Literature DB >> 25832477

Reduced Expression of miR-23a Suppresses A20 in TLR-stimulated Macrophages.

Ping Peng1, Zhiyi Li, Xinyan Liu.   

Abstract

High levels of miR-23a expression in human primary macrophages suggested that miR-23a might have an important role in innate immune cells. Therefore, we investigated whether miR-23a regulates the secretion of cytokines by immune cells. Herein, we demonstrate that the expression of miR-23a was reduced in toll-like receptor (TLR)-stimulated macrophages. By targeting A20, miR-23a could affect NF-κB activity and the expression of downstream NF-κB-target genes that encode proinflammatory mediators, such as IL-6 and TNF-α. In summary, our study describes a novel role for miR-23a in the regulation of inflammatory cytokine production in macrophages, which could yield new insights into the regulatory role of miRNAs in the inflammatory response.

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Year:  2015        PMID: 25832477     DOI: 10.1007/s10753-015-0156-7

Source DB:  PubMed          Journal:  Inflammation        ISSN: 0360-3997            Impact factor:   4.092


  25 in total

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3.  MicroRNAs are expressed and processed by human primary macrophages.

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4.  The ubiquitin-modifying enzyme A20 is required for termination of Toll-like receptor responses.

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Journal:  Nat Immunol       Date:  2004-08-29       Impact factor: 25.606

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Review 6.  Cytokines and chemokines: At the crossroads of cell signalling and inflammatory disease.

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Review 8.  A20-mediated negative regulation of canonical NF-κB signaling pathway.

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6.  Seminal Plasma Modulates miRNA Expression by Sow Genital Tract Lining Explants.

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10.  miR-23a, miR-146a and miR-301a confer predisposition to Vogt-Koyanagi-Harada syndrome but not to Behcet's disease.

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