ArticleMolecular endocrinology (Baltimore, Md.)2016
FGFR2IIIb-MAPK Activity Is Required for Epithelial Cell Fate Decision in the Lower Müllerian Duct.
Article in Molecular endocrinology (Baltimore, Md.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- A transient epithelial plasticity state defines the developmental window for uterine gland specification.bioRxiv : the preprint server for biology · 2026Article
- Retinoic acid antagonizes estrogen signaling to maintain adult uterine cell fate.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Uterine organoids reveal insights into epithelial specification and plasticity in development and disease.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Decoding Müllerian Duct Epithelial Regionalization.Molecular reproduction and development · 2025Review
- The histone methyltransferase KMT2D is essential for embryo implantation via regulating precise differentiation of endometrial cells.Cell death discovery · 2024Article
- Estrogen receptor alpha regulates uterine epithelial lineage specification and homeostasis.iScience · 2023Article
- Article
- Development of an in vitro carcinogenesis model of human papillomavirus-induced cervical adenocarcinoma.Cancer science · 2022Article
- Menstural function preservation treatment of a primary vaginal clear cell carcinoma with ovarian transposition and vaginal brachytherapy.Gynecologic oncology reports · 2021Article
- Mechanistic Drivers of Müllerian Duct Development and Differentiation Into the Oviduct.Frontiers in cell and developmental biology · 2021Review
- SIX1 cooperates with RUNX1 and SMAD4 in cell fate commitment of Müllerian duct epithelium.Cell death and differentiation · 2020Article
- A tale of two tracts: history, current advances, and future directions of research on sexual differentiation of reproductive tracts†.Biology of reproduction · 2019Review
- Ovarian insufficiency and CTNNB1 mutations drive malignant transformation of endometrial hyperplasia with altered PTEN/PI3K activities.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Transient inhibition of p53 homologs protects ovarian function from two distinct apoptotic pathways triggered by anticancer therapies.Cell death and differentiation · 2019Article
- Bioactivity Determination of a Therapeutic Recombinant Human Keratinocyte Growth Factor by a Validated Cell-based Bioassay.Molecules (Basel, Switzerland) · 2019Article
- Cellular kinetics ofEndocrine-related cancer · 2018Article
- Patient-derived xenograft model for uterine leiomyoma by sub-renal capsule grafting.Journal of biological methods · 2018Article
- Regulation of FGF10 Signaling in Development and Disease.Frontiers in genetics · 2018Review
- Subtype-Specific Tumor-Associated Fibroblasts Contribute to the Pathogenesis of Uterine Leiomyoma.Cancer research · 2017Article
- The Role of Fgf Signaling on Epithelial Cell Differentiation in Mouse Vagina.In vivo (Athens, Greece)Article
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Cell fate of lower Müllerian duct epithelium (MDE), to become uterine or vaginal epithelium, is determined by the absence or presence of ΔNp63 expression, respectively. Previously, we showed that SMAD4 and runt-related transcription factor 1 (RUNX1) were independently required for MDE to express ΔNp63. Here, we report that vaginal mesenchyme directs vaginal epithelial cell fate in MDE through paracrine activation of fibroblast growth factor (FGF) receptor-MAPK pathway. In the developing reproductive tract, FGF7 and FGF10 were enriched in vaginal mesenchyme, whereas FGF receptor 2IIIb was expressed in epithelia of both the uterus and vagina. When Fgfr2 was inactivated, vaginal MDE underwent uterine cell fate, and this differentiation defect was corrected by activation of MEK-ERK pathway. In vitro, FGF10 in combination with bone morphogenetic protein 4 and activin A (ActA) was sufficient to induce ΔNp63 in MDE, and ActA was essential for induction of RUNX1 through SMAD-independent pathways. Accordingly, inhibition of type 1 receptors for activin in neonatal mice induced uterine differentiation in vaginal epithelium by down-regulating RUNX1, whereas conditional deletion of Smad2 and Smad3 had no effect on vaginal epithelial differentiation. In conclusion, vaginal epithelial cell fate in MDE is induced by FGF7/10-MAPK, bone morphogenetic protein 4-SMAD, and ActA-RUNX1 pathway activities, and the disruption in any one of these pathways results in conversion from vaginal to uterine epithelial cell fate.
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