title: Inducible microRNA-214 contributes to the suppression of NF-κB-mediated inflammatory response via targetingmyd88gene in fish.
abstract: Upon recognition of bacterial pathogens by pattern recognition receptors, cells are activated to produce pro-inflammatory cytokines and type I IFN by multiple signaling pathways. Every step of the process must be precisely regulated to prevent dysregulation. MicroRNAs (miRNAs) have been shown to be important regulators with profound effects on inflammatory response. Nevertheless, the miRNA-mediated regulatory mechanism remains unclear in fish species. Here, we addressed the role of miiuy croaker miR-214 in the bacteria triggered inflammatory response. miR-214 could significantly be up-regulated byVibro harveyiand LPS stimulation. Up-regulating miR-214 subsequently inhibits the production of inflammatory cytokines by targetingmyd88to avoid excessive inflammation. Moreover, the negative regulatory mechanism of miR-214 has been demonstrated to be via the myd88-mediated NF-κB pathway. This is the first to focus on miR-214 acting as the negative regulator involved in the bacteria-triggered inflammatory response and thus may provide knowledge on the host-cell regulator responses to microbial infection.
authors.affiliation: From the Laboratory of Fish Biogenetics & Immune Evolution, College of Marine Science, Zhejiang Ocean University, Zhoushan 316022, China.
authors.forename: Qing
authors.initials: Q
authors.lastname: Chu
authors.affiliation: From the Laboratory of Fish Biogenetics & Immune Evolution, College of Marine Science, Zhejiang Ocean University, Zhoushan 316022, China.
authors.forename: Yuena
authors.initials: Y
authors.lastname: Sun
authors.affiliation: From the Laboratory of Fish Biogenetics & Immune Evolution, College of Marine Science, Zhejiang Ocean University, Zhoushan 316022, China.
authors.forename: Junxia
authors.initials: J
authors.lastname: Cui
authors.affiliation: From the Laboratory of Fish Biogenetics & Immune Evolution, College of Marine Science, Zhejiang Ocean University, Zhoushan 316022, China tianjunxu@163.com.
authors.forename: Tianjun
authors.initials: T
authors.lastname: Xu
mesh_terms: D000818:Animals; D001424:Bacterial Infections / Q000276:immunology; D016207:Cytokines; D005399:Fishes; D007249:Inflammation / Q000382:microbiology*; D008070:Lipopolysaccharides; D035683:MicroRNAs / Q000276:immunology*; D053594:Myeloid Differentiation Factor 88 / Q000235:genetics*; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000378:metabolism*; D015398:Signal Transduction / Q000276:immunology
chemical_list: D016207:Cytokines; D008070:Lipopolysaccharides; D035683:MicroRNAs; D053594:Myeloid Differentiation Factor 88; D016328:NF-kappa B
keywords: MyD88; NF-κB; cellular immune response; excessive inflammation; gene regulation; microRNA (miRNA); microRNA mechanism; microRNA-214; myeloid differentiation primary response gene (88) (MYD88); negatively regulation