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MicroRNAs are short transcripts specifically inhibiting protein translation. Neutrophils can release extracellular vesicles (EVs). In this study, we characterized profile of microRNA trafficked by EVs in GPA. Fifty patients with GPA were enrolled in the study, 25 at acute phase and 25 in remission. EVs were isolated from the blood serum, characterized by their number, size distribution. Following unbiased screening for microRNA expression, differentially expressed candidates were measured by quantitative real-time PCR. Circulating DNA-myeloperoxidase complexes and apoptosis-related transcripts in peripheral blood neutrophils were quantified. We identified four differentially expressed microRNAs from EVs in granulomatosis with polyangiitis (GPA). MirRs-223-3p, 664a-3p, and 200b-3p were overexpressed and miR-769-5p suppressed in the disease. A distinction between GPA and healthy controls was the best for miR-223-3p, whereas miR-664a-3p discriminated between active vs. remission of GPA. Correct classification of the disease based on multivariate discriminant analysis was between 92% for acute phase and 85% for all study participants. Bioinformatics tools identified genes transcripts potentially targeted by the microRNAs belonging to pathways of focal adhesion, mTOR signaling and neutrophil extracellular traps formation. Two microRNAs positively correlating with the disease activity were involved in neutrophil extracellular traps formation and apoptosis inhibition. A comprehensive characteristics of microRNAs trafficked in bloodstream inside EVs correlates well with our understanding of the mechanisms of GPA and suggests the importance of EVs in progression of the disease.<\/jats:p>","DOI":"10.1093\/cei\/uxac022","type":"journal-article","created":{"date-parts":[[2022,3,3]],"date-time":"2022-03-03T21:02:26Z","timestamp":1646341346000},"page":"103-113","source":"Crossref","is-referenced-by-count":10,"title":["Profile of circulating extracellular vesicles microRNA correlates with the disease activity in granulomatosis with polyangiitis"],"prefix":"10.1093","volume":"208","author":[{"given":"Marcin","family":"Surmiak","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Jagiellonian University Medical College , 8 Skawinska Str., 31-066 Krak\u00f3w , Poland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Katarzyna","family":"Wawrzycka-Adamczyk","sequence":"additional","affiliation":[{"name":"Clinic of Rheumatology and Immunology, University Hospital , 2 Jakubowskiego Str., 30-668 Krak\u00f3w , Poland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Joanna","family":"Kosa\u0142ka-W\u0119giel","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Jagiellonian University Medical College , 8 Skawinska Str., 31-066 Krak\u00f3w , Poland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stanis\u0142aw","family":"Pola\u0144ski","sequence":"additional","affiliation":[{"name":"Division of Biochemical and Molecular Diagnostics, University Hospital , 8 Skawinska Str., 31-066 Krak\u00f3w , Poland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7635-8103","authenticated-orcid":false,"given":"Marek","family":"Sanak","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Jagiellonian University Medical College , 8 Skawinska Str., 31-066 Krak\u00f3w , Poland"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2022,3,3]]},"reference":[{"key":"2022121213274630500_CIT0001","first-page":"157","article-title":"Wegener\u2019 s granulomatosis, autoimmunity to neutrophil proteinase 3.","volume":"51","author":"Watorek","year":"2003","journal-title":"Arch Immunol Ther Exp"},{"key":"2022121213274630500_CIT0002","first-page":"630","article-title":"Clinical and immunological aspects of Wegener\u2019 s granulomatosis (WG) and other syndromes resembling WG.","volume":"2","author":"Lamprecht","year":"2000","journal-title":"Rheumatology"},{"key":"2022121213274630500_CIT0003","doi-asserted-by":"crossref","first-page":"683","DOI":"10.1038\/nrrheum.2015.144","article-title":"Vasculitis syndromes: PR3 on apoptotic cells promotes inflammation in GPA.","volume":"11","author":"Onuora","year":"2015","journal-title":"Nat Rev Rheumatol"},{"key":"2022121213274630500_CIT0004","doi-asserted-by":"crossref","first-page":"1160","DOI":"10.1016\/j.autrev.2017.09.012","article-title":"Neutrophil extracellular traps (NETs) in autoimmune diseases: a comprehensive review.","volume":"16","author":"Lee","year":"2017","journal-title":"Autoimmun Rev"},{"key":"2022121213274630500_CIT0005","first-page":"249","article-title":"Expression profile of proinflammatory genes in neutrophil-enriched granulocytes stimulated with native anti-PR3 autoantibodies.","volume":"63","author":"Surmiak","year":"2012","journal-title":"J Physiol Pharmacol"},{"key":"2022121213274630500_CIT0006","doi-asserted-by":"crossref","first-page":"3","DOI":"10.1189\/jlb.1202611","article-title":"Neutrophil-activating potential of antineutrophil cytoplasm autoantibodies.","volume":"74","author":"Rarok","year":"2003","journal-title":"J Leukoc Biol"},{"key":"2022121213274630500_CIT0007","doi-asserted-by":"crossref","first-page":"89","DOI":"10.1016\/j.copbio.2019.01.005","article-title":"Extracellular vesicles: exosomes, microparticles, their parts, and their targets to enable their biomanufacturing and clinical applications.","volume":"60","author":"Kao","year":"2019","journal-title":"Curr Opin Biotechnol"},{"key":"2022121213274630500_CIT0008","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1007\/s11060-013-1084-8","article-title":"Biogenesis of extracellular vesicles (EV): exosomes, microvesicles, retrovirus-like vesicles, and apoptotic bodies.","volume":"s113","author":"Akers","year":"2013","journal-title":"J. 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