ArticleMolecular endocrinology (Baltimore, Md.)2014
TGFBR1 is required for mouse myometrial development.
Article in Molecular endocrinology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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
20 citing papers in PubMed, 36 citations in OpenAlex.
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- Rediscovering thebioRxiv : the preprint server for biology · 2024Article
- Single-cell transcriptomic profiling of the neonatal oviduct and uterus reveals new insights into upper Müllerian duct regionalization.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Morphogenesis of the female reproductive tract along antero-posterior and dorso-ventral axes is dependent on Amhr2+ mesenchyme in mice†.Biology of reproduction · 2022Article
- Contribution of the Wolffian duct mesenchyme to the formation of the female reproductive tract.PNAS nexus · 2022Article
- Functional similarity between TGF-beta type 2 and type 1 receptors in the female reproductive tract.Scientific reports · 2021Article
- Transforming growth factor beta signaling and decidual integrity in mice†.Biology of reproduction · 2020Article
- Enhancer of Zeste 2 Polycomb Repressive Complex 2 Subunit Is Required for Uterine Epithelial Integrity.The American journal of pathology · 2019Article
- A novel mouse model of testicular granulosa cell tumors.Molecular human reproduction · 2018Article
- Article
- TGFβ superfamily signaling and uterine decidualization.Reproductive biology and endocrinology : RB&E · 2017Review
- The TGF-β Family in the Reproductive Tract.Cold Spring Harbor perspectives in biology · 2017Review
- Conditional abrogation of transforming growth factor-β receptor 1 in PTEN-inactivated endometrium promotes endometrial cancer progression in mice.The Journal of pathology · 2017Article
- Constitutively active transforming growth factor β receptor 1 in the mouse ovary promotes tumorigenesis.Oncotarget · 2016Article
- Deletion of Arid1a in Reproductive Tract Mesenchymal Cells Reduces Fertility in Female Mice.Biology of reproduction · 2016Article
- PAI-1 secretion of endometrial and endometriotic cells is Smad2/3- and ERK1/2-dependent and influences cell adhesion.American journal of translational research · 2016Article
- Constitutive activation of transforming growth factor Beta receptor 1 in the mouse uterus impairs uterine morphology and function.Biology of reproduction · 2015Article
- Uterine epithelial cell proliferation and endometrial hyperplasia: evidence from a mouse model.Molecular human reproduction · 2014Article
- Transforming growth factor β signaling in uterine development and function.Journal of animal science and biotechnology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The smooth muscle layer of the uterus (ie, myometrium) is critical for a successful pregnancy and labor. We have shown that the conditional deletion of TGFβ type 1 receptor (TGFBR1) in the female reproductive tract leads to remarkable smooth muscle defects. This study was aimed at defining the cellular and molecular basis of the myometrial defects. We found that TGFBR1 is required for myometrial configuration and formation during early postnatal uterine development. Despite the well-established role of TGFβ signaling in vascular smooth muscle cell differentiation, the majority of smooth muscle genes were expressed in Tgfbr1 conditional knockout (cKO) uteri at similar levels as controls during postnatal uterine development, coinciding with the presence but abnormal distribution of proteins for select smooth muscle markers. Importantly, the uteri of these mice had impaired synthesis of key extracellular matrix proteins and dysregulated expression of platelet-derived growth factors. Furthermore, platelet-derived growth factors induced the migration of uterine stromal cells from both control and Tgfbr1 cKO mice in vitro. Our results suggest that the myometrial defects in Tgfbr1 cKO mice may not directly arise from an intrinsic deficiency in uterine smooth muscle cell differentiation but are linked to the impaired production of key extracellular matrix components and abnormal uterine cell migration during a critical time window of postnatal uterine development. These findings will potentially aid in the design of novel therapies for reproductive disorders associated with myometrial defects.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.