Literature DB >> 28235799

Inducible microRNA-214 contributes to the suppression of NF-κB-mediated inflammatory response via targeting myd88 gene in fish.

Qing Chu1, Yuena Sun1, Junxia Cui1, Tianjun Xu2.   

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 by Vibro harveyi and LPS stimulation. Up-regulating miR-214 subsequently inhibits the production of inflammatory cytokines by targeting myd88 to 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.
© 2017 by The American Society for Biochemistry and Molecular Biology, Inc.

Entities:  

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

Mesh:

Substances:

Year:  2017        PMID: 28235799      PMCID: PMC5392675          DOI: 10.1074/jbc.M117.777078

Source DB:  PubMed          Journal:  J Biol Chem        ISSN: 0021-9258            Impact factor:   5.157


  43 in total

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7.  MicroRNA miR-214 Inhibits Snakehead Vesiculovirus Replication by Promoting IFN-α Expression via Targeting Host Adenosine 5'-Monophosphate-Activated Protein Kinase.

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