{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T15:07:51Z","timestamp":1787584071877,"version":"build-2736575974"},"reference-count":45,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2017,5,18]],"date-time":"2017-05-18T00:00:00Z","timestamp":1495065600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2017,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:sec><jats:label\/><jats:p>Osteoarthritis (OA) is characterized by progressive destruction of articular cartilage, resulting in significant disability. Inflammatory cytokines commonly initiate the extreme changes in the synovium and cartilage microenvironment of the OA patients, subsequently resulting in cell dysfunctions, especially synoviocyte dysfunction. We revealed that the expression of osteopontin (OPN), which has been reported to regulate expression of various inflammatory factors associating with the pathogenesis of OA including matrix metalloprotease 13 (MMP13), interlukine\u20106 and 8 (IL\u20106 and IL\u20108), is significantly upregulated in OA tissues. In the present study, online tools were used to screen out the candidate miRNAs of OPN. Among the candidate miRNAs, miR\u2010181c inhibited OPN mRNA expression the most strongly. Ectopic expression of miR\u2010181c significantly repressed synoviocyte proliferation, as well as the levels of OPN, MMP13, IL\u20106, and IL\u20108. Further, the candidate lncRNAs of miR\u2010181c were screened out by using DianaTools; among which NEAT1 showed to inversely regulate miR\u2010181c. By performing Luciferase assays, we revealed that NEAT1 competed with OPN for miR\u2010181c binding. After NEAT1 knockdown, MMP13, IL\u20106, and IL\u20108 expression was reduced; the synoviocyte proliferation was repressed, as well as OPN protein levels; the suppressive effect of NETA1 knockdown on synoviocyte proliferation and the indicated factors were partially reversed by miR\u2010181c inhibition. In OA tissues, OPN mRNA, and NEAT1 expression was upregulated, whereas miR\u2010181c expression was downregulated, indicating that targeting NEAT1 to rescue miR\u2010181c expression so as to inhibit OPN expression and synoviocyte proliferation might be an efficient strategy for OA treatment. J. Cell. Biochem. 118: 3775\u20133784, 2017. \u00a9 2017 Wiley Periodicals, Inc.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcb.26025","type":"journal-article","created":{"date-parts":[[2017,4,5]],"date-time":"2017-04-05T21:02:47Z","timestamp":1491426167000},"page":"3775-3784","source":"Crossref","is-referenced-by-count":69,"title":["NEAT1\/miR\u2010181c Regulates Osteopontin (OPN)\u2010Mediated Synoviocyte Proliferation in Osteoarthritis"],"prefix":"10.1002","volume":"118","author":[{"given":"Qiyuan","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Emergency Medicine The Second Xiangya Hospital Central South University Changsha Hunan China"},{"name":"Emergency Medicine and Difficult Diseases Institute Central South University Changsha Hunan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9999-4695","authenticated-orcid":false,"given":"Wanchun","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of 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