Gene Expression Analysis of Inflammation, Apoptosis, and DNA Repair Mechanisms in the Pathogenesis of Ankylosing Spondylitis

Sevil Ceyhan Doğan; Tugba Agbektas; Cemile Zontul; Mert Ataş; Gonca Kabak; Ayça Taş; Yavuz Siliğ

doi:10.17776/csj.1962481

Gene Expression Analysis of Inflammation, Apoptosis, and DNA Repair Mechanisms in the Pathogenesis of Ankylosing Spondylitis

Abstract

Ankylosing spondylitis (AS) is a chronic inflammatory rheumatic disease characterized by persistent inflammation, oxidative stress, immune dysregulation, and abnormal bone remodeling. Recent evidence suggests that microRNA-mediated post-transcriptional regulation and DNA damage response pathways may contribute to AS pathogenesis. This study aimed to investigate the expression profiles of selected microRNAs and genes associated with inflammation, apoptosis, and DNA repair mechanisms in patients with AS. A total of 30 patients diagnosed with AS and 30 healthy controls were included in the study. Gene and microRNA expression levels, including miRNA-574-5p, miRNA-30c-5p, MDM2, RAD51, NFKB1, BAX, ERCC1, and ATR, were analyzed using quantitative real-time PCR (qRT-PCR). Inflammatory parameters, including C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and interleukin-6 (IL-6), were also evaluated. The results demonstrated significantly increased miRNA-574-5p expression and significantly decreased MDM2 expression in the AS group compared with controls (p<0.05). CRP and IL-6 levels were also significantly elevated in patients with AS. Logistic regression analysis identified miRNA-574-5p, MDM2, and CRP as independently associated with AS. Receiver operating characteristic (ROC) analysis revealed that miRNA-574-5p and MDM2 exhibited significant diagnostic performance for distinguishing AS patients from healthy individuals. Correlation analyses demonstrated a positive association between miRNA-574-5p and BAX, whereas a negative correlation was observed between miRNA-574-5p and ESR. These findings suggest that altered miRNA-574-5p and MDM2 expression may contribute to inflammatory activity, apoptosis, and cellular stress responses in AS. Overall, the findings suggest that altered miRNA-574-5p and MDM2 expression may be associated with ankylosing spondylitis and represent candidate molecular biomarkers that warrant further validation in larger independent cohorts.

Keywords

Ankylosing spondylitis, Apoptosis, DNA repair, Inflammation

Ethical Statement

Approval Date: March 26, 2026; No: 2026-03/74

References

Braun, J., & Sieper, J. (2007). Ankylosing spondylitis. The Lancet, 369, 1379–1390. https://doi.org/10.1016/S0140-6736(07)60635-7
Taurog, J. D., Chhabra, A., & Colbert, R. A. (2016). Ankylosing spondylitis and axial spondyloarthritis. The New England Journal of Medicine, 374, 2563–2574. https://doi.org/10.1056/NEJMra1406182
Hayden, M. S., & Ghosh, S. (2011). NF-κB in immunobiology. Cell Research, 21, 223–244. https://doi.org/10.1038/cr.2011.13
Vousden, K. H., & Prives, C. (2009). Blinded by the light: The growing complexity of p53. Cell, 137, 413–431. https://doi.org/10.1016/j.cell.2009.04.037
Ciccia, A., & Elledge, S. J. (2010). The DNA damage response: Making it safe to play with knives. Molecular Cell, 40, 179–204. https://doi.org/10.1016/j.molcel.2010.09.019
Ku, T., Li, B., Gao, R., Zhang, Y., Yan, W., Ji, X., Li, G., & Sang, N. (2017). NF-κB-regulated microRNA-574-5p underlies synaptic and cognitive impairment in response to atmospheric PM2.5 aspiration. Particle and Fibre Toxicology, 14, Article 34. https://doi.org/10.1186/s12989-017-0215-3
Yang, J. Y. (2024). miR-574-5p in epigenetic regulation and Toll-like receptor signaling. Cell Communication and Signaling, 22, Article 567. https://doi.org/10.1186/s12964-024-01934-x
Ceolotto, G., Giannella, A., Albiero, M., Kuppusamy, M., Radu, C., Simioni, P., Garlaschelli, K., Baragetti, A., Catapano, A. L., Lori, E., Fadini, G. P., Avogaro, A., & de Kreutzenberg. (2017). miR-30c-5p regulates macrophage-mediated inflammation and pro-atherosclerosis pathways. Cardiovascular Research, 113, 1627–1638. https://doi.org/10.1093/cvr/cvx157
Pérez-Sánchez, A., Barrajón-Catalán, E., Herranz-López, M., & Micol, V. (2018). Nutraceuticals for skin care: A comprehensive review of human clinical studies. Nutrients, 10, Article 403. https://doi.org/10.3390/nu10040403
Das, K., & Rao, L. V. M. (2022). The role of microRNAs in inflammation. International Journal of Molecular Sciences, 23(24), Article 15479. https://doi.org/10.3390/ijms232415479

