Kocak, AyseAvsar, Aydan KokenHarmancı, DuyguAkdogan, GulBirlik, A. Merih2023-06-162023-06-1620212618-65002148-5046https://doi.org/10.46497/ArchRheumatol.2021.8581https://search.trdizin.gov.tr/yayin/detay/511479https://hdl.handle.net/20.500.14365/2658Objectives: This study aims to investigate the possible fibrotic role of meprin metalloproteases and possible fibrotic effects of activator protein-1 (AP-1) in scleroderma patients. Patients and methods: Between April 2018 and April 2019, a total of 85 scleroderma patients (9 males, 76 females; mean age: 54.9 +/- 12.1 years; range, 22 to 80 years) who met the 2013 American College of Rheumatology/European League Against Rheumatism criteria and 80 healthy control individuals (10 males, 70 females; mean age 42.9 +/- 10.2 years; range, 19 to 65 years) were included. Patients' data and blood samples were collected. Messenger ribonucleic acid expressions of interleukin (IL)-6, AP-1 subunits, and tumor necrosis factor-alpha (TNF-alpha) were analyzed by quantitative real-time polymerase chain reaction. Serum meprin alpha and beta protein levels were analyzed using the enzyme-linked immunosorbent assay. Results: Meprin alpha and meprin beta protein levels increased in scleroderma patients. The AP-1 subunits (c-Fos, c-Jun), IL-6, and TNF-alpha increased in scleroderma patients, compared to controls. Conclusion: Our results provide evidence showing that increased meprins levels may be related to AP-1 levels and increased meprins levels may responsible for increased inflammatory TNF-alpha and IL-6 levels. All these data suggest meprins as promising therapeutic targets to restore the balance between inflammation and extracellular matrix deposition in scleroderma.eninfo:eu-repo/semantics/openAccessActivator protein-1meprin-alphameprin-betasclerodermaSystemic-SclerosisProcollagen ProteinasesBetaAlphaCleavagePathogenesisClassificationMechanismsCancerArticle10.46497/ArchRheumatol.2021.85812-s2.0-85122513950