Expression Profile of Human Gingival Fibroblasts Induced by Interleukin-1 beta Reveals Central Role of Nuclear Factor-Kappa B Stabilizing Human Gingival Fibroblasts During Inflammation

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dc.contributor.authorVardar-Sengul, Saynur
dc.contributor.authorArora, Shilpi
dc.contributor.authorBaylas, Haluk
dc.contributor.authorMercola, Dan
dc.date.accessioned2019-10-27T20:52:11Z
dc.date.available2019-10-27T20:52:11Z
dc.date.issued2009
dc.departmentEge Üniversitesien_US
dc.description.abstractBackground: Interleukin (IL)-1 beta is a key cytokine in the pathogenesis of periodontitis, and it induces inflammatory mediators in periodontal diseases. We developed immortalized human gingival fibroblasts (HGFs), investigated the effects of IL-1 beta on the gene expression using expression arrays containing similar to 40,000 genes, and tested the role of nuclear factor-kappa B (NF-kappa B) in maintaining an activated HGF population. Methods: Total RNA was isolated from IL-1 beta-induced and mock-induced control cells. Gene expression analyses were performed using expression arrays and confirmed by quantitative real-time polymerase chain reaction. Western blot analysis to show inhibitor of kappa B-alpha (I kappa B alpha) phosphorylation and immunostaining of cells for NF-kappa B nuclear translocation were performed. Apoptosis was confirmed by assay of poly ADP-ribose polymerase (PARP) cleavage. Results: A total of 382 probe sets corresponding to 254 genes were differentially expressed in IL-1 beta-induced cells (P <0.001). A total of 215 genes were upregulated, and 39 genes were downregulated. Most notable NF-kappa B pathway members (NF kappa B1, NF kappa B2, I kappa B alpha, I kappa B epsilon, I kappa B zeta, REL, RELB, and TA-NFKBH) were upregulated. I kappa B alpha was phosphorylated, and NF-kappa B accumulated in the nucleus. An IL-1 beta-induced set of 27 genes was downregulated by an NF-kappa B inhibitor, leading to a decreased number of viable cells and suggesting an antiapoptotic role for NF-kappa B. Conclusions: IL-1 beta leads to a large number of significant expression changes consistent with a pathologic role in periodontitis, including enhancement of inflammatory cytokines, chemokines, transcription factors, matrix metalloproteinases, adhesion molecules, and especially NF-kappa B-dependent antiapoptotic genes. NF-kappa B activation blocks apoptosis, thereby stabilizing the HGF population in inflammation. J Periodontol 2009;80:833-849.en_US
dc.description.sponsorshipNational Institutes of Health, Bethesda, MarylandUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USA [UO1CA114810-03]en_US
dc.description.sponsorshipThis study was supported, in part, by the National Institutes of Health, Bethesda, Maryland (grant UO1CA114810-03). The authors report no conflicts of interest related to this study.en_US
dc.identifier.doi10.1902/jop.2009.080483en_US
dc.identifier.endpage849en_US
dc.identifier.issn0022-3492
dc.identifier.issn1943-3670
dc.identifier.issue5en_US
dc.identifier.pmid19405838en_US
dc.identifier.startpage833en_US
dc.identifier.urihttps://doi.org/10.1902/jop.2009.080483
dc.identifier.urihttps://hdl.handle.net/11454/43200
dc.identifier.volume80en_US
dc.identifier.wosWOS:000265992200018en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofJournal of Periodontologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectFibroblastsen_US
dc.subjectgene expressionen_US
dc.subjectinterleukin-1 betaen_US
dc.subjectmicroarraysen_US
dc.subjectnuclear factor-kappa Ben_US
dc.subjectreal-time polymerase chain reactionen_US
dc.titleExpression Profile of Human Gingival Fibroblasts Induced by Interleukin-1 beta Reveals Central Role of Nuclear Factor-Kappa B Stabilizing Human Gingival Fibroblasts During Inflammationen_US
dc.typeArticleen_US

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