{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T15:27:36Z","timestamp":1787066856089,"version":"build-2736575974"},"reference-count":0,"publisher":"S. Karger AG","issue":"3-4","license":[{"start":{"date-parts":[[2016,1,1]],"date-time":"2016-01-01T00:00:00Z","timestamp":1451606400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2016,1,1]],"date-time":"2016-01-01T00:00:00Z","timestamp":1451606400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cell Physiol Biochem"],"published-print":{"date-parts":[[2016]]},"abstract":"<jats:p>Background\/Aims: The primary objective of this study was to investigate the role of miR-146a in inducing the inflammatory infiltration of macrophages in polymyositis\/dermatomyositis (PM\/DM) through targeting TNF receptor associated factor 6 (TRAF6), which may further down-regulate the Interleukin-17 (IL-17)\/Intercellular Adhesion Molecule 1 (ICAM-1) pathway. Methods: Biopsies were collected from PM\/DM patients and healthy volunteers. PM\/DM model establishment and macrophage isolation were performed on Sprague Dawley (SD) rats. Model rats and macrophages were treated with anti-IL-17, anti-ICAM-1, miR-146a mimics, miR-146a inhibitors, and TRAF6 siRNAs. Serum creatine phosphokinase (S-CK) expression was assessed using double antibody sandwich enzyme-linked immunosorbent assay (ELISA) assay, and immunohistochemistry assay was performed to analyze CD163 expression in muscle samples. Furthermore, we used transwell assay to test cell migration; RT-PCR and western blot were carried out to determine the expression of miR-146a, TRAF6, IL-17, and ICAM-1. Results: The S-CK, TRAF6, IL-17 and ICAM-1 levels were higher in PM\/DM patients compared with healthy controls and were down-regulated after the conventional treatment. Treatment with miR-146a mimics, anti-IL-17 and anti-ICAM-1 decreased the expression of IL-17 and ICAM-1, whereas miR-146a inhibitors exerted the opposite effects. The effects of miR-146a inhibitors were suppressed by treatment with TRAF6 siRNA. In addition, the luciferase reporter assay validated the targeting relationship between miR-146a and TRAF6. Conclusions: MiR-146a regulates inflammatory macrophage infiltration in PM\/DM by targeting TRAF6 and affecting the IL-17\/ICAM-1 pathway.<\/jats:p>","DOI":"10.1159\/000452563","type":"journal-article","created":{"date-parts":[[2016,11,24]],"date-time":"2016-11-24T17:01:31Z","timestamp":1480006891000},"page":"486-498","source":"Crossref","is-referenced-by-count":33,"title":["MiR-146a Regulates Inflammatory Infiltration by Macrophages in Polymyositis\/Dermatomyositis by Targeting TRAF6 and Affecting IL-17\/ICAM-1 Pathway"],"prefix":"10.1159","volume":"40","author":[{"given":"Yuanqin","family":"Yin","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fei","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jing","family":"Shi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Songlin","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jingjing","family":"Cai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Youhong","family":"Jiang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"127","published-online":{"date-parts":[[2016,11,25]]},"container-title":["Cellular Physiology and Biochemistry"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/452563","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/452563","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.karger.com\/Article\/Pdf\/452563","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,4,23]],"date-time":"2025-04-23T13:23:09Z","timestamp":1745414589000},"score":1,"resource":{"primary":{"URL":"https:\/\/karger.com\/article\/doi\/10.1159\/000452563"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2016]]},"references-count":0,"journal-issue":{"issue":"3-4","published-online":{"date-parts":[[2016,12,9]]}},"URL":"https:\/\/doi.org\/10.1159\/000452563","archive":["Portico"],"relation":{},"ISSN":["1015-8987","1421-9778"],"issn-type":[{"value":"1015-8987","type":"print"},{"value":"1421-9778","type":"electronic"}],"subject":[],"published":{"date-parts":[[2016]]}}}