LncRNA uc003pxg.1 与miR-339-5p相互作用 促进血管内皮细胞的增殖,迁移和血管生成
Ping Li1,2, Feng Wang1,3, Anna Yue1
1Department of Cardiology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou, P. R. China.
Korean circulation journal
|December 29, 2024
概括
长非编码RNA uc003pxg.1 和微RNA miR-339-5p 在冠心病中起着关键作用. uc003pxg.1的上调和miR-339-5p的下调促进了血管动脉样硬化的发展.
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
- 遗传学 是一个遗传学.
背景情况:
- 冠心病 (CHD) 的发病过程涉及复杂的分子机制.
- 长非编码RNAs (lncRNAs) 和microRNAs (miRNAs) 都与心血管疾病有关.
研究的目的:
- 调查 lncRNA uc003pxg.1 和 miR-339-5p 在冠心病发展中的作用.
- 阐明它们调节内皮细胞功能的基础上的分子机制.
主要方法:
- 在临床样本和人静脉内皮细胞 (HUVEC) 中量化uc003pxg.1和miR-339-5p的表达.
- 使用高通量测序和生物信息学识别目标基因.
- 在体外转染实验中使用si-uc003pxg.1,miR-339-5p模仿剂和抑制剂.
- 使用EDU,CCK-8,scratch和Transwell试验评估细胞增殖,迁移和血管生成.
- 通过RT-qPCR和西式涂抹检测基因和蛋白质表达.
主要成果:
- 在临床样本和HUVEC中观察到uc003pxg.1和miR-339-5p表达之间的负相关性.
- 对uc003pxg.1和miR-339-5p的下调模仿减少了HUVEC的增殖,迁移和血管生成.
- 这些干预措施降低了转化生长因子-β1 (TGF-β1),α-平滑肌肉活性蛋白 (α-SMA),CD31,原蛋白I,原蛋白III和内分泌蛋白的表达.
结论:
- 在体外,uc003pxg.1的上调和miR-339-5p的下调促进细胞增殖,迁移和血管生成.
- 这些分子变化与TGF-β1,α-SMA,CD31,原蛋白I,原蛋白III和内分泌蛋白的表达增加有关.
- 这些发现表明,uc003pxg.1和miR-339-5p在促进血管动脉样硬化发展方面起着作用.
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