SIAE-Mediated Loss of Sialic Acid Acetylation Contributes to Ulcerative Colitis
This study demonstrates that SIAE is significantly upregulated in ulcerative colitis (UC) tissues and TNF-α-stimulated HT-29 cells, leading to a marked reduction in sialic acid acetylation and cell surface sialic acid levels. These changes correlate with decreased expression of cell adhesion molecules, suggesting a disruption of the mucosal barrier integrity. Consequently, SIAE-mediated sialic acid de-acetylation emerges as a critical factor in UC pathogenesis, potentially serving as both a valuable biomarker and a promising therapeutic target.
Authors
- Chunyan Hou (ORCID: https://orcid.org/0000-0001-5966-1899)
- Shuang Yang (ORCID: https://orcid.org/0000-0001-7958-0594)
- Guoqiang Ma (ORCID: https://orcid.org/0000-0002-0475-3267)
- Junfeng Ma (ORCID: https://orcid.org/0000-0002-5183-5425)
- Duanmin Hu (ORCID: https://orcid.org/0000-0002-7347-8051)
- Xiaotong Wang (ORCID: https://orcid.org/0000-0001-6024-4435)
- Lei Xu (ORCID: https://orcid.org/0009-0004-1374-2211)
- Ying Zheng (ORCID: https://orcid.org/0000-0003-3014-1587)
- S. Nair B�o
- Jiani Qian
Institutions
- Georgetown University (US)
- Georgetown University Medical Center (US)
- Soochow University (CN)
- Second Affiliated Hospital of Soochow University (CN)
- First Affiliated Hospital of Soochow University (CN)
Publication Details
- Journal
- Journal of Inflammation Research
- Published
- 2025-04-01
- DOI
- https://doi.org/10.2147/jir.s512139
- Citations
- 5
- Primary Topic
- Liver Diseases and Immunity
- Type
- article
- Field-Weighted Citation Impact
- 6.61
Funders
- National Natural Science Foundation of China
- Soochow University
- Priority Academic Program Development of Jiangsu Higher Education Institutions
- State Key Laboratory of Radiation Medicine and Protection