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干扰 HSA_CIRC_0001226 LPS 诱导的豆-2B 细胞损伤通过规范 MIR-940/TGFBR2 路径

Song Mo¹, Qushen Yi, Xuezhu Bei

¹Department of Intensive Care Unit, Liuzhou Worker's Hospital, The Fourth Affiliated Hospital of Guangxi Medical University, Liuzhou, China.

Shock (Augusta, Ga.)

|October 13, 2023

概括

循环RNAcirc_0001226通过海绵miR-940和调节TGFBR2.2,加剧败血症相关的急性肺损伤 (SA-ALI). 减少circ_0001226可以缓解SA-ALI模型中LPS诱导的细胞增殖和炎症.

科学领域:

分子生物学分子生物学
细胞生物学细胞生物学
免疫学免疫学免疫学

背景情况:

败血症相关的急性肺损伤 (SA-ALI) 构成严重的健康风险.
循环RNAs (circRNAs) 与急性肺损伤 (ALI) 的进展有关.

研究的目的:

为了研究circ_0001226在脂聚糖 (LPS) 诱导的BEAS-2B细胞中的作用和机制,模拟SA-ALI.
阐明涉及circ_0001226,miR-940和转化生长因子β受体II (TGFBR2) 的调节途径.

主要方法:

使用LPS刺激的BEAS-2B细胞建立了一个SA-ALI细胞模型.
量化基因和蛋白质的表达 (circ_0001226,miR-940,TGFBR2,PCNA,Bax) 使用RT-qPCR和西欧涂抹.
通过CCK-8,EDU,流细胞计和ELISA评估细胞增殖,细胞亡和炎症性细胞因子水平 (IL-6,IL-1β,TNF-α).
通过使用双露西法酶记者和RNA拉下测试,研究了分子相互作用.

主要成果:

在SA-ALI血清和LPS治疗细胞中,Circ_0001226和TGFBR2的上调,而miR-940的下调.
在LPS诱导的BEAS-2B细胞中,Circ_0001226干扰增强了细胞增殖,减少了细胞亡和炎症.
在机械上,circ_0001226作为miR-940的分子海绵,从而调节TGFBR2的表达.

结论:

Circ_0001226的缺乏减轻了LPS诱导的增殖抑制和BEAS-2B细胞中的炎症反应.
该机制涉及circ_0001226与miR-940结合,并随后调节TGFBR2.2.
Circ_0001226是SA-ALI的一个潜在治疗点.

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