Barnabei, L., Laplantine, E., Mbongo, W., Rieux-Laucat, F., & Weil, R. (2021). NF-κB: At the borders of autoimmunity and inflammation. Frontiers in Immunology, 12, Article 716469. https://doi.org/10.3389/fimmu.2021.716469
Korn, T., Bettelli, E., Oukka, M., & Kuchroo, V. K. (2009). IL-17 and Th17 cells. Annual Review of Immunology, 27, 485–517. https://doi.org/10.1146/annurev.immunol.021908.132710
Fan, X., Wang, E., & Zhang, L. (2017). MicroRNA-mediated regulatory networks in inflammation and immune responses. Cellular & Molecular Immunology, 14, 1–10. https://doi.org/10.1186/ar4194
Takayanagi, H. (2007). Osteoimmunology: Shared mechanisms and crosstalk between the immune and bone systems. Nature Reviews Immunology, 7, 292–304. https://doi.org/10.1038/nri2062
Wade, M., Li, Y. C., & Wahl, G. M. (2013). MDM2, MDMX and p53 in oncogenesis and cancer therapy. Nature Reviews Cancer, 13, 83–96. https://doi.org/10.1038/nrc3430
Jackson, S. P., & Bartek, J. (2009). The DNA-damage response in human biology and disease. Nature, 461, 1071–1078. https://doi.org/10.1038/nature08467
Webster, G. A., & Perkins, N. D. (1999). Transcriptional cross talk between NF-κB and p53. Molecular and Cellular Biology, 19, 3485–3495. https://doi.org/10.1128/MCB.19.5.3485
Ak, P., & Levine, A. J. (2010). p53 and NF-κB: Different strategies for responding to stress lead to a functional antagonism. The FASEB Journal, 24, 3643–3652. https://doi.org/10.1096/fj.10-160549
Hunter, C. A., & Jones, S. A. (2015). IL-6 as a keystone cytokine in health and disease. Nature Immunology, 16, 448–457. https://doi.org/10.1038/ni.3153
Lubberts, E. (2015). The IL-23–IL-17 axis in inflammatory arthritis. Nature Reviews Rheumatology, 11, 415–429. https://doi.org/10.1038/nrrheum.2015.53
Sherlock, J. P., Joyce-Shaikh, B., Turner, S. P., Chao, C. C., Sathe, M., Grein, J., Gorman, C. D., Bowman, E. P. B., McClanahan, T. K., Yearley, J. H., Eberl, G., Buckley, C. D., Kastelein, R. A., Pierce, R. H., Laface, D. M., & Cua, D. J. (2012). IL-23 induces spondyloarthropathy by acting on ROR-γt+ CD3+ CD4− CD8− entheseal resident T cells. Nature Medicine, 18, https://doi.org/1069–1076. 10.1038/nm.2817
Gabay, C. (2006). Interleukin-6 and chronic inflammation. Arthritis Research & Therapy, 8, S3. https://doi.org/10.1186/ar1917

