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Hsa_circ_0005548通过miR-362-3p/ETS1轴对人类大脑微血管内皮细胞的OGD/R诱导损伤进行敲击修复

Chunlei Chen¹, Jiguo Xu¹, Tianrun Huang¹

¹Department of Urology, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai, China.

The International journal of neuroscience

|August 30, 2023

概括

这项研究表明,降低hsa_circ_0005548水平可以防止缺血性中风 (IS) 细胞损伤. 这种保护通过miR-362-3p/ETS1通路进行介导,为IS提供了潜在的治疗点.

科学领域:

分子生物学分子生物学
细胞生物学细胞生物学
生物化学生物化学

背景情况:

缺血性中风 (IS) 是导致残疾和死亡的主要原因.
循环RNAs (circRNAs) 越来越多地被认为是它们在疾病中的调节作用.
了解IS中circRNAs的特定机制对于开发新疗法至关重要.

研究的目的:

研究hsa_circ_0005548在缺血性中风中的作用和机制.
在细胞中风模型中阐明hsa_circ_0005548,miR-362-3p和ETS-1之间的相互作用.

主要方法:

在人脑微血管内皮细胞不朽化 (HBMEC-IM) 中使用氧气-葡萄糖剥夺/再输液 (OGD/R) 建立了体外缺血性中风模型.
量化基因和蛋白质表达,使用RT-qPCR和西布洛特.
通过CCK8,EDU,流细胞计和ELISA评估细胞活力,增殖,亡和炎症.
使用双露西法酶记者和RNA免疫沉降 (RIP) 试验,研究了分子相互作用.

主要成果:

在HBMEC-IM细胞中,OGD/R治疗增加了hsa_circ_0005548和ETS-1水平,同时降低了miR-362-3p.
降低hsa_circ_0005548的调节缓解了OGD/R诱导的细胞损伤.
hsa_circ_0005548直接针对miR-362-3p,miR-362-3p针对ETS-1进行攻击.
沉默miR-362-3p扭转了hsa_circ_0005548敲击的保护作用.

结论:

Hsa_circ_0005548通过海绵化miR-362-3p促进缺血性中风细胞损伤,这反过来又提高了ETS-1的调节.
针对hsa_circ_0005548/miR-362-3p/ETS-1轴可能代表缺血性中风的新治疗策略.

关键词:

在ETS1中,ETS1是ETS1.据了解,Hsa_circ_000554848是该公司的一名员工.缺血性中风中风在 miR-362-3p 中使用.

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