Development and Function of Uterine Glands in Domestic Animals

2019 ◽  
Vol 7 (1) ◽  
pp. 125-147 ◽  
Author(s):  
Thomas E. Spencer ◽  
Andrew M. Kelleher ◽  
Frank F. Bartol

All mammalian uteri contain glands that synthesize or transport and secrete substances into the uterine lumen. Uterine gland development, or adenogenesis, is uniquely a postnatal event in sheep and pigs and involves differentiation of glandular epithelium from luminal epithelium, followed by invagination and coiling morphogenesis throughout the stroma. Intrinsic transcription factors and extrinsic factors from the ovary and pituitary as well as the mammary gland (lactocrine) regulate uterine adenogenesis. Recurrent pregnancy loss is observed in the ovine uterine gland knockout sheep, providing unequivocal evidence that glands and their products are essential for fertility. Uterine gland hyperplasia and hypertrophy during pregnancy are controlled by sequential actions of hormones from the ovary and/or pituitary as well as the placenta. Gland-derived histotroph is transported by placental areolae for fetal growth. Increased knowledge of uterine gland biology is expected to improve pregnancy outcomes, as well as the health and productivity of mothers and their offspring.

2018 ◽  
Author(s):  
◽  
Andrew Michael Kelleher

[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] Pregnancy loss is the most common complication of human gestation, and roughly one-half of conceptions result in pregnancy loss, most frequently in the first two weeks of gestation. In humans, uterine gland dysfunction is thought to result in pregnancy loss and complications, such as preeclampsia, and fetal growth restriction. Available studies in mice support the hypothesis that uterine glands and forkhead box A2 (FOXA2), a uterine gland specific transcription factor, have important biological roles in blastocyst attachment, implantation, and stromal cell decidualization. Thus, aims of this dissertation included: (1) interrogation of the uterine transcriptome and secretome with and without uterine glands during the periimplantation period of pregnancy; and (2) elucidation of the impact of uterine glands and FOXA2 on endometrial receptivity, blastocyst implantation, and stromal cell decidualization. Those objectives were addressed by utilizing mouse models lacking uterine glands and/or FOXA2 in conjunction with in-depth histomorphological, transcriptomic and proteomic analysis. Results of these studies established: (1) uterine glands substantially impact homeostasis of the uterine environment; (2) leukemia inhibitory factor (LIF), and other gland-derived products, are not present within the uterine fluid during the periimplantation period; (3) FOXA2 regulates uterine expression of Lif; (4) LIF-repletion is sufficient for pregnancy establishment but not maintenance in glandless mice; (5) FOXA2- independent uterine gland-derived factors are required for a successful pregnancy. Collectively, these studies provide original evidence that uterine glands are critical for synchronous embryo-endometrial interactions and coordinate on-time implantation and stromal cell decidualization, thereby impacting embryo viability and pregnancy success. These studies also identified novel glandular factors that may be of significance to implantation and post-implantation processes in mice and humans.


Author(s):  
Sidra Asad Ali ◽  
Bushra Moiz ◽  
Lumaan Sheikh

Abstract Objective: To determine the association of Factor V Leiden / prothrombin gene mutation in Pakistani women with adverse pregnancy outcomes. Method: The prospective study was conducted at the Aga Khan University Hospital, Karachi, from January 1 to December 31, 2016, and comprised females ?40 years having history of two or more foetal losses with no apparent aetiology. Restriction fragment length polymorphism- Polymerase chain reaction was performed using MnlI and HindIII restriction enzymes for factor V Leiden G1691A and prothrombin gene mutation G20210A. Females with two or more consecutive normal pregnancies were enrolled as the control group. Data was analysed using SPSS 19. Results: Of the 172 participants with a mean age of 29.3±5.9 years (range: 19-38 years). 86(50%) each were healthy controls and those with recurrent pregnancy loss. There were 238 livebirths among the controls compared to 13 in the other group. Factor V Leiden G1691A was identified in 2(2.3%) women, and prothrombin gene mutation G20210A in 1(1.2%) woman in the patient group, while no mutation was identified in the control group. Conclusion: The prevalence of Factor V Leiden / prothrombin gene mutation in women with recurrent pregnancy loss was found to be very low. Continuous....


2018 ◽  
Vol 46 (7) ◽  
pp. 764-770 ◽  
Author(s):  
Maor Kabessa ◽  
Avi Harlev ◽  
Michael Friger ◽  
Ruslan Sergienko ◽  
Baila Litwak ◽  
...  

Abstract Background: Recurrent pregnancy loss (RPL) is defined by two or more failed clinical pregnancies. Three to four percent of the couples with RPL have chromosomal aberrations (CA) in at least one partner. The parent’s structural chromosomal abnormalities may cause an unbalanced karyotype in the conceptus which could lead to implantation failure, early or late pregnancy loss, or delivery of a child with severe physical and/or mental disabilities. Objective: To compare live birth rates of couples with CA to couples with normal karyotypes and to investigate medical and obstetric characteristics and pregnancy outcomes of couples with CA and RPL who attend an RPL clinic at a tertiary hospital. Methods: A retrospective cohort study, including 349 patients with two or more consecutive pregnancy losses. The study group consisted of 52 patients with CA, and the control group consisted of 297 couples with normal karyotype. All patients were evaluated and treated in the RPL clinic at Soroka University Medical Center and had at least one subsequent spontaneous pregnancy. Results: The demographic and clinical characteristics were not found to be statistically different between the two groups. The group of carriers of CA had 28/52 (53.8%) live births in their index pregnancy vs. the normal 202/297 (68%) (P=0.067, CI 95%) in the control group. No statistically significant etiology was found between the study group and the control group. A statistically significant difference in live birth rates was found when comparing the total amount of pregnancies [index pregnancy (IP)+post index pregnancy (PIP)] between the study group and the control group (54.16% vs. 67.82%, respectively, P=0.0328). Conclusion: Patients with RPL and CA who have spontaneous pregnancies, have a good prognosis (63.4%) of a successful pregnancy with at least one of the pregnancies (index or post index) resulting in a live birth.


2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Ryo Seishima ◽  
Carly Leung ◽  
Swathi Yada ◽  
Katzrin Bte Ahmed Murad ◽  
Liang Thing Tan ◽  
...  

AbstractWnt signaling is critical for directing epithelial gland development within the uterine lining to ensure successful gestation in adults. Wnt-dependent, Lgr5-expressing stem/progenitor cells are essential for the development of glandular epithelia in the intestine and stomach, but their existence in the developing reproductive tract has not been investigated. Here, we employ Lgr5-2A-EGFP/CreERT2/DTR mouse models to identify Lgr5-expressing cells in the developing uterus and to evaluate their stem cell identity and function. Lgr5 is broadly expressed in the uterine epithelium during embryogenesis, but becomes largely restricted to the tips of developing glands after birth. In-vivo lineage tracing/ablation/organoid culture assays identify these gland-resident Lgr5high cells as Wnt-dependent stem cells responsible for uterine gland development. Adjacent Lgr5neg epithelial cells within the neonatal glands function as essential niche components to support the function of Lgr5high stem cells ex-vivo. These findings constitute a major advance in our understanding of uterine development and lay the foundations for investigating potential contributions of Lgr5+ stem/progenitor cells to uterine disorders.


Sign in / Sign up

Export Citation Format

Share Document