Mechanism of mesenchymal stromal cells reversing fibrosis of the uterine endometrium after injury
10.11665/j.issn.1000-5048.2025120801
- VernacularTitle:间充质基质细胞逆转子宫内膜纤维化的机制研究
- Author:
Shiqi LI
1
;
Yue DANG
;
Qingqing ZHOU
;
Xin SHANG
;
Jiali LIU
Author Information
1. 中国药科大学药物代谢动力学重点实验室, 南京210009
- Publication Type:Journal Article
- Keywords:
endometrial injury;
mesenchymal stromal cells;
collagen fiber;
TGF-β/SMAD pathway
- From:
Journal of China Pharmaceutical University
2026;57(3):360-368
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the effect of mesenchymal stromal cells (MSCs) on the fibrosis progression and endometrial regeneration in mouse models of endometrial injury, a mouse endometrial injury model was established by physical scraping combined with lipopolysaccharide (LPS) chemical induction, and the endometrium morphology and collagen deposition were evaluated by HE and Masson staining after unilateral administration of MSCs. RT-qPCR and immunofluorescence were used to detect the expression of epithelial markers Epcam and collagen I (Col1). Primary endometrial epithelial cells were isolated to assess p21 expression. Fibrosis-related genes and signaling pathways were validated using transcriptome sequencing and RT-qPCR. The experimental results showed that MSCs increased endometrial thickness and number of glands (P<0.05), up-regulated the expression of Epcam (P<0.01), while significantly reducing uterine collagen fiber deposition (P<0.05) and the expression of p21 in primary epithelial cells (P<0.0001). Transcriptomic analysis revealed that MSCs attenuated collagen deposition by modulating genes involved in the TGF-β signaling pathway. This study elucidates that MSCs facilitate uterine repair by reversing endometrial fibrosis and promoting epithelial regeneration, and their role is related to the regulation of the TGF-β/SMAD pathway and suppression of aberrant collagen accumulation.
