Urotensin-II Prevents Cartilage Degeneration in a Monosodium Iodoacetate-Induced Rat Model of Osteoarthritis

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dc.authoridOkuyan, Hamza Malik/0000-0001-7616-3330
dc.contributor.authorTerzi, Menderes Yusuf
dc.contributor.authorOkuyan, Hamza Malik
dc.contributor.authorKaraboga, Ihsan
dc.contributor.authorGokdemir, Cemil Emre
dc.contributor.authorTap, Duygu
dc.contributor.authorKalacı, Aydıner
dc.date.accessioned2024-09-18T20:52:59Z
dc.date.available2024-09-18T20:52:59Z
dc.date.issued2022
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractOsteoarthritis (OA) is a common degenerative articular disorder caused by traumatic or spontaneous factors such as genetics, obesity, and advanced age. Comprehending the pathogenic mechanism of OA ensures the development of novel disease-modifying therapeutics rather than conventional palliative drugs with undesired side effects. Urotensin-II (UII) is a multifunctional short cyclic peptide implicated in several disorders. We aimed to analyze the effects of intraarticular UII treatment in a monosodium iodoacetate (MIA)-induced OA rat model. We divided animals into six groups to test three different concentrations of UII with histopathological and immunohistochemical analyses of bone morphogenetic protein-2 (BMP-2), nuclear factor kappa B subunit 1 (NF-kappa B), and intrinsic UII expression. We analyzed serum levels of cartilage related and inflammatory markers post-OA. We observed a noticeable amelioration of the MIA-induced knee damage in UII-treated animals after gross morphology examination. Mankin scoring after histopathological stainings revealed a partial prevention of articular tissue damage in UII-treated animals. We found a significant reduction in BMP-2 and NF-kappa B while an increase in intrinsic UII expressions upon exogenous UII injection after immunohistochemical analyses. The Mankin scores were significantly correlated with BMP-2, NF-kappa B, and intrinsic UII levels. There was no significant alteration in serum markers after UII treatment. We are the first group showing the protective effect of UII on the destructed knee joints of osteoarthritic rats by downregulating the BMP-2 and NF-kappa B and upregulating intrinsic UII expressions. To uncover the mechanistic role of UII during OA, further experiments are warranted. [GRAPHICS] .en_US
dc.identifier.doi10.1007/s10989-022-10448-4
dc.identifier.issn1573-3149
dc.identifier.issn1573-3904
dc.identifier.issue5en_US
dc.identifier.scopus2-s2.0-85135611044en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.urihttps://doi.org/10.1007/s10989-022-10448-4
dc.identifier.urihttps://hdl.handle.net/20.500.12483/11521
dc.identifier.volume28en_US
dc.identifier.wosWOS:000838076200001en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.relation.ispartofInternational Journal of Peptide Research and Therapeuticsen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectOsteoarthritisen_US
dc.subjectUrotensin-IIen_US
dc.subjectCartilage destructionen_US
dc.subjectMonosodium iodoacetateen_US
dc.subjectBMP-2en_US
dc.subjectNF-kappa Ben_US
dc.titleUrotensin-II Prevents Cartilage Degeneration in a Monosodium Iodoacetate-Induced Rat Model of Osteoarthritisen_US
dc.typeArticleen_US

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