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http://purl.uniprot.org/citations/26315540http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/26315540http://www.w3.org/2000/01/rdf-schema#comment"

Objective

Systemic lupus erythematosus (SLE) is characterized by the uncontrolled production of inflammatory cytokines, among which type I interferon (IFN) is recognized as a crucial pathogenic factor. The expression of microRNA-146a (miR-146a) is reduced in the white blood cells of SLE patients and accounts for their overactivated inflammatory responses. However, the mechanism of the reduction of miR-146a is still not fully understood. This study was undertaken to test whether the key pathogenic cytokine, type I IFN, is responsible for the dysregulation of miR-146a in SLE.

Methods

Gene and protein expression was measured in all cells by reverse transcription-quantitative polymerase chain reaction, Northern blotting, or Western blotting. In THP-1 cells, expression of monocyte chemotactic protein-induced protein 1 (MCPIP-1) was knocked down with a lentivirus encoding a short hairpin RNA targeting MCPIP1. The cells were pretreated with type I IFN and assessed for gene expression levels of miR-146a. White blood cells from patients with SLE were analyzed for the expression of the IFN-inducible genes MCPIP1 and miR-146a, and the gene expression data were compared for correlation.

Results

Pretreatment of THP-1 cells with type I IFN attenuated the induction of miR-146a posttranscriptionally, by down-regulating the expression of pre-miR-146a but not pri-miR-146a or its original unspliced transcript. Expression of MCPIP-1, which was enhanced by type I IFN, was found to be responsible for the inhibition of miR-146a. In white blood cells from patients with SLE, MCPIP1 expression was elevated, and its expression correlated positively with the IFN score and negatively with the miR-146a transcript level.

Conclusion

Type I IFN inhibits the maturation of miR-146a through the up-regulation of MCPIP-1, and thus contributes to the uncontrolled inflammation and excessive inflammatory gene expression in SLE."xsd:string
http://purl.uniprot.org/citations/26315540http://purl.org/dc/terms/identifier"doi:10.1002/art.39398"xsd:string
http://purl.uniprot.org/citations/26315540http://purl.uniprot.org/core/author"Cao J."xsd:string
http://purl.uniprot.org/citations/26315540http://purl.uniprot.org/core/author"Li J."xsd:string
http://purl.uniprot.org/citations/26315540http://purl.uniprot.org/core/author"Liu Z."xsd:string
http://purl.uniprot.org/citations/26315540http://purl.uniprot.org/core/author"Tang Y."xsd:string
http://purl.uniprot.org/citations/26315540http://purl.uniprot.org/core/author"Zhang F."xsd:string
http://purl.uniprot.org/citations/26315540http://purl.uniprot.org/core/author"Yao Y."xsd:string
http://purl.uniprot.org/citations/26315540http://purl.uniprot.org/core/author"Cui H."xsd:string
http://purl.uniprot.org/citations/26315540http://purl.uniprot.org/core/author"Guo Q."xsd:string
http://purl.uniprot.org/citations/26315540http://purl.uniprot.org/core/author"Shen N."xsd:string
http://purl.uniprot.org/citations/26315540http://purl.uniprot.org/core/author"Qu B."xsd:string
http://purl.uniprot.org/citations/26315540http://purl.uniprot.org/core/author"Jallal B."xsd:string
http://purl.uniprot.org/citations/26315540http://purl.uniprot.org/core/author"Teng J."xsd:string
http://purl.uniprot.org/citations/26315540http://purl.uniprot.org/core/author"Morehouse C."xsd:string
http://purl.uniprot.org/citations/26315540http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/26315540http://purl.uniprot.org/core/name"Arthritis Rheumatol"xsd:string
http://purl.uniprot.org/citations/26315540http://purl.uniprot.org/core/pages"3209-3218"xsd:string
http://purl.uniprot.org/citations/26315540http://purl.uniprot.org/core/title"Type I Interferon Inhibition of MicroRNA-146a Maturation Through Up-Regulation of Monocyte Chemotactic Protein-Induced Protein 1 in Systemic Lupus Erythematosus."xsd:string
http://purl.uniprot.org/citations/26315540http://purl.uniprot.org/core/volume"67"xsd:string
http://purl.uniprot.org/citations/26315540http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/26315540
http://purl.uniprot.org/citations/26315540http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/26315540
http://purl.uniprot.org/uniprot/#_B3KSD3-mappedCitation-26315540http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26315540
http://purl.uniprot.org/uniprot/#_C0LED9-mappedCitation-26315540http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/26315540
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