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一种新型硬骨鱼 microRNA 在细菌感染过程中调控自噬和 NF-κB 激活。

A novel teleost microRNA regulates autophagy and NF-κB activation during bacterial infection.

机构信息

College of Marine Science and Engineering, Qingdao Agricultural University, Qingdao, China; CAS Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Center for Ocean Mega-Science, Chinese Academy of Sciences, Qingdao, China.

CAS Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Center for Ocean Mega-Science, Chinese Academy of Sciences, Qingdao, China.

出版信息

Fish Shellfish Immunol. 2023 Jun;137:108778. doi: 10.1016/j.fsi.2023.108778. Epub 2023 Apr 30.

Abstract

MicroRNAs (miRNAs) are a class of non-coding RNAs with regulatory functions in many cellular processes, including immune defense. In this study, we identified novel-m0089-3p, a novel miRNA with unknown function, in the teleost fish Japanese flounder (Paralichthys olivaceus) and investigated its immune function. Novel-m0089-3p was found to target the autophagy-associated gene ATG7 and negatively regulate ATG7 expression via interaction with the 3' UTR of ATG7. During the infection of the bacterial pathogen Edwardsiella tarda, novel-m0089-3p expression was induced in flounder, which in turn repressed ATG7 expression. Overexpression of novel-m0089-3p or blocking ATG7 expression inhibited autophagy and promoted the intracellular replication of E. tarda. Novel-m0089-3p overexpression, as well as E. tarda infection, activated NF-κB and stimulated the expression of inflammatory cytokines. Together these results revealed an important role of novel-m0089-3p in response to bacterial infection.

摘要

微小 RNA(miRNAs)是一类具有调节功能的非编码 RNA,参与许多细胞过程,包括免疫防御。在这项研究中,我们在硬骨鱼牙鲆(Paralichthys olivaceus)中鉴定了一种新型 miRNA——novel-m0089-3p,该 miRNA 具有未知的功能,并研究了其免疫功能。novel-m0089-3p 被发现靶向自噬相关基因 ATG7,并通过与 ATG7 的 3'UTR 相互作用负调控 ATG7 的表达。在细菌病原体迟缓爱德华氏菌(Edwardsiella tarda)感染期间,novel-m0089-3p 在牙鲆中被诱导表达,进而抑制 ATG7 的表达。novel-m0089-3p 的过表达或阻断 ATG7 的表达抑制了自噬作用,并促进了 E. tarda 的细胞内复制。novel-m0089-3p 的过表达以及 E. tarda 感染激活了 NF-κB,并刺激了炎症细胞因子的表达。这些结果共同揭示了 novel-m0089-3p 在细菌感染反应中的重要作用。

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