{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,30]],"date-time":"2025-10-30T22:30:05Z","timestamp":1761863405010},"reference-count":50,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2014,11,13]],"date-time":"2014-11-13T00:00:00Z","timestamp":1415836800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"National Research Foundation of Kore"},{"name":"Korean Government","award":["2012R1A5A2051384"],"award-info":[{"award-number":["2012R1A5A2051384"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Periodontal Research"],"published-print":{"date-parts":[[2015,10]]},"abstract":"<jats:sec><jats:title>Background and Objective<\/jats:title><jats:p>Resistin was recently reported to play a role in inflammation\u2010related diseases such as arthritis. However, the precise role of resistin in chronic inflammatory diseases, such as periodontal disease, remains unclear. The aim of this study was to investigate the combined effects of nicotine and lipopolysaccharide (<jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>) on the expression of resistin and to assess whether resistin expression influences the levels of inflammatory cytokines, extracellular matrix (<jats:styled-content style=\"fixed-case\">ECM<\/jats:styled-content>) molecules and <jats:styled-content style=\"fixed-case\">MMP<\/jats:styled-content>s in human periodontal ligament cells (<jats:styled-content style=\"fixed-case\">PDLC<\/jats:styled-content>s) stimulated with both nicotine and <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Material and Methods<\/jats:title><jats:p>PDLCs were pretreated with isoproterenol or resistin\u2010specific small interfering RNA (siRNA), stimulated with LPS plus nicotine for 24\u00a0h, and then monitored for the production of inflammatory mediators. The concentrations of prostaglandin E2 (PGE2) and nitric oxide (NO) were measured by radioimmunoassay and the Griess method, respectively. RT\u2010PCR and western blot analysis were used to measure the levels of <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> and protein, respectively. Western blot analysis was also used to assess the activation of various signal\u2010transduction pathways.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Treatment with nicotine plus LPS up\u2010regulated the expression of resistin <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> and the production of resistin protein in PDLCs in a time\u2010 and concentration\u2010dependent manner. Isoproterenol\u2010mediated interference with the function of resistin, or siRNA\u2010mediated knockdown of resistin expression, markedly attenuated the LPS plus nicotine\u2010mediated stimulation of PGE2 and NO production, the production of cyclooxygenase\u20102 (COX\u20102) and inducible nitric oxide synthase proteins and the expression of proinflammatory cytokines [tumor necrosis factor\u2010\u03b1, interleukin (IL)\u20101\u03b2, IL\u20106 and IL\u201012] and MMPs (MMP\u20101, MMP\u20102 and MMP\u20109); however, these treatments restored the expression of ECM molecules. Furthermore, pretreatment with isoproterenol or resistin\u2010specific siRNA blocked nicotine plus LPS\u2010induced activation of phosphoinositide\u20103\u2010kinase, glycogen synthase kinase\u20103 beta, \u03b2\u2010catenin, p38, ERK, JNK and nuclear factor\u2010\u03baB.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>This is the first study to show that the inhibition of resistin, by either a pharmacological or a genetic silencing approach, has anti\u2010inflammatory effects. These effects include decreased levels of inflammatory cytokines and the prevention of <jats:styled-content style=\"fixed-case\">ECM<\/jats:styled-content> breakdown in a nicotine plus <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>\u2010stimulated <jats:styled-content style=\"fixed-case\">PDLC<\/jats:styled-content> model.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jre.12240","type":"journal-article","created":{"date-parts":[[2014,11,13]],"date-time":"2014-11-13T11:03:04Z","timestamp":1415876584000},"page":"602-613","source":"Crossref","is-referenced-by-count":14,"title":["Role of resistin in the inflammatory response induced by nicotine plus lipopolysaccharide in human periodontal ligament cells <i>in vitro<\/i>"],"prefix":"10.1111","volume":"50","author":[{"given":"S.\u2010K.","family":"Kang","sequence":"first","affiliation":[{"name":"Department of Oral Medicine School of Dentistry Kyung Hee University Seoul 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