MiR-130a-3p通过调节内皮细胞中MAPK8的表达来抑制内皮炎症
Mingming Gu1, Kun Liu1, Hui Xiong1
1Department of Cardiothoracic Surgery, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu Province, China.
Heliyon
|February 1, 2024
概括
微RNA-130a-3p (miR-130a-3p) 通过促进内皮细胞的增殖和减少炎症来预防动脉样硬化. 上调 miR-130a-3p 抵消氧化 LDL 的作用,这表明它是一个治疗点.
科学领域:
- 分子生物学分子生物学
- 心血管研究研究心血管研究
- 细胞生物学 细胞生物学
背景情况:
- 动脉样硬化 (AS) 是一种慢性炎症性疾病.
- 内皮细胞功能障碍是AS病变的关键因素.
- 微RNA在调节与AS相关的细胞过程中起着至关重要的作用.
研究的目的:
- 研究微RNA-130a-3p (miR-130a-3p) 在暴露于氧化低密度脂蛋白 (ox-LDL) 的内皮细胞 (ECs) 中的作用.
- 探索 miR-130a-3p 在用牛脂LDL 处理的 EC 中的潜在分子机制.
- 评估miR-130a-3p在AS中的治疗潜力.
主要方法:
- 人类静脉内皮细胞 (HUVEC) 用ox-LDL.进行了治疗.
- 用CCK-8,EDU和流式细胞计量来评估细胞增殖和细胞亡.
- 细胞因子表达和蛋白质水平通过ELISA和西欧 blot.测量.
- 生物信息学和双露西法酶记者测定确定了MAPK8作为miR-130a-3p.p的直接目标.
主要成果:
- 在ox-LDL处理的HUVEC中,miR-130a-3p的下调.
- 对miR-130a-3p的升级促进了HUVEC的扩散,并抑制了亡.
- miR-130a-3p抑制了炎症标记物 (TNF-α,IL-6) 和粘附分子 (VCAM-1,ICAM-1,E-selectin) 的作用.
- MAPK8被ox-LDL上调;它的沉默模仿了miR-130a-3p的保护作用.
结论:
- miR-130a-3p对内皮细胞产生保护作用,防止ox-LDL诱导的损伤.
- miR-130a-3p针对MAPK8,调解其抗炎和抗亡功能.
- 在动脉样硬化治疗中,miR-130a-3p是一个有前途的治疗标.
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