ArticleThe Journal of endocrinology2017
Gain-of-function β-catenin in the uterine mesenchyme leads to impaired implantation and decidualization.
Article in The Journal of endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 27 citations in OpenAlex.
- LPS Disrupts Endometrial Receptivity by Inhibiting STAT1 Phosphorylation in Sheep.International journal of molecular sciences · 2024Article
- Mechanisms of Bushen Tiaoxue Granules against controlled ovarian hyperstimulation-induced abnormal morphology of endometrium based on network pharmacology.Journal of ovarian research · 2024Article
- Homeobox regulator Wilms Tumour 1 is displaced by androgen receptor at cis-regulatory elements in the endometrium of PCOS patients.Frontiers in endocrinology · 2024Article
- Molecular Targets for Nonhormonal Treatment Based on a Multistep Process of Adenomyosis Development.Reproductive sciences (Thousand Oaks, Calif.) · 2023Review
- miR-1246 is implicated as a possible candidate for endometrium remodelling facilitating implantation in buffalo (Bubalus bubalis).Veterinary medicine and science · 2023Article
- Basigin is necessary for normal decidualization of human uterine stromal cells.Human reproduction (Oxford, England) · 2022Article
- Wnt4, Wnt6 and β-catenin expression in human placental tissue - is there a link with first trimester miscarriage? Results from a pilot study.Reproductive biology and endocrinology : RB&E · 2022Article
- Shoutai Wan Improves Embryo Survival by Regulating Aerobic Glycolysis of Trophoblast Cells in a Mouse Model of Recurrent Spontaneous Abortion.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- C-Peptide Promotes Cell Migration by Controlling Matrix Metallopeptidase-9 Activity Through Direct Regulation of β-Catenin in Human Endometrial Stromal Cells.Frontiers in cell and developmental biology · 2022Article
- Abnormal cGMP-dependent protein kinase I-mediated decidualization in preeclampsia.Hypertension research : official journal of the Japanese Society of Hypertension · 2021Article
- Prednisolone Alters Endometrial Decidual Cells and Affects Decidual-Trophoblast Interactions.Frontiers in cell and developmental biology · 2021Article
- Article
- Interleukin-17A-promoted MSC2 polarization related with new bone formation of ankylosing spondylitis.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Embryo implantation and endometrial decidualization are critical events that occur during early pregnancy in humans and mice, and perturbation in either can result in infertility. WNT signaling through the canonical β-catenin pathway plays a pivotal role in embryonic Müllerian duct development, postnatal uterine maturation and establishment of pregnancy. Loss of β-catenin in the Müllerian duct mesenchyme (MDM)-derived stroma and myometrium results in impaired decidualization and infertility, whereas gain-of-function (GOF) results in the formation of mesenchymal tumors and sub-fertility attributed to malformed oviducts. We hypothesized that GOF β-catenin further contributes to sub-fertility through improper stromal and epithelial cell signaling during embryo implantation and decidualization. We show that mice with GOF β-catenin in MDM-derived stroma and myometrium have reduced implantation sites after embryo transfer and decreased decidualization. On day 4.5 of pseudopregnancy or in mice treated with progesterone and estrogen to mimic early pregnancy, the estrogen-LIF-ERK and progesterone-IHH pathways remain predominantly intact in GOF β-catenin mice; however, JAK/STAT signaling is altered. pSTAT3 is significantly reduced in GOF β-catenin mice and expression of downstream epithelial junctional complex factors,
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