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Background:With the mounting number of intrauterine operations, the incidence of intrauterine adhesion continues to rise. However, the specific pathogenesis of intrauterine adhesion has not been clear and there is no fundamental treatment so far. Objective:IUA is an endometrial fibrosis illness that gravely jeopardizes the reproductive health of women of reproductive age. We elucidated the pathogenesis of IUA at the protein level to provide a more effective research basis for diagnosis and treatment. Methods: This study collected 15 endometrial tissue samples and divided them into three comparison groups (Adhesion/Control group, Endometrium/Adhesion group, and Endometrium/Control group). Label-free quantitative proteomics was used to identify differentially expressed proteins and performed a comprehensive bioinformatics analysis. The research was followed by a quantitative analysis of selected target proteins using a parallel reaction monitoring method. Results: 1328, 290, and 1335 differential proteins were found in each comparison group. Many features of the differential proteins were also identified by GO enrichment analysis and KEGG pathways analysis. Parallel reaction monitoring analysis was performed to quantify 14 target proteins (PGM5, CAMK2G, ABHD6, MYLK, SYNPO2, LTF, PTPN11, TGF-β1, SLC4A1, PROS1, IRAG1, ADIPOQ, HLA-DRB3, COQ6). Among them, TGF-β1 was previously reported as a significant protein in intrauterine adhesion, while other proteins were newly discovered. Conclusions: These proteins are anticipated to develop as biomarkers for intrauterine adhesion and have a specific role in diagnosis and therapy.
Ren et al. (Sun,) studied this question.
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