NF-?B and MAPKs are involved in resistin-caused ADAMTS-5 induction in human chondrocytes

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dc.authoridYaykasli, Emine/0000-0001-6471-0106|Yaykasli, Kursat/0000-0001-7550-6370;
dc.contributor.authorHatipoglu, Omer F.
dc.contributor.authorYaykasli, Kursat O.
dc.contributor.authorDogan, Mustafa
dc.contributor.authorYaykasli, Emine
dc.contributor.authorBender, Onur
dc.contributor.authorYasar, Tugce
dc.contributor.authorTapan, Safa
dc.date.accessioned2025-10-24T18:10:31Z
dc.date.available2025-10-24T18:10:31Z
dc.date.issued2015
dc.departmentMalatya Turgut Özal Üniversitesi
dc.description.abstractPurpose: Chronic inflammation is an important etiological factor in the development of arthritic diseases. Several factors contribute to aggregation of chronic inflammation, including the presence of excess adipose tissue. Methods: The putative induction mechanisms of ADAMTS-5 by resistin were investigated in normal primary human articular chondrocytes. Expression levels of the ADAMTS-5 gene were determined at several resistin doses and durations. Results: Human chondrocytes were activated and associated with upregulated ADAMTS-5 gene expression after exposure to resistin (also known as adipose tissue-specific secretary factor, ADSF). Release of ADAMTS-5 leads to joint cartilage degradation, a key event in the development of arthritic diseases rheumatoid arthritis (RA) and osteoarthritis (OA). Activation of chondrocytes was associated with upregulated NF-kappa B protein levels in a time-dependent fashion. Co-incubation of human chondrocytes with JNK and p38 inhibitors lead to abrogated levels of NF-kappa B, indicating that these MAPKs are important in the activation of chondrocytes after stimulation with resistin. Similarly, ADAMTS-5 expression levels were abrogated when co-incubated with p38, NF-kappa B, JNK, MEK and PI3K inhibitors. Our results demonstrate that resistin, released from adipose tissue, may be involved in the development of RA and OA in obese patients through degradation of joint cartilage via ADAMTS-5 released from activated chondrocytes.
dc.identifier.endpageE254
dc.identifier.issn0147-958X
dc.identifier.issn1488-2353
dc.identifier.issue4
dc.identifier.scopus2-s2.0-84939155068
dc.identifier.scopusqualityQ2
dc.identifier.startpageE248
dc.identifier.urihttps://hdl.handle.net/20.500.12899/4228
dc.identifier.volume38
dc.identifier.wosWOS:000359119100021
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.language.isoen
dc.publisherCanadian Soc Clinical Investigation
dc.relation.ispartofClinical And Investigative Medicine
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_20251023
dc.subjectRheumatoid-Arthritis; Gene-Expression; Leptin; Inflammation; Protein; Obesity; Metalloproteinases; Osteoarthritis; Destruction; Disintegrin
dc.titleNF-?B and MAPKs are involved in resistin-caused ADAMTS-5 induction in human chondrocytes
dc.typeArticle

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