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http://purl.uniprot.org/citations/28096568http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/28096568http://www.w3.org/2000/01/rdf-schema#comment"Identification of mediators triggering microglia activation and transference of noncoding microRNA (miRNA) into exosomes are critical to dissect the mechanisms underlying neurodegeneration. We used lipopolysaccharide-(LPS-) induced N9 microglia activation to explore new biomarkers/signaling pathways and to identify inflammatory miRNA (inflamma-miR) in cells and their derived exosomes. Upregulation of iNOS and MHC-II (M1-markers) and downregulation of arginase 1, FIZZ1 (M2-markers), and CX3CR1 (M0/M2 polarization) confirmed the switch of N9 LPS-treated cells into the M1 phenotype, as described for macrophages/microglia. Cells showed increased proliferation, activated TLR4/TLR2/NF-κB pathway, and enhanced phagocytosis, further corroborated by upregulated MFG-E8. We found NLRP3-inflammasome activation in these cells, probably accounting for the increased extracellular content of the cytokine HMGB1 and of the MMP-9 we have observed. We demonstrate for the first time that the inflamma-miR profiling (upregulated miR-155 and miR-146a plus downregulated miR-124) in M1 polarized N9 cells, noticed by others in activated macrophages/microglia, was replicated in their derived exosomes, likely regulating the inflammatory response of recipient cells and dissemination processes. Data show that LPS-treated N9 cells behave like M1 polarized microglia/macrophages, while providing new targets for drug discovery. In particular, the study yields novel insights into the exosomal circulating miRNA during neuroinflammation important for emerging therapeutic approaches targeting microglia activation."xsd:string
http://purl.uniprot.org/citations/28096568http://purl.org/dc/terms/identifier"doi:10.1155/2016/6986175"xsd:string
http://purl.uniprot.org/citations/28096568http://purl.uniprot.org/core/author"Gomes C."xsd:string
http://purl.uniprot.org/citations/28096568http://purl.uniprot.org/core/author"Cunha C."xsd:string
http://purl.uniprot.org/citations/28096568http://purl.uniprot.org/core/author"Brites D."xsd:string
http://purl.uniprot.org/citations/28096568http://purl.uniprot.org/core/author"Vaz A.R."xsd:string
http://purl.uniprot.org/citations/28096568http://purl.uniprot.org/core/date"2016"xsd:gYear
http://purl.uniprot.org/citations/28096568http://purl.uniprot.org/core/name"Mediators Inflamm"xsd:string
http://purl.uniprot.org/citations/28096568http://purl.uniprot.org/core/pages"6986175"xsd:string
http://purl.uniprot.org/citations/28096568http://purl.uniprot.org/core/title"Exploring New Inflammatory Biomarkers and Pathways during LPS-Induced M1 Polarization."xsd:string
http://purl.uniprot.org/citations/28096568http://purl.uniprot.org/core/volume"2016"xsd:string
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http://purl.uniprot.org/citations/28096568http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/28096568
http://purl.uniprot.org/uniprot/P63158#attribution-53B62B612F1C1E4E9150AFEACD291F05http://purl.uniprot.org/core/sourcehttp://purl.uniprot.org/citations/28096568
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http://purl.uniprot.org/uniprot/#_P63158-mappedCitation-28096568http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28096568