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lncRNA AK085865 Promotes Macrophage M2 Polarization in CVB3-Induced VM by Regulating ILF2-ILF3 Complex-Mediated miRNA-192 Biogenesis

Yingying Zhang, Xueqin Li, Chen Wang, Mengying Zhang, Hui Yang, Kun Lv

2020Molecular Therapy — Nucleic Acids52 citationsDOIOpen Access PDF

Abstract

mice. Moreover, miR-192 overexpression promoted macrophage M2 polarization in vitro, and interleukin-1 receptor-associated kinase 1 (IRAK1) was identified as a direct target. miR-192 overexpression effectively rescued mice from lethal myocarditis caused by CVB3 infection and switched myocardial-infiltrating macrophages to a predominant M2 phenotype. Collectively, our findings uncover a critical mechanism of AK085865 in the regulation of macrophage polarization in vitro and in vivo and provide a potential, clinically significant therapeutic target.

Topics & Concepts

Macrophage polarizationGene knockdownM2 MacrophageDownregulation and upregulationCancer researchBiologymicroRNACell biologyMacrophageRNA interferenceIn vitroChemistryCell cultureRNAGeneGeneticsCancer-related molecular mechanisms researchRNA modifications and cancerRNA Research and Splicing
lncRNA AK085865 Promotes Macrophage M2 Polarization in CVB3-Induced VM by Regulating ILF2-ILF3 Complex-Mediated miRNA-192 Biogenesis | Litcius