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微小RNA-1985通过靶向MNK1增强扇贝对聚肌苷酸:聚胞苷酸(poly(I:C))刺激的氧化还原能力。

MicroRNA-1985 enhances the redox capability of scallop () in response to poly(I:C) stimulation by targeting MNK1.

作者信息

Yu Linghui, Deng Huiqi, Liu Shaohua, Xia Jianpin, Hao Zhenlin, Yin Donghong, Zhan Yaoyao, Chang Yaqing

机构信息

College of Bioscience and Biotechnology, Shenyang Agricultural University, Shenyang, Liaoning, China.

Key Laboratory of Mariculture & Stock Enhancement in North China's Sea, Ministry of Agriculture and Rural Affairs, Dalian Ocean University, Dalian, Liaoning, China.

出版信息

Front Immunol. 2025 May 8;16:1556591. doi: 10.3389/fimmu.2025.1556591. eCollection 2025.

Abstract

To clarify the microRNA (miRNA)-target gene axis is involved in response to pathogen-associated molecular pattern (PAMP)-induced oxidative stress in shellfish, the full-length cDNA of a novel 1 () homolog gene from the scallop () was cloned and characterized. The interaction between miR-1985 and was verified, and then the responses and possible molecular function of miR-1985, , and miR-1985/ axis to poly(I:C) (a classic virus-related PAMP) stimulation in were explored and preliminarily dissected. The results indicate: 1) The full-length cDNA of was 5354 bp, with a high level of sequence conservation across mollusks. 2) MiR-1985 bound to the 3'-UTR of and negatively regulated the expression of . 3) MNK1 may repress the relative expression of superoxide dismutase () by binding its promoter. 4) Both silencing and miR-1985 overexpression promoted the expression and enzymatic activity of SOD. 5) The miR-1985/ axis may be involved in the response to poly(I:C) stimulation by elevating the activity of the SOD/catalase axis. To summarize, all observations from this study indicated that may enhance its redox capability via the miR-1985//SOD/CAT cascade and thereby alleviate PAMP-induced oxidative stress.

摘要

为阐明微小RNA(miRNA)-靶基因轴参与贝类对病原体相关分子模式(PAMP)诱导的氧化应激反应,克隆并鉴定了扇贝()中一个新的1()同源基因的全长cDNA。验证了miR-1985与的相互作用,然后探索并初步剖析了miR-1985、和miR-1985/轴对聚肌胞苷酸(poly(I:C),一种典型的病毒相关PAMP)刺激的反应及其可能的分子功能。结果表明:1)的全长cDNA为5354 bp,在软体动物中具有高度的序列保守性。2)MiR-1985与的3'-UTR结合并负调控的表达。3)MNK1可能通过结合其启动子抑制超氧化物歧化酶()的相对表达。4)沉默和miR-1985过表达均促进了SOD的表达和酶活性。5)miR-1985/轴可能通过提高SOD/过氧化氢酶轴的活性参与对poly(I:C)刺激的反应。总之,本研究的所有观察结果表明,可能通过miR-1985//SOD/CAT级联增强其氧化还原能力,从而减轻PAMP诱导的氧化应激。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ced/12095029/45487257078e/fimmu-16-1556591-g001.jpg

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