#123 : Caveolin-1 Function and Regulation in Mouse Uterus During Early Pregnancy and Under Human In Vitro Decidualization
Background and Aims: Endometrial decidualization is a step in establishing and maintaining pregnancy. Senescence was considered to accompany with decidualization. Failure to clear senescence during decidualization could cause pregnancy abnormalities. Caveolin-1, as a scaffold protein, play a role in...
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| Format: | Article |
| Language: | English |
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World Scientific Publishing
2023-12-01
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| Series: | Fertility & Reproduction |
| Online Access: | https://www.worldscientific.com/doi/10.1142/S2661318223743758 |
| Summary: | Background and Aims: Endometrial decidualization is a step in establishing and maintaining pregnancy. Senescence was considered to accompany with decidualization. Failure to clear senescence during decidualization could cause pregnancy abnormalities. Caveolin-1, as a scaffold protein, play a role in senescence, but the expression, regulation and function were not very clear in uterine endometrium. Here, we investigated the profile of Caveolin-1 in mouse and human decidualization to tease out the potential relationship among the Caveolin-1, senescence and decidualization. Method: ICR strain mice and immortalized human endometrial stromal cells (ESCs) were used. Immunofluorescence, Western-Blot, Real-time PCR were used to detect the levels of molecules. Results: In endometrium of mice during early pregnancy, the expression of Caveolin-1 gradually decreased in stroma and epithelium before embryo implantation. However, the level of Caveolin-1 converts in stromal cell after implantation. Estrogen could stimulate expression of Caveolin-1 in epithelium and progesterone could up-regulate level of Caveolin-1 in endometrial stromal cells. In vitro, expression of Caveolin-1 was up-regulated during decidualization in mESCs, while the level of Caveolin-1 was reduced during decidualization in hESCs. siRNA of Caveolin-1 could promote the expression of IGFBP-1 (decidualization biomarker) and senescence in hESCs, while over-expression of Caveolin-1 had the opposite results. In mESCs, Caveolin-1 seems to play a different role in decidualization, over-expression of Caveolin-1 could promote decidualization and senescence in mESCs, but siRNA depressed it. Blastocysts-derived TNF and hCG stimulated Caveolin-1 in mice and depressed it in human decidual cells, respectively. Caveolin-1 levels are also regulated by high glucose and insulin. Conclusion: Caveolin-1 play a role in ESCs decidualization, but the mode of action was different between species. A low level of Caveolin-1 will benefit for human decidualization, disorder of Caveolin-1 could impair decidualization. |
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| ISSN: | 2661-3182 2661-3174 |