The relationship of promoter methylation of calcium voltage-gated channel alpha 1 and interleukin-16 to primary osteoarthritis

L. Kehribar, Z. Betul Celik, D. Yalcin Kehribar, İ. Eseoglu, C. Gunaydin, M. Aydin

Department of Orthopaedics and Traumatology, Faculty of Medicine, Samsun University, Samsun, Turkey. kehribardemet@gmail.com

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• Orthopedics

OBJECTIVE: Osteoarthritis is the most prevalent joint disease worldwide and the primary cause of musculoskeletal dysfunction. Epigenetic changes in various genes, particularly methylation, have been implicated as possible underlying causes of primary osteoarthritis. The aim of our study was to investigate the promoter methylation status of the calcium voltage-gated channel alpha 1 subunit G (CACNA1G) and interleukin-16 (IL-16) genes, which are strongly associated with calcium channel activity and antigen presentation, respectively, in primary osteoarthritis patients.

PATIENTS AND METHODS: Twenty-one patients with primary osteoarthritis and 25 healthy controls were included in our study. The methylation status of CACNA1G and IL-16 genes was analyzed with methylation-specific Polymerase Chain Reaction (PCR), and the serum levels of IL-16 were determined with Enzyme-Linked Immunosorbent Assay (ELISA).

RESULTS: The age of the patients was 63.95±8.41 years, and they were 15 females and 6 males. The promoter of the CACNA1G gene was found to be hypermethylated in primary osteoarthritis patients (p<0.001). In contrast, the promoter of the IL-16 gene was found to be hypomethylated compared to the control (p<0.001). The serum levels of IL-16 increased in parallel with the hypomethylated promoter status of IL-16 gene in primary osteoarthritis patients compared to the control (p<0.001).

CONCLUSIONS: Our study indicates that the methylation status of CACNA1G and IL-16 gene promoters are epigenetically altered in patients with primary osteoarthritis. Moreover, increased serum IL-16 levels in osteoarthritis patients may be associated with hypomethylation of the IL-16 gene promoter.

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