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A preliminary study of possible fibrotic role of meprin metalloproteases in scleroderma patients
Ayşe Koçak1, Aydan Köken Avşar2, Duygu Harmancı1
1Department of Molecular Medicine, Dokuz Eylül University Faculty of Medicine, Izmir, Turkey.
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.
Insights
Scleroderma patients show increased levels of meprin metalloproteases and activator protein-1 (AP-1). These findings suggest meprins may drive inflammation and extracellular matrix deposition, offering potential therapeutic targets.
Area of Science:
- Biochemistry
- Immunology
- Rheumatology
Background:
- Scleroderma is a chronic autoimmune disease characterized by fibrosis and inflammation.
- The role of meprin metalloproteases and activator protein-1 (AP-1) in scleroderma pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the fibrotic role of meprin metalloproteases.
- To examine the fibrotic effects of activator protein-1 (AP-1) in scleroderma patients.
Main Methods:
- Quantitative real-time polymerase chain reaction (PCR) was used to analyze messenger ribonucleic acid (mRNA) expressions of interleukin (IL)-6, AP-1 subunits (c-Fos, c-Jun), and tumor necrosis factor-alpha (TNF-α).
- Enzyme-linked immunosorbent assay (ELISA) was employed to measure serum meprin alpha and beta protein levels.
- The study included 85 scleroderma patients and 80 healthy controls.
Main Results:
- Serum levels of meprin alpha and meprin beta were significantly elevated in scleroderma patients compared to controls.
- Expressions of AP-1 subunits (c-Fos, c-Jun), IL-6, and TNF-α were also increased in scleroderma patients.
- A positive correlation was observed between meprin levels and AP-1 levels.
Conclusions:
- Increased meprin levels in scleroderma patients may be associated with elevated AP-1 levels.
- Meprin overexpression might contribute to increased inflammatory mediators like TNF-α and IL-6.
- Meprin metalloproteases represent potential therapeutic targets for managing inflammation and fibrosis in scleroderma.
