Association between TGF-β1 and β-catenin expression in the vaginal wall of patients with pelvic organ prolapse
The aim of this study is to investigate the mechanism of action and correlation between transforming growth factor beta 1 (TGF-β1) and β-catenin in pelvic organ prolapse (POP). The study compared vaginal wall tissues from two groups: 20 patients with POP (POP group) and 20 who had hysterectomies for benign conditions (control group). Hematoxylin and Eosin and Masson staining visualized collagen, while TUNEL staining detected apoptosis. Protein and mRNA expression levels of TGF-β1, β-catenin, matrix metallopeptidase 2 (MMP2), tissue inhibitor of metalloproteinases 2 (TIMP2), and collagen, type I, alpha 1 (COL1A1) were assessed using immunohistochemistry, quantitative real-time polymerase chain reaction, and western blot techniques. Relationships between the protein expressions of TGF-β1 and β-catenin, β-catenin and COL1A1, and TGF-β1 and COL1A1 were analyzed. In the POP group, vaginal wall collagen fibers were sparse, disorganized, and fragmented, with fewer fibers and more apoptotic cells compared to the control group. Protein and mRNA levels of TGF-β1, β-catenin, TIMP2, and COL1A1 were significantly lower, while MMP2 was higher (<i>p</i> < 0.05). Positive correlations were found between TGF-β1, β-catenin, and COL1A1. Reduced TGF-β1 and β-catenin levels may trigger POP by affecting pelvic floor collagen metabolism.
Authors
- Ye Zhao (ORCID: https://orcid.org/0000-0002-9561-6435)
- Shurui Zhao (ORCID: https://orcid.org/0000-0002-0822-3140)
- Dan Xu (ORCID: https://orcid.org/0000-0003-0284-746X)
- Fei Xue (ORCID: https://orcid.org/0000-0003-2086-6699)
- Ying Ma (ORCID: https://orcid.org/0000-0003-0661-9931)
Institutions
- Shanxi Medical University (CN)
- First Hospital of Shanxi Medical University (CN)
Publication Details
- Journal
- Open Life Sciences
- Published
- 2025-01-01
- DOI
- https://doi.org/10.1515/biol-2022-1058
- Primary Topic
- Pelvic floor disorders treatments
- Type
- article
- Field-Weighted Citation Impact
- 0.00