affiliated to Xuzhou Medical University, (Nanjing Drum Tower Hospital Group Suqian Hospital), Suqian, 223800, China. pingchenzan87@126.com.
Cellular and molecular biology (Noisy-le-Grand, France)
|October 9, 2023
概括
微RNA-204-5p (miR-204-5p) 针对P4HB减少深静脉血栓症 (DVT) 模型中的炎症和亡. 在DVT患者中降低miR-204-5p水平突显了其治疗潜力.
科学领域:
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
- 生物化学 生化学
背景情况:
- 深静脉血栓症 (DVT) 是一种严重的血管疾病.
- 背后的DVT的分子机制,特别是涉及微RNA及其点,需要进一步阐明.
- 人静脉内皮细胞 (HUVEC) 是研究血管炎症和亡的关键模型.
研究的目的:
- 研究miR-204-5p在HUVEC细胞中向P4HB的调控机制.
- 探索miR-204-5p和P4HB在内脏瘤发病过程中的作用.
- 评估miR-204-5p作为DVT治疗标的潜力.
主要方法:
- 分析了来自DVT患者和健康对照者的血清样本.
- 生物信息预测 (Targetscan) 确定P4HB作为一个miR-204-5p目标.
- 双 luciferase 记者测定,qRT-PCR,CCK-8 测定,流动细胞测量,西部涂抹,免疫光和ELISA 用于评估基因表达,细胞活力,细胞亡,氧化应激和炎症标志物在 CoCl2-诱导的低氧/缺血下HUVECs.
主要成果:
- miR-204-5p的表达显著减少,而P4HB的表达在DVT患者的血清中升高.
- miR-204-5p直接向和负调节的P4HB表达.
- 在HUVEC中,miR-204-5p的过度表达增加了细胞活力,抑制了细胞灭亡,并减少了活性氧物种 (ROS) 和炎症性细胞因子 (TNF-α,IL-1β,IL-6) 的产生. 相反,P4HB过度表达抵消了这些保护作用.
结论:
- miR-204-5p通过降低P4HB的调节,对HUVEC中缺氧/缺血诱导的损伤产生保护作用.
- 在DVT的背景下,miR-204-5p/P4HB轴在调节炎症和亡方面发挥着至关重要的作用.
- miR-204-5p 是一个有前途的 DVT 治疗候选药物.
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