The role of estrogen in uterine receptivity and blastocyst implantation

2003 ◽  
Vol 14 (5) ◽  
pp. 197-199 ◽  
Author(s):  
Carlos Simon ◽  
Francisco Domínguez ◽  
Diana Valbuena ◽  
Antonio Pellicer
Keyword(s):  
Uterine Receptivity ◽  
Blastocyst Implantation

scholarly journals Progesterone supplementation extends uterine receptivity for blastocyst implantation in mice

Reproduction ◽  
2007 ◽  
Vol 133 (2) ◽  
pp. 487-493 ◽  
Author(s):  
Haengseok Song ◽  
Kyuyong Han ◽  
Hyunjung Lim
Keyword(s):  
Cell Proliferation ◽  
Embryo Transfer ◽  
Thymidine Incorporation ◽  
Expression Patterns ◽  
Physiological Changes ◽  
Uterine Receptivity ◽  
Blastocyst Implantation ◽  
Progesterone Supplementation

We previously showed that blastocyst can initiate implantation beyond the normal ‘window’ of uterine receptivity on day 5 of pregnancy and pseudopregnancy (PSP) in mice. In this study, we investigated whether uterine receptivity for blastocyst implantation can be further extended on day 6 of PSP and the role of progesterone (P4) on this event. Embryo transfers, experimentally induced decidualization,in situhybridization and [3H]thymidine incorporation were performed. Blastocysts initiate attachment reaction within 48 h when transferred on day 5, but not on day 6 of PSP. Likewise, decidualization reaction occurred on days 4 and 5 of PSP, but completely failed on day 6. However, P4supplementation partially retains uterine receptivity for blastocyst implantation and decidualization on day 6 of PSP. In addition, certain indicators of uterine receptivity, such as cell proliferation profile and expression patterns of implantation-related genes were similarly observed on days 4 and 5 of PSP, but not on day 6. Consistent with embryo transfer and decidualization, exogenous administration of P4partially restores these indicators on day 6 of PSP. We concluded that critical physiological changes occur between days 4 and 5 of PSP, leading to uterine non-receptivity on day 6, but P4is able to extend the uterine receptivity through day 6.

scholarly journals The critical role of uterine CD31 as a post-progesterone signal in early pregnancy

Reproduction ◽  
2017 ◽  
Vol 154 (5) ◽  
pp. 595-605 ◽  
Author(s):  
Seo-Ho Lee ◽  
Byung-Ju Kim ◽  
Uh-Hyun Kim
Keyword(s):  
Early Pregnancy ◽  
Critical Role ◽  
Hormone Treatment ◽  
Endothelial Cell Migration ◽  
Male Mice ◽  
Uterine Receptivity ◽  
Female Mice ◽  
Blastocyst Implantation ◽  
And Function

CD31 has been shown to play a role in endothelial cell migration and angiogenesis, which are critical to the formation and function of the endometrium and myometrium in uterine development during early pregnancy. However, the role of CD31 in uterine receptivity during blastocyst implantation is poorly understood. The pregnancy rate in CD31−/− female mice mated with CD31+/+ male mice was higher than that observed in CD31+/+ female mice mated with CD31+/+ male mice. During the receptive phase of implantation, uterine glands were more developed in CD31−/− mice than in CD31+/+ mice, and the uterine weights of CD31−/− mice were increased. Leukemia inhibitory factor (LIF) was highly expressed in the CD31−/− mice during implantation and the expression of LIF was up-regulated by estradiol-17β (E2) + progesterone (P4) in ovariectomized CD31−/− mice, compared with CD31+/+ mice at 8 h after hormone treatment. E2-induced protein synthesis was inhibited by P4 in the CD31+/+ uterus, but not in the uterus of CD31−/− mice. Also, STAT3, HAND2, LIF, and mTOR signals were enhanced in CD31−/− mice. Stromal DNA replication was highly activated in the uterus of CD31−/− mice, manifested by upregulated cyclin series signaling and PCNA expression after E2 + P4treatment. Collectively, CD31 inhibits E2-mediated epithelial proliferation via recruitment and phosphorylation of SHP-2 upon receiving P4signal in early pregnancy.

