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Circ_0006944通过调节miR-205-5p/UBL4A通路而加剧LPS诱导的HK2细胞损伤

Fan Zhou^1,2, Dong Liu^2,3, Junwei Ye^2,3

¹Department of Infectious Diseases, Huangshi Central Hospital, Affiliated Hospital of Hubei Polytechnic University, Edong Healthcare Group, Hubei, China.

|November 23, 2023

概括

循环RNAcirc_0006944通过调节miR-205-5p/UBL4A通路使败血症相关的急性损伤 (SA-AKI) 恶化. 这一发现突出了circ_0006944作为SA-AKI的潜在生物标志物和治疗点.

科学领域:

分子生物学分子生物学
细胞生物学细胞生物学
病理学病理学病理学

背景情况:

循环RNAs (circRNAs) 与人类疾病有关,包括败血症相关的急性损伤 (SA-AKI).
在SA-AKI中circ_0006944的特定作用和机制在很大程度上仍未被描述.

研究的目的:

调查circ_0006944在SA-AKI.病变发生过程中的功能和分子机制.
探索circ_0006944作为SA-AKI的诊断和治疗点的潜力.

主要方法:

脂聚糖 (LPS) 用于建立急性损伤 (AKI) 的体外模型.
使用定量实时聚合酶连锁反应 (qRT-PCR) 和西部涂抹来评估基因和蛋白质表达.
用CCK-8,EDU,流细胞计,ELISA和MDA/SOD试验来评估细胞增殖,亡,炎症和氧化应激.
采用双露西法酶报告者和RIP试验来确认circ_0006944,miR-205-5p和UBL4A之间的相互作用.

主要成果:

在SA-AKI患者和LPS诱导的HK2细胞中发现Circ_0006944的上调.
与circ_0006944的干扰显著减弱了LPS诱导的HK2细胞增殖抑制,细胞亡,炎症和氧化应激.
Circ_0006944充当了miR-205-5p的分子海绵,miR-205-5p的目标是UBL4A,形成了circ_0006944/miR-205-5p/UBL4A轴.
过度表达UBL4A部分扭转了miR-205-5p抑制的保护作用.

结论:

Circ_0006944通过海绵化miR-205-5p加剧SA-AKI的发展,这反过来又调节了UBL4A的表达.
该circ_0006944/miR-205-5p/UBL4A通路代表了SA-AKI的潜在治疗标和诊断生物标记物.

关键词:

这就是SA-akiaki.这就是UBL4A.环_000694444 在线阅读在 miR-205-5p 中.

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Hedgehog Signaling Pathway

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