Short-Term Progesterone Treatment of Neonatal Mice Prevents Uterine Gland Development.

2009 ◽  
Vol 81 (Suppl_1) ◽  
pp. 100-100
Author(s):  
Paul S. Cooke ◽  
Gail C. Ekman ◽  
Joantine C.J. van Esterik ◽  
Philip J. Dziuk ◽  
Sherrie G. Clark ◽  
...  
2020 ◽  
Vol 7 (1) ◽  
pp. 126
Author(s):  
Craig Kreikemeier-Bower ◽  
Pascal Polepole ◽  
Katherine Pinkerton ◽  
Luwen Zhang

2012 ◽  
Vol 86 (5) ◽  
Author(s):  
Justyna Filant ◽  
Huaijun Zhou ◽  
Thomas E. Spencer

Animals ◽  
2018 ◽  
Vol 9 (1) ◽  
pp. 9 ◽  
Author(s):  
Paula Martinez-Ros ◽  
Alejandro Rios-Abellan ◽  
Antonio Gonzalez-Bulnes

The present study characterizes, for sheep, the occurrence and timing of the onset of estrus behavior and ovulation and the yields obtained (ovulation rate, progesterone secretion, and fertility) after Controlled Internal Drug Release (CIDR) insertion for five, six, seven, or fourteen days, with or without equine chorionic gonadotrophin (eCG) in ewes of the Segureña meat breed. All the treatments showed above 80% of females displaying estrus, but the onset of estrus was earlier and more synchronized when using eCG and, among groups with eCG, onset of estrus was earlier in the sheep treated for 14 days than in the short-term treatments (p < 0.05 for all). Administration of eCG after either short- or long-term treatments assured the occurrence of fertile ovulations in all the animals. Conversely, ovulatory success without eCG was found to be dependent on treatment length, with a high percentage of animals ovulating after five days of treatment (83.3%) and very low percentages after treatment for six or seven days (40% and 20%, respectively). Ovulation rate and progesterone secretion were similar among animals ovulating, but ovulation failures predetermined the fertility yields obtained in response to the treatments. Hence, the best results were found after treatment for 14 days plus eCG, and for 5 days without eCG (83.3 for both, p < 0.05 when compared to the other groups with different treatment lengths and with or without eCG).


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.


2018 ◽  
Author(s):  
C. Allison Stewart ◽  
M. David Stewart ◽  
Ying Wang ◽  
Rui Liang ◽  
Yu Liu ◽  
...  

AbstractFemale mice homozygous for an engineered Gnrhr E90K mutation have reduced gonadotropin-releasing hormone signaling, leading to infertility. Their ovaries have numerous antral follicles but no corpora lutea, indicating a block to ovulation. These mutants have high levels of circulating estradiol and low progesterone, indicating a state of persistent estrus. This mouse model provided a unique opportunity to examine the lack of cyclic levels of ovarian hormones on uterine gland biology. Although uterine gland development appeared similar to controls during prepubertal development, it was compromised during adolescence in the mutants. By 20 weeks of age, uterine gland development was comparable to controls, but pathologies, including squamous neoplasia, tubal neoplasia, and cribriform glandular structures, were observed. Induction of ovulations by periodic human chorionic gonadotropin treatment did not rescue post-pubertal uterine gland development. Interestingly, progesterone receptor knockout mice, which lack progesterone signaling, also have defects in post-pubertal uterine gland development. However, progesterone treatment did not rescue post-pubertal uterine gland development. These studies indicate that chronically elevated levels of estradiol with low progesterone and therefore an absence of cyclic ovarian hormone secretion disrupts post-pubertal uterine gland development and homeostasis.


2011 ◽  
Vol 85 (Suppl_1) ◽  
pp. 129-129
Author(s):  
Sarah Reardon ◽  
William Burke ◽  
James A. MacLean ◽  
Francesco J. DeMayo ◽  
John P. Lydon ◽  
...  

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

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