Leptin induces ADAMTS-4, ADAMTS-5, and ADAMTS-9 genes expression by mitogen-activated protein kinases and NF-kappa B signaling pathways in human chondrocytes

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dc.contributor.authorYaykaşlı, Kürşat Oğuz
dc.contributor.authorHatipoğlu, Ömer Faruk
dc.contributor.authorYaykaşlı, Emine
dc.contributor.authorYıldırım, Kübra
dc.contributor.authorKaya, Ertuğrul
dc.contributor.authorÖzşahin, Mustafa
dc.contributor.authorGündüz, Esra
dc.date.accessioned2020-04-30T23:18:54Z
dc.date.available2020-04-30T23:18:54Z
dc.date.issued2015
dc.departmentDÜ, Tıp Fakültesi, Dahili Tıp Bilimleri Bölümüen_US
dc.descriptionYaykasli, Kursat/0000-0001-7550-6370; Hatipoglu, Omer Faruk/0000-0002-1012-001X; Yaykasli, Emine/0000-0001-6471-0106; Kaya, Ertugrul/0000-0003-0081-682Xen_US
dc.descriptionWOS: 000347382000012en_US
dc.descriptionPubMed: 25045124en_US
dc.description.abstractElucidation of the causes of inflammation has vital importance in the development of new approaches for the treatment of arthritic diseases. The degradation of aggrecan by upregulated disintegrin and metalloproteinase with trombospondin motifs (ADAMTSs) is the key event in the development of both rheumatoid arthritis (RA) and osteoarthritis (OA). Increased levels of leptin in both RA and OA have been demonstrated, thus linking leptin to arthritic diseases, but the mechanism has not been clarified. This study investigated the putative role of signaling pathways (p38, JNK, MEK1, NF-?B, and PI3) involved in leptin-induced cartilage destruction. Normal human articular chondrocytes were cultured with recombinant human leptin at 100, 250, 500, and 1000ng/mL doses for 6, 12, 24, and 48h, after which ADAMTS-4, -5, and -9 genes expression were determined by real time-polymerase chain reaction (RT-PCR) and Western Blot methods. The signaling pathways involved in leptin-induced ADAMTSs upregulation were also investigated by using inhibitors of signaling pathways. It was demonstrated that ADAMTSs expression level was peaked at 1000ng/mL doses for 48hours, and MAPKs (p38, JNK, and MEK) and NF-?B signaling pathways involving in leptin triggered ADAMTSs upregulation. Obesity as a risk for RA and OA may contribute to the inflammation of both RA and OA diseases by secreting adipokines like leptin. We hypothesize that leptin is involved in the development of RA and OA accompanied with obesity by increasing ADAMTS-4, -5, and -9 genes expression via MAPKs and NF-?B signaling pathways.en_US
dc.description.sponsorshipTUBITAK (Scientific and Technical Research Council of Turkey)Turkiye Bilimsel ve Teknolojik Arastirma Kurumu (TUBITAK) [SBAG/111S218]en_US
dc.description.sponsorshipThis study was supported by TUBITAK (The Scientific and Technical Research Council of Turkey), (Project Number: SBAG/111S218).en_US
dc.identifier.doi10.1002/cbin.10336en_US
dc.identifier.endpage112en_US
dc.identifier.issn1065-6995
dc.identifier.issn1095-8355
dc.identifier.issue1en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage104en_US
dc.identifier.urihttps://doi.org/10.1002/cbin.10336
dc.identifier.urihttps://hdl.handle.net/20.500.12684/3574
dc.identifier.volume39en_US
dc.identifier.wosWOS:000347382000012en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakPubMeden_US
dc.indekslendigikaynakScopusen_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofCell Biology Internationalen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectmatrix metalloproteinasesen_US
dc.subjectinflammationen_US
dc.subjectleptinen_US
dc.subjectADAMTSen_US
dc.subjectMAPKsen_US
dc.titleLeptin induces ADAMTS-4, ADAMTS-5, and ADAMTS-9 genes expression by mitogen-activated protein kinases and NF-kappa B signaling pathways in human chondrocytesen_US
dc.typeArticleen_US

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