4.2 Article

DNA Methylation and mRNA Expression of B7-H3 Gene in Ankylosing Spondylitis: A Case-Control Study

Journal

IMMUNOLOGICAL INVESTIGATIONS
Volume 51, Issue 7, Pages 2025-2034

Publisher

TAYLOR & FRANCIS INC
DOI: 10.1080/08820139.2022.2095285

Keywords

Ankylosing spondylitis; B7-H3; DNA methylation; epigenetics; mRNA

Categories

Funding

  1. National Natural Science Foundation of China [81773514, 82073655]
  2. funds for academic and technical leaders in Anhui province [2017D140]
  3. Clinical Medicine Discipline construction project of Anhui Medical University [2021lcxk043]

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This study explored the association between the B7-H3 gene and AS in an eastern Chinese Han population. The researchers found that hypomethylation of the B7-H3 gene promoter was observed in AS patients, and B7-H3 gene expression was significantly enhanced in AS patients. These findings suggest that epigenetic modifications of B7-H3 are associated with susceptibility to AS.
Background Ankylosing spondylitis (AS) is a common inflammatory arthritis, with a high prevalence in patients in their mid-20s. Its pathogenesis is not well understood; however, genetic factors likely play a critical role. Epigenetic DNA changes may be involved in the pathogenesis of AS. In this study, we explored the methylation and transcription levels of the B7-H3 gene and its association with AS in an eastern Chinese Han population. Methods Peripheral blood of AS patients and healthy controls was used to extract genomic DNA and B7-H3 methylation levels were analyzed using sodium bisulfite followed by multiplex polymerase chain reaction. SPSS software was used to determine the statistical significance of the results. Results Hypomethylation of the promoter of the B7-H3 gene was observed in AS patients, whereas the B7-H3 gene expression was significantly enhanced in AS patients. Conclusion Epigenetic modifications of B7-H3 were associated with susceptibility to AS. Hypomethylation of the B7-H3 promoter, which leads to B7-H3 overexpression, may be involved in the pathogenesis of AS.

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