scholarly journals Uterine Patterning, Endometrial Gland Development, and Implantation Failure in Mice Exposed Neonatally to Genistein

2020 ◽  
Vol 128 (3) ◽  
pp. 037001 ◽  
Author(s):  
Wendy N. Jefferson ◽  
Elizabeth Padilla-Banks ◽  
Alisa A. Suen ◽  
Lindsey J. Royer ◽  
Sharon M. Zeldin ◽  
...  
2017 ◽  
Vol 100 (4) ◽  
pp. 3243-3256 ◽  
Author(s):  
Meghan L. Wilson ◽  
Sarah R. McCoski ◽  
Adam J. Geiger ◽  
R. Michael Akers ◽  
Sally E. Johnson ◽  
...  

2020 ◽  
Author(s):  
Ryan M. Marquardt ◽  
Tae Hoon Kim ◽  
Jung-Yoon Yoo ◽  
Hanna E. Teasley ◽  
Asgerally T. Fazleabas ◽  
...  

AbstractThough endometriosis and infertility are clearly associated, the pathophysiological mechanism remains unclear. Previous work has linked endometrial ARID1A loss to endometriosis-related endometrial non-receptivity. Here, we show in mice that ARID1A binds and regulates transcription of the Foxa2 gene required for endometrial gland function. Uterine specific deletion of Arid1a compromises gland development and diminishes Foxa2 and Lif expression. Deletion of Arid1a with Ltf-iCre in the adult mouse endometrial epithelium preserves gland development while still compromising gland function. Mice lacking endometrial epithelial Arid1a are severely sub-fertile due to defects in implantation, decidualization, and endometrial receptivity from disruption of the LIF-STAT3-EGR1 pathway. FOXA2 is also reduced in the endometrium of women with endometriosis in correlation with diminished ARID1A, and both ARID1A and FOXA2 are reduced in non-human primates induced with endometriosis. Our findings describe a role for ARID1A in the endometrial epithelium supporting early pregnancy establishment through the maintenance of gland function.


2010 ◽  
Vol 83 (3) ◽  
pp. 396-403 ◽  
Author(s):  
Jae-Wook Jeong ◽  
Inseok Kwak ◽  
Kevin Y. Lee ◽  
Tae Hoon Kim ◽  
Michael J. Large ◽  
...  

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Silvia León ◽  
Daniela Fernandois ◽  
Alexandra Sull ◽  
Judith Sull ◽  
Michele Calder ◽  
...  

2005 ◽  
Vol 71 (3) ◽  
pp. 347-357 ◽  
Author(s):  
Maria B. Padua ◽  
Şaban Tekin ◽  
Thomas E. Spencer ◽  
Peter J. Hansen

Reproduction ◽  
2008 ◽  
Vol 135 (3) ◽  
pp. 357-365 ◽  
Author(s):  
Kanako Hayashi ◽  
Anne R O'Connell ◽  
Jennifer L Juengel ◽  
Ken P McNatty ◽  
George H Davis ◽  
...  

Postnatal development of the uterus involves, particularly, development of uterine glands. Studies with ovariectomized ewe lambs demonstrated a role for ovaries in uterine growth and endometrial gland development between postnatal days (PNDs) 14 and 56. The uterotrophic ovarian factor(s) is presumably derived from the large numbers of growing follicles in the neonatal ovary present after PND 14. The Inverdale gene mutation (FecXI) results in an increased ovulation rate in heterozygous ewes; however, homozygous ewes (II) are infertile and have ‘streak’ ovaries that lack normal developing of preantral and antral follicles. Uteri were obtained on PND 56 to determine whether postnatal uterine development differs between wild-type (++) and II Inverdale ewes. When compared with wild-type ewes, uterine weight of II ewes was 52% lower, and uterine horn length tended to be shorter, resulting in a 68% reduction in uterine weight:length ratio in II ewes. Histomorphometrical analyses determined that endometria and myometria of II ewes were thinner and intercaruncular endometrium contained 38% fewer endometrial glands. Concentrations of estradiol in the neonatal ewes were low and not different between ++ and II ewes, but II ewes had lower concentrations of testosterone and inhibin-α between PNDs 14 and 56. Receptors for androgen and activin were detected in the neonatal uteri of both ++ and II ewes. These results support the concept that developing preantral and/or antral follicles of the ovary secrete uterotrophic factors, perhaps testosterone or inhibin-α, that acts in an endocrine manner to stimulate uterine growth and endometrial gland development in the neonatal ewes.


2010 ◽  
Vol 84 (2) ◽  
pp. 308-319 ◽  
Author(s):  
K. Hayashi ◽  
S. Yoshioka ◽  
S. N. Reardon ◽  
E. B. Rucker ◽  
T. E. Spencer ◽  
...  

2018 ◽  
Vol 100 (1) ◽  
pp. 49-60 ◽  
Author(s):  
Guillaume St-Jean ◽  
Alexandre Boyer ◽  
Gustavo Zamberlam ◽  
Philippe Godin ◽  
Marilène Paquet ◽  
...  

2007 ◽  
Vol 77 (Suppl_1) ◽  
pp. 146-146
Author(s):  
Jae-Wook Jeong ◽  
Kevin Lee ◽  
Inseok Kwak ◽  
Klaus Kaestner ◽  
John Lydon ◽  
...  

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Silvia León ◽  
Daniela Fernandois ◽  
Alexandra Sull ◽  
Judith Sull ◽  
Michele Calder ◽  
...  

Abstract Uterine growth and endometrial gland formation (adenogenesis) and function, are essential for fertility and are controlled by estrogens and other regulators, whose nature and physiological relevance are yet to be elucidated. Kisspeptin, which signals via Kiss1r, is essential for fertility, primarily through its central control of the hypothalamic-pituitary-ovarian axis, but also likely through peripheral actions. Using genetically modified mice, we addressed the contributions of central and peripheral kisspeptin signaling in regulating uterine growth and adenogenesis. Global ablation of Kiss1 or Kiss1r dramatically suppressed uterine growth and almost fully prevented adenogenesis. However, while uterine growth was fully rescued by E2 treatment of Kiss1 −/− mice and by genetic restoration of kisspeptin signaling in GnRH neurons in Kiss1r −/− mice, functional adenogenesis was only marginally restored. Thus, while uterine growth is largely dependent on ovarian E2-output via central kisspeptin signaling, peripheral kisspeptin signaling is indispensable for endometrial adenogenesis and function, essential aspects of reproductive competence.


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