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

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dc.authoridKaya, Ertugrul/0000-0003-0081-682X|Yaykasli, Kursat/0000-0001-7550-6370|Yaykasli, Emine/0000-0001-6471-0106;
dc.contributor.authorYaykasli, Kursat Oguz
dc.contributor.authorHatipoglu, Omer Faruk
dc.contributor.authorYaykasli, Emine
dc.contributor.authorYildirim, Kubra
dc.contributor.authorKaya, Ertugrul
dc.contributor.authorOzsahin, Mustafa
dc.contributor.authorUslu, Mustafa
dc.date.accessioned2025-10-24T18:08:46Z
dc.date.available2025-10-24T18:08:46Z
dc.date.issued2015
dc.departmentMalatya Turgut Özal Üniversitesi
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.
dc.description.sponsorshipTUBITAK (Scientific and Technical Research Council of Turkey) [SBAG/111S218]
dc.description.sponsorshipThis study was supported by TUBITAK (The Scientific and Technical Research Council of Turkey), (Project Number: SBAG/111S218).
dc.identifier.doi10.1002/cbin.10336
dc.identifier.endpage112
dc.identifier.issn1065-6995
dc.identifier.issn1095-8355
dc.identifier.issue1
dc.identifier.pmid25045124
dc.identifier.scopus2-s2.0-84921019135
dc.identifier.scopusqualityQ2
dc.identifier.startpage104
dc.identifier.urihttps://doi.org/10.1002/cbin.10336
dc.identifier.urihttps://hdl.handle.net/20.500.12899/3279
dc.identifier.volume39
dc.identifier.wosWOS:000347382000012
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherWiley
dc.relation.ispartofCell Biology International
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_20251023
dc.subjectmatrix metalloproteinases; inflammation; leptin; ADAMTS; MAPKs
dc.titleLeptin induces ADAMTS-4, ADAMTS-5, and ADAMTS-9 genes expression by mitogen-activated protein kinases and NF-?B signaling pathways in human chondrocytes
dc.typeArticle

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