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http://purl.uniprot.org/citations/24987958http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24987958http://www.w3.org/2000/01/rdf-schema#comment"A critical role of the Toll-like receptor(TLR) and its downstream molecules, including IL-1 receptor-associated kinase 1(IRAK1) and tumor necrosis factor receptor-associated factor 6(TRAF6), in the pathogenesis of liver ischemia/reperfusion (I/R) injury has been documented. Recently a microRNA, miR-146a, was identified as a potent negative regulator of the TLR signaling pathway. In this study, we investigated the role of miR-146a to attenuate TLR signaling and liver I/R injury in vivo and in vitro. miR-146a was decreased in mice Kupffer cells following hepatic I/R, whereas IRAK1 and TRAF6 increased. Overexpression of miR-146a directly decreased IRAK1 and TRAF6 expression and attenuated the release of proinflammatory cytokines through the inactivation of NF-κB P65 in hypoxia/reoxygenation (H/R)-induced macrophages, RAW264.7 cells. Knockdown experiments demonstrated that IRAK1 and TRAF6 are two potential targets for reducing the release of proinflammatory cytokines. Moreover, co-culture assays indicated that miR-146a decreases the apoptosis of hepatocytes after H/R. In vivo administration of Ago-miR-146a, a stable version of miR-146a in vivo, protected against liver injury in mice after I/R via inactivation of the TLR signaling pathway. We conclude that miR-146a ameliorates liver ischemia/reperfusion injury in vivo and hypoxia/reoxygenation injury in vitro by directly suppressing IRAK1 and TRAF6."xsd:string
http://purl.uniprot.org/citations/24987958http://purl.org/dc/terms/identifier"doi:10.1371/journal.pone.0101530"xsd:string
http://purl.uniprot.org/citations/24987958http://purl.uniprot.org/core/author"Jiang W."xsd:string
http://purl.uniprot.org/citations/24987958http://purl.uniprot.org/core/author"Lu Y."xsd:string
http://purl.uniprot.org/citations/24987958http://purl.uniprot.org/core/author"Liu G."xsd:string
http://purl.uniprot.org/citations/24987958http://purl.uniprot.org/core/author"Kong L."xsd:string
http://purl.uniprot.org/citations/24987958http://purl.uniprot.org/core/author"Tang W."xsd:string
http://purl.uniprot.org/citations/24987958http://purl.uniprot.org/core/author"Ding W."xsd:string
http://purl.uniprot.org/citations/24987958http://purl.uniprot.org/core/author"Pu L."xsd:string
http://purl.uniprot.org/citations/24987958http://purl.uniprot.org/core/author"Ni Q."xsd:string
http://purl.uniprot.org/citations/24987958http://purl.uniprot.org/core/author"Kong L.'"xsd:string
http://purl.uniprot.org/citations/24987958http://purl.uniprot.org/core/date"2014"xsd:gYear
http://purl.uniprot.org/citations/24987958http://purl.uniprot.org/core/name"PLoS One"xsd:string
http://purl.uniprot.org/citations/24987958http://purl.uniprot.org/core/pages"e101530"xsd:string
http://purl.uniprot.org/citations/24987958http://purl.uniprot.org/core/title"miR-146a ameliorates liver ischemia/reperfusion injury by suppressing IRAK1 and TRAF6."xsd:string
http://purl.uniprot.org/citations/24987958http://purl.uniprot.org/core/volume"9"xsd:string
http://purl.uniprot.org/citations/24987958http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/24987958
http://purl.uniprot.org/citations/24987958http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/24987958
http://purl.uniprot.org/uniprot/#_B1AUW6-mappedCitation-24987958http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24987958
http://purl.uniprot.org/uniprot/#_Q540G0-mappedCitation-24987958http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24987958
http://purl.uniprot.org/uniprot/#_Q62406-mappedCitation-24987958http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24987958
http://purl.uniprot.org/uniprot/#_Q8BR10-mappedCitation-24987958http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24987958
http://purl.uniprot.org/uniprot/#_Q99J34-mappedCitation-24987958http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24987958
http://purl.uniprot.org/uniprot/#_Q8K4N5-mappedCitation-24987958http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24987958