Müllerian Duct Development

2017 ◽  
pp. 90-101
Author(s):  
Maribel Acién ◽  
Pedro Acién
2017 ◽  
Vol 233 (1) ◽  
pp. 119-130 ◽  
Author(s):  
Amanda L Patterson ◽  
Jamieson Pirochta ◽  
Stephanie Y Tufano ◽  
Jose M Teixeira

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, Ctnna1 and Cldn1, is increased. We also show that purified stromal cells from GOF β-catenin uteri, when removed from epithelial cell influence and provided with the appropriate hormonal stimuli, are able to decidualize in vitro indicating that the cells are intrinsically capable of decidualization. Taken together, these results suggest that dysregulated β-catenin activity in the stroma affects epithelial cell STAT3 signaling and ultimately embryo implantation and stromal decidualization.


genesis ◽  
2008 ◽  
Vol 46 (4) ◽  
pp. 205-213 ◽  
Author(s):  
Richard J. Davis ◽  
Mark Harding ◽  
Yalda Moayedi ◽  
Graeme Mardon

1982 ◽  
Vol 92 (1) ◽  
pp. 16-26 ◽  
Author(s):  
Akira Hayashi ◽  
Patricia K. Donahoe ◽  
Gerald P. Budzik ◽  
Robert L. Trelstad

2018 ◽  
Vol 7 (3) ◽  
pp. e310 ◽  
Author(s):  
Zahida Yesmin Roly ◽  
Brendan Backhouse ◽  
Andrew Cutting ◽  
Tiong Yang Tan ◽  
Andrew H. Sinclair ◽  
...  

2012 ◽  
Vol 211 ◽  
pp. S81
Author(s):  
Moa Säfholm ◽  
Anna Norder ◽  
Cecilia Berg

2020 ◽  
Vol 244 (2) ◽  
pp. 395-413 ◽  
Author(s):  
Zahida Yesmin Roly ◽  
Andrew T Major ◽  
Alex Fulcher ◽  
Martin A Estermann ◽  
Claire E Hirst ◽  
...  

The embryonic Müllerian ducts give rise to the female reproductive tract (fallopian tubes, uterus and upper vagina in humans, the oviducts in birds). Embryonic Müllerian ducts initially develop in both sexes, but later regress in males under the influence of anti-Müllerian hormone. While the molecular and endocrine control of duct regression in males have been well studied, early development of the ducts in both sexes is less well understood. Here, we describe a novel role for the adhesion G protein-coupled receptor, GPR56, in development of the Müllerian ducts in the chicken embryo. GPR56 is expressed in the ducts of both sexes from early stages. The mRNA is present during the elongation phase of duct formation, and it is restricted to the inner Müllerian duct epithelium. The putative ligand, Collagen III, is abundantly expressed in the Müllerian duct at the same developmental stages. Knockdown of GPR56 expression using in ovo electroporation results in variably truncated ducts, with a loss of expression of both epithelial and mesenchymal markers of duct development. Over-expression of GPR56 in vitro results in enhanced cell proliferation and cell migration. These results show that GPR56 plays an essential role in avian Müllerian duct development through the regulation of duct elongation.


2021 ◽  
Vol 108 (2) ◽  
pp. 337-345
Author(s):  
Na Chen ◽  
Sen Zhao ◽  
Angad Jolly ◽  
Lianlei Wang ◽  
Hongxin Pan ◽  
...  

2014 ◽  
Vol 03 (03) ◽  
pp. 150-158
Author(s):  
Richa Niranjan ◽  
A K Singh ◽  
Anjoo Yadav

AbstractDevelopmental anomalies of the Mullerian duct system represent some of the most fascinating disorders that obstetricians and gynaecologists encounter. The uterus is formed during embryogenesis by the fusion of the two paramesonephric ducts (Mullerian ducts). This process usually fuses the two Mullerian ducts into a single uterine body, but fails to take place in the affected women who maintain their double Mullerian systems. A bicornuate uterus is a type of a uterine malformation where upper part of uterus forms two horns. The fusion process of upper part of Mullerian duct is altered. As a result, cranial part of the uterus becomes bifurcated. As Mullerian duct anomalies are of anatomic interest, this article discusses epidemiology, embryological development, genetics of development and malformation and lastly various classifications based on Mullerian duct development. Pregnancy in bicornuate uterus is usually of high risk with reproductive outcomes like recurrent abortions, preterm delivery or malpresentation. Classifying Mullerian duct anomalies bears merit because it correlates anatomic anomalies with arrests in morphogenesis. Establishing an accurate diagnosis is essential for planning treatment and management strategies.


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