循环RNA DHTKD1针对miR-338-3p/ETS1轴调节人类支气管上皮细胞的炎症反应
Fenhong Qian1, Shanchuan He1, Xianmiao Yang1
1Department of Respiratory and Critical Care Medicine, Affiliated Hospital of Jiangsu University, Zhenjiang, Jiangsu 212001, P.R. China.
循环RNA DHTKD1 (circDHTKD1) 通过通过miR-338-3p调节ETS1来加剧喘炎症. 向circDHTKD1可能为喘治疗提供新的治疗策略.
科学领域:
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
背景情况:
- 喘是一种慢性呼吸道炎症疾病,涉及呼吸道上皮质.
- 循环RNAs (circRNAs) 在喘病因发生中的作用尚未完全理解.
- 在呼吸道炎症中研究circRNAs如circDHTKD1至关重要.
研究的目的:
- 确定炎症期间人类支气管上皮细胞中circRNA DHTKD1 (circDHTKD1) 的功能和分子机制.
- 阐明 circDHTKD1 在脂聚糖 (LPS) 诱导的呼吸道炎症中的作用.
- 探索circDHTKD1作为喘治疗点的潜力.
主要方法:
- 通过使用LPS刺激的BEAS-2B细胞建立了体外呼吸道炎症模型.
- 通过细胞计数工具-8测定来评估细胞活力.
- 使用RT-qPCR和西方涂抹对circDHTKD1,miR-338-3p,ETS1和ERK通路组件的量化RNA和蛋白质表达水平.
- 通过双露西法酶记者测定证实circDHTKD1/miR-338-3p相互作用,并使用ELISA测量炎症细胞因子.
主要成果:
- 在BEAS-2B细胞中,LPS上调circDHTKD1和下调miR-338-3p.
- circDHTKD1直接准了miR-338-3p,对ETS1的表达进行了负面调节.
- 抑制circDHTKD1或miR-338-3p可以模仿炎症性细胞因子和ETS1水平的降低.
- 抑制ETS1抑制了LPS诱导的细胞因子产生和ERK通路激活.
结论:
- circDHTKD1通过miR-338-3p轴向上调节ETS1,加剧支气管上皮细胞中LPS触发的炎症.
- circDHTKD1促进呼吸道炎症和ERK通路的激活.
- circDHTKD1代表了喘的潜在治疗点.
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