Uterine epithelial LIF receptors contribute to implantation chamber formation in blastocyst attachment

Endocrinology ◽  
2021 ◽  
Author(s):  
Yamato Fukui ◽  
Yasushi Hirota ◽  
Tomoko Saito-Fujita ◽  
Shizu Aikawa ◽  
Takehiro Hiraoka ◽  
...  
Keyword(s):  
Hormone Receptor ◽  
Leukemia Inhibitory Factor ◽  
Ovarian Hormones ◽  
Signal Transducer ◽  
Blastocyst Implantation ◽  
Implantation Process ◽  
Uterine Glands ◽  
Transcription 3

Abstract Recent studies have demonstrated that the formation of an implantation chamber composed of a uterine crypt, an implantation-competent blastocyst, and uterine glands is a critical step in blastocyst implantation in mice. Leukemia inhibitory factor (LIF) activates signal transducer and activator of transcription 3 (STAT3) precursors via uterine LIF receptors (LIFRs), allowing successful blastocyst implantation. Our recent study revealed that the role of epithelial STAT3 is different from that of stromal STAT3. However, both are essential for blastocyst attachment, suggesting the different roles of epithelial and stromal LIFR in blastocyst implantation. However, how epithelial and stromal LIFR regulate the blastocyst implantation process remains unclear. To investigate the roles of LIFR in the uterine epithelium and stroma, we generated Lifr-floxed/lactoferrin (Ltf)-iCre (Lifr eKO) and Lifr-floxed/anti-Mullerian hormone receptor type 2 (Amhr2)-Cre (Lifr sKO) mice with deleted epithelial and stromal LIFR, respectively. Surprisingly, fertility and blastocyst implantation in the Lifr sKO mice were normal despite stromal STAT3 inactivation. In contrast, blastocyst attachment failed, and no implantation chambers were formed in the Lifr eKO mice with epithelial inactivation of STAT3. In addition, normal responsiveness to ovarian hormones was observed in the peri-implantation uteri of the Lifr eKO mice. These results indicate that the epithelial LIFR-STAT3 pathway initiates the formation of implantation chambers, leading to complete blastocyst attachment, and that stromal STAT3 regulates blastocyst attachment without stromal LIFR control. Thus, uterine epithelial LIFR is critical to implantation chamber formation and blastocyst attachment.

scholarly journals The Autophagy Gene Atg16L1 is Necessary for Endometrial Decidualization

Endocrinology ◽  
2019 ◽  
Vol 161 (1) ◽  
Author(s):  
Arin K Oestreich ◽  
Sangappa B Chadchan ◽  
Pooja Popli ◽  
Alexandra Medvedeva ◽  
Marina N Rowen ◽  
...  
Keyword(s):  
Reproductive Tract ◽  
Implantation Rate ◽  
Conditional Knockout ◽  
Uterine Receptivity ◽  
Placental Development ◽  
Human Escs ◽  
Embryo Survival ◽  
Autophagy Gene ◽  
Decidual Cells

Abstract Uterine receptivity is critical for establishing and maintaining pregnancy. For the endometrium to become receptive, stromal cells must differentiate into decidual cells capable of secreting factors necessary for embryo survival and placental development. Although there are multiple reports of autophagy induction correlated with endometrial stromal cell (ESC) decidualization, the role of autophagy in decidualization has remained elusive. To determine the role of autophagy in decidualization, we utilized 2 genetic models carrying mutations to the autophagy gene Atg16L1. Although the hypomorphic Atg16L1 mouse was fertile and displayed proper decidualization, conditional knockout in the reproductive tract of female mice reduced fertility by decreasing the implantation rate. In the absence of Atg16L1, ESCs failed to properly decidualize and fewer blastocysts were able to implant. Additionally, small interfering RNA knock down of Atg16L1 was detrimental to the decidualization response of human ESCs. We conclude that Atg16L1 is necessary for decidualization, implantation, and overall fertility in mice. Furthermore, considering its requirement for human endometrial decidualization, these data suggest Atg16L1 may be a potential mediator of implantation success in women.

scholarly journals The Role of Mitochondria from Mature Oocyte to Viable Blastocyst

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Scott Chappel
Keyword(s):  
Cell Division ◽  
Animal Studies ◽  
Oocyte Quality ◽  
Mature Oocyte ◽  
Reproductive Age ◽  
Mitochondrial Activity ◽  
Dna Deletions ◽  
Blastocyst Implantation ◽  
Cytoplasmic Transfer

The oocyte requires a vast supply of energy after fertilization to support critical events such as spindle formation, chromatid separation, and cell division. Until blastocyst implantation, the developing zygote is dependent on the existing pool of mitochondria. That pool size within each cell decreases with each cell division. Mitochondria obtained from oocytes of women of advanced reproductive age harbor DNA deletions and nucleotide variations that impair function. The combination of lower number and increased frequency of mutations and deletions may result in inadequate mitochondrial activity necessary for continued embryo development and cause pregnancy failure. Previous reports suggested that mitochondrial activity within oocytes may be supplemented by donor cytoplasmic transfer at the time of intracytoplasmic sperm injection (ICSI). Those reports showed success; however, safety concerns arose due to the potential of two distinct populations of mitochondrial genomes in the offspring. Mitochondrial augmentation of oocytes is now reconsidered in light of our current understanding of mitochondrial function and the publication of a number of animal studies. With a better understanding of the role of this organelle in oocytes immediately after fertilization, blastocyst and offspring, mitochondrial augmentation may be reconsidered as a method to improve oocyte quality.

