Role of MicroRNAs in Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a common autoimmune disease. The hallmarks of RA are synovial inflammation and hyperplasia, autoantibody production, systemic features, and deformity. A lot of researchers have paid attention to the possibility that microRNAs (miRNAs) play a role in the pathogenesis of RA. miRNAs are a class of small noncoding RNAs, which have 18–25 nucleotides. These small RNAs modify gene expression by binding to target messenger RNA (mRNA), and they block the translation or induce the degradation of target mRNA. Biological relevance of miRNAs has been investigated in physiological and pathological conditions. A growing body of evidence suggests that miRNAs participate in the inflammatory disorders including RA. In this chapter, an overview of biogenesis and function of miRNAs has been presented to introduce researchers to the changes and functional regulation of the key miRNAs in RA and to provide current knowledge in miRNA and RA. It is important to understand the relationship between the key miRNAs and RA pathology as modulation of specific miRNA alterations could be of great pharmaceutical interest in the future

A preliminary study of possible fibrotic role of meprin metalloproteases in scleroderma patients

© 2021 Turkish League Against Rheumatism.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±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-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