microRNA-148 is involved in NF-κB signaling pathway regulation after LPS stimulation by targeting IL-1β in miiuy croaker

microRNA-148 is involved in NF-κB signaling pathway regulation after LPS stimulation by targeting IL-1β in miiuy croaker
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microRNA-148通过靶向IL-1β参与黄花鱼LPS刺激后NF-kappa B信号通路的调节

DOI:
10.1016/j.fsi.2021.08.028
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发表时间:
2021-09-01
影响因子:
4.7
通讯作者:
Sun, Yuena
Sun, Yuena
中科院分区:
农林科学2区
文献类型:
--
作者:
Dong, Wenjing;Gao, Wenya;Sun, Yuena

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炎症反应是清除有害刺激的保护过程,构成了对感染性病原体的防御。清除病原体感染需要适当的免疫和炎症反应,但过度的炎症反应可导致不受控制的炎症、自身免疫性疾病或病原体传播。越来越多的证据表明,mirna是先天免疫和炎症的重要和多功能调节因子。然而,在低等脊椎动物的炎症反应中,mirna的调控网络在很大程度上是未知的。在本研究中,采用生物信息学和实验技术相结合的方法来研究miR-148的功能。IL-1 β是生物信息学预测的miR-148的假设靶基因。此外,我们通过双荧光素酶报告基因实验验证了miR-148对IL-1 β -3' utr的靶向作用。miR-148在蛋白和mRNA水平上以剂量依赖性的方式抑制IL-1 β的表达。重要的是,miR-148通过抑制IL-1 β参与lps诱导的NF-kappa B信号通路的调控。这些结果将提高我们对miRNAs在鱼类免疫应答中的调控作用的认识。
The inflammatory response is a protective process to clear detrimental stimuli, constitutes the defense against infectious pathogens. Clearing pathogen infection requires appropriate immune and inflammatory response, but excessive inflammatory response can lead to uncontrolled inflammation, autoimmune disease, or pathogen transmission. Accumulating evidences show that miRNAs are important and multifunctional regulators of innate immunity and inflammation. However, in the inflammatory response of lower vertebrates, the miRNAs regu-latory networks are largely unknown. In this study, a combination of bioinformatics and experimental techniques were used to investigate the functions of miR-148. IL-1 beta is a hypothetical target gene of miR-148 predicted by bioinformatics. In addition, dual-luciferase reporter gene experiment was used to verify the targeting effect of miR-148 on IL-1 beta-3'UTR. miR-148 inhibits IL-1 beta expression in a dose-dependent manner at protein and mRNA levels. It is important that miR-148 participates in regulation of LPS-induced the NF-kappa B signaling pathway by inhibiting IL-1 beta. These results will improve our understanding of the regulation of miRNAs in fish on the immune response.