A preliminary study of possible fibrotic role of meprin metalloproteases in scleroderma patients
Archives of Rheumatology, vol.36, no.4, pp.510-517, 2021 (SCI-Expanded, Scopus, TRDizin)
- Publication Type: Article / Article
- Volume: 36 Issue: 4
- Publication Date: 2021
- Doi Number: 10.46497/archrheumatol.2021.8581
- Journal Name: Archives of Rheumatology
- Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, CINAHL, EMBASE, TR DİZİN (ULAKBİM)
- Page Numbers: pp.510-517
- Keywords: Activator protein-1, meprin-alpha, meprin-beta, scleroderma
- Dokuz Eylül University Affiliated: Yes
Abstract
Objectives: 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 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 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-α) 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-α 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-α 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.