Details

Primary Language

English

Subjects

Gene Expression

Journal Section

Research Article

Authors

Sevil Ceyhan Doğan
0000-0003-1570-8848
Türkiye

Tugba Agbektas ^*
0009-0004-4533-0019
Türkiye

Cemile Zontul
0000-0002-1436-5145
Türkiye

Mert Ataş
0000-0002-6713-5888
Türkiye

Gonca Kabak
0009-0004-2430-5076
Türkiye

Ayça Taş
0000-0002-7132-1325
Türkiye

Yavuz Siliğ
0000-0002-0562-7457
Türkiye

Publication Date

August 31, 2026

Submission Date

June 2, 2026

Acceptance Date

August 17, 2026

Published in Issue

Year 2026 Volume: 47 Number: 4

DOI

https://doi.org/10.17776/csj.1962481

IZ

https://izlik.org/JA77RU24BG

APA

Ceyhan Doğan, S., Agbektas, T., Zontul, C., Ataş, M., Kabak, G., Taş, A., & Siliğ, Y. (2026). Gene Expression Analysis of Inflammation, Apoptosis, and DNA Repair Mechanisms in the Pathogenesis of Ankylosing Spondylitis. Cumhuriyet Science Journal, 47(4), 690-700. https://doi.org/10.17776/csj.1962481

AMA

1.Ceyhan Doğan S, Agbektas T, Zontul C, et al. Gene Expression Analysis of Inflammation, Apoptosis, and DNA Repair Mechanisms in the Pathogenesis of Ankylosing Spondylitis. CSJ. 2026;47(4):690-700. doi:10.17776/csj.1962481

Chicago

Ceyhan Doğan, Sevil, Tugba Agbektas, Cemile Zontul, et al. 2026. “Gene Expression Analysis of Inflammation, Apoptosis, and DNA Repair Mechanisms in the Pathogenesis of Ankylosing Spondylitis”. Cumhuriyet Science Journal 47 (4): 690-700. https://doi.org/10.17776/csj.1962481.

EndNote

Ceyhan Doğan S, Agbektas T, Zontul C, Ataş M, Kabak G, Taş A, Siliğ Y (August 1, 2026) Gene Expression Analysis of Inflammation, Apoptosis, and DNA Repair Mechanisms in the Pathogenesis of Ankylosing Spondylitis. Cumhuriyet Science Journal 47 4 690–700.

IEEE

[1]S. Ceyhan Doğan et al., “Gene Expression Analysis of Inflammation, Apoptosis, and DNA Repair Mechanisms in the Pathogenesis of Ankylosing Spondylitis”, CSJ, vol. 47, no. 4, pp. 690–700, Aug. 2026, doi: 10.17776/csj.1962481.

ISNAD

Ceyhan Doğan, Sevil - Agbektas, Tugba - Zontul, Cemile - Ataş, Mert - Kabak, Gonca - Taş, Ayça - Siliğ, Yavuz. “Gene Expression Analysis of Inflammation, Apoptosis, and DNA Repair Mechanisms in the Pathogenesis of Ankylosing Spondylitis”. Cumhuriyet Science Journal 47/4 (August 1, 2026): 690-700. https://doi.org/10.17776/csj.1962481.

JAMA

1.Ceyhan Doğan S, Agbektas T, Zontul C, Ataş M, Kabak G, Taş A, Siliğ Y. Gene Expression Analysis of Inflammation, Apoptosis, and DNA Repair Mechanisms in the Pathogenesis of Ankylosing Spondylitis. CSJ. 2026;47:690–700.

MLA

Ceyhan Doğan, Sevil, et al. “Gene Expression Analysis of Inflammation, Apoptosis, and DNA Repair Mechanisms in the Pathogenesis of Ankylosing Spondylitis”. Cumhuriyet Science Journal, vol. 47, no. 4, Aug. 2026, pp. 690-0, doi:10.17776/csj.1962481.

Vancouver

1.Sevil Ceyhan Doğan, Tugba Agbektas, Cemile Zontul, Mert Ataş, Gonca Kabak, Ayça Taş, Yavuz Siliğ. Gene Expression Analysis of Inflammation, Apoptosis, and DNA Repair Mechanisms in the Pathogenesis of Ankylosing Spondylitis. CSJ. 2026 Aug. 1;47(4):690-70. doi:10.17776/csj.1962481

As of 2026, Cumhuriyet Science Journal will be published in six issues per year, released in February, April, June, August, October, and December

Gene Expression Analysis of Inflammation, Apoptosis, and DNA Repair Mechanisms in the Pathogenesis of Ankylosing Spondylitis

Abstract

Keywords

Ethical Statement

References

Details

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Published in Issue

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