scholarly journals PARP1 during embryo implantation and its upregulation by oestradiol in mice

Reproduction ◽  
2014 ◽  
Vol 147 (6) ◽  
pp. 765-780 ◽  
Author(s):  
Anubha Joshi ◽  
Sahil Mahfooz ◽  
Vineet Kumar Maurya ◽  
Vijay Kumar ◽  
Chadchan Sangappa Basanna ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Embryo Implantation ◽  
Transcript Level ◽  
Tissue Remodelling ◽  
Native Form ◽  
Ovarian Steroids ◽  
Blastocyst Implantation ◽  
Implantation Sites ◽  
Implantation Period

Pregnancy requires successful implantation of an embryo, which occurs during a restricted period defined as ‘receptivity of the endometrium’ and is influenced by the ovarian steroids progesterone and oestradiol. The role of poly(ADP-ribose)polymerase-1 (PARP1) in apoptosis is well established. However, it is also involved in cell differentiation, proliferation and tissue remodelling. Previous studies have described the presence of PARP in the uterus, but its exact role in embryo implantation is not yet elucidated. Hence, in this study, we studied the expression of PARP1 in the uterus during embryo implantation and decidualisation, and its regulation by ovarian steroids. Our results show upregulation of the native form of PARP1 (∼116 kDa) in the cytosolic and nuclear compartments of implantation and non-implantation sites at day 5 (0500 h), followed by downregulation at day 5 (1000 h), during the embryo implantation period. The transcript level of Parp1 was also augmented during day 5 (0500 h). Inhibition of PARP1 activity by the drug EB-47 decreased the number of embryo implantation sites and blastocysts at day 5 (1000 h). Further, cleavage of native PARP1 was due to the activity of caspase-3 during the peri-implantation stage (day 5 (0500 h)), and is also required for embryo implantation, as inhibition of its activity compromised blastocyst implantation. The native (∼116 kDa) and cleaved (∼89 kDa) forms of PARP1 were both elevated during decidualisation of the uterus. Furthermore, the expression level of PARP1 in the uterus was found to be under the control of the hormone oestrogen. Our results clearly demonstrate that PARP1 participates in the process of embryo implantation.

scholarly journals Extended uterine receptivity for blastocyst implantation and full-term fetal development in mice with vitrified-warmed ovarian tissue autotransplantation

2012 ◽  
Vol 11 (3) ◽  
pp. 123-128 ◽  
Author(s):  
Hiromichi Matsumoto ◽  
Kenji Ezoe ◽  
Akinori Mitsui ◽  
Emiko Fukui ◽  
Masanori Ochi ◽  
...  
Keyword(s):  
Fetal Development ◽  
Ovarian Tissue ◽  
Full Term ◽  
Uterine Receptivity ◽  
Blastocyst Implantation

scholarly journals Gram-Negative Bacterial LPS Induced Poor Uterine Receptivity and Implantation Failure in Mouse: Alterations in IL-1β Expression in the Preimplantation Embryo and Uterine Horns

2005 ◽  
Vol 13 (3) ◽  
pp. 125-133 ◽  
Author(s):  
Kaushik Deb ◽  
Madan Mohan Chaturvedi ◽  
Yogesh Kumar Jaiswal
Keyword(s):  
Cross Sections ◽  
Pregnancy Loss ◽  
Embryo Implantation ◽  
Preimplantation Embryos ◽  
Soluble Form ◽  
Implantation Failure ◽  
Perinatal Complications ◽  
Uterine Receptivity ◽  
Gram Negative ◽  
Blastocyst Implantation

Genito-urinary tract or systemic infections of the gram-negative bacteria in pregnant women, causes abortions, preterm labor, and several other perinatal complications. LPS is the most potent antigenic component of the gram-negative bacterial cell wall and is known to modulate the expression of various proinflammatory cytokines. Here we investigate the role of the soluble form of IL-1 i.e., IL-1β in the ‘minimum dose’ of LPS induced pregnancy loss in mice. Uterine cross-sections on each day of the preimplantation period of pregnancy were examined histopathologically for finding out LPS induced changes in the uterine preparation for embryo implantation. The expression of IL-1β in the various stages of the preimplantation period of pregnancy was studied by RT-PCR in the embryos and the uterine horns of the LPS treated and normal pregnant mice. We found that LPS significantly alters the proliferation of the glandular epithelium, luminal epithelium and stroma during the preimplantation period. We also found large infiltration of macrophages into the uterine horns of the LPS treated animals. The level and pattern of IL-1β expression in the preimplantation embryos and uterine horns were also altered in LPS treated animals. These observations indicate that LPS can alter the uterine preparation for blastocyst implantation, which could be due to the change in the IL-1β expression in the uterine horns. However, a change in the expression pattern of IL-1β in the preimplantation embryos underlines the significance of this molecule in LPS induced pregnancy loss or implantation failure in mouse.

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