ArticleReproductive sciences (Thousand Oaks, Calif.)2023
Increased Expression of TGF-β1 Contributes to the Downregulation of Progesterone Receptor Expression in the Eutopic Endometrium of Infertile Women with Minimal/Mild Endometriosis.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- The role of TGF-β superfamily in endometriosis: a systematic review.Frontiers in immunology · 2025Pooled it
- Menstrual Effluent in the Pathogenesis and Diagnosis of Endometriosis-A Systematic Review.Diagnostics (Basel, Switzerland) · 2026Review
- Role of Salivary MicroRNA as a Marker of Progesterone Resistance in Endometriosis: Preliminary Results from a Single-Institution Experience.Biomolecules · 2025Article
- Integral Roles of the TGFβ Signaling Pathway in Uterine Function and Disease.Endocrinology · 2025Review
- The IL-33-ST2 axis plays a vital role in endometriosis via promoting epithelial-mesenchymal transition by phosphorylating β-catenin.Cell communication and signaling : CCS · 2024Article
- Progestin-based pharmacotherapy in fertility preservation in early endometrial cancer.Frontiers in oncology · 2024Review
- Progesterone resistance in endometriosis: A pathophysiological perspective and potential treatment alternatives.Reproductive medicine and biologyReview
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Endometriosis is a hormone-dependent disease associated with impaired immunoregulation. In our recent study, we have characterized the trascriptomic transformation of eutopic endometrium from patients with minimal/mild endometriosis and controls across the menstrual cycle. However, the regulatory mechanism of altered immune microenvironment in eutopic endometrial stromal cells (ESCs) remains unclear. Here, we want to explore the regulation of immune cell to progesterone resistance and endometrial receptivity in the eutopic ESCs by cytokine (TGF-β1), and to understand the effect of TGF-β1 on the decidualization of the eutopic ESCs. Primary culture of eutopic ESCs was performed to explore the effects of TGF-β1 on the expression of Smad and progesterone receptor (PR) and the in vitro decidualization. Additionally, co-immunoprecipitation (Co-IP) was used to explore the direct interaction between Smad and PR. We found an attenuate expression of PRB protein (p=0.026) after using TGF-β1 in eutopic ESCs, although the difference of PRA before and after treatment was not significant (p=0.678). Similarly, the results of qRT-PCR showed that the mRNA level of PR (p<0.001), PRB (p=0.003) and HOXA10 (p<0.001) decreased significantly after TGF-β1 treatment, but that increased (p<0.023, for all) after SB431542 treatment in the eutopic ESCs. Moreover, TGF-β1 has a negative effect on the in vitro decidualization of eutopic ESCs (p=0.003). And the group with treatment of both TGF-β1 and SB435142 in eutopic ESCs showed significant decidual-like changes with increased prolactin level (p=0.01). We did not observe any physical interaction between the PR and p-Smad3/Smad3 proteins by using Co-IP. By activating TGF-β/Smad signaling in eutopic ESCs, elevated TGF-β1 from CD45+ immune cells could attenuate expression of PR, and further decrease endometrial receptivity.
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