Embryo Implantation: War in Times of Love

Ashary, Nancy; Tiwari, Abhishek; Modi, Deepak

doi:10.1210/en.2017-03082

Cited by 158 publications

(122 citation statements)

References 85 publications

Supporting

Mentioning

117

Contrasting

Unclassified

Order By: Relevance

“…For successful implantation, however, gene expression in the endometrium in addition is regulated by the implanting blastocyst by precisely synchronized embryo-maternal interactions [60,61,62]. Both compartments of the endometrium are involved in this process: on the one hand, the epithelium has to allow adhesion of the embryo and invasion through the epithelium, on the other hand the stromal cells must be transformed to decidua cells which regulate trophoblast invasion and provide the placental blood supply necessary for embryo nutrition.…”

Section: Cell–cell Junctions During Implantation and Decidualizationmentioning

confidence: 99%

Direct Cell–Cell Interactions in the Endometrium and in Endometrial Pathophysiology

Grund

Grümmer

2018

IJMS

View full text Add to dashboard Cite

Cell contacts exhibit a considerable influence on tissue physiology and homeostasis by controlling paracellular and intercellular transport processes, as well as by affecting signaling pathways. Since they maintain cell polarity, they play an important role in cell plasticity. The knowledge about the junctional protein families and their interactions has increased considerably during recent years. In contrast to most other tissues, the endometrium undergoes extensive physiological changes and reveals an extraordinary plasticity due to its crucial role in the establishment and maintenance of pregnancy. These complex changes are accompanied by changes in direct cell–cell contacts to meet the various requirements in the respective developmental stage. Impairment of this sophisticated differentiation process may lead to failure of implantation and embryo development and may be involved in the pathogenesis of endometrial diseases. In this article, we focus on the knowledge about the distribution and regulation of the different junctional proteins in the endometrium during cycling and pregnancy, as well as in pathologic conditions such as endometriosis and cancer. Decoding these sophisticated interactions should improve our understanding of endometrial physiology as well as of the mechanisms involved in pathological conditions.

show abstract

Section: Cell–cell Junctions During Implantation and Decidualizationmentioning

confidence: 99%

Direct Cell–Cell Interactions in the Endometrium and in Endometrial Pathophysiology

Grund

Grümmer

2018

IJMS

View full text Add to dashboard Cite

show abstract

“…A high expression of L-selectin and its ligand, MECA-79, during the embryo implantation period has been proposed to help increase the stickiness of the endometrial epithelium toward the implanting blastocyst [25]. The sticky surface will anchor the blastocyst firmly to the endometrial wall for the invasion phase to start [26]. As the expression of MECA-79 in the uterus was markedly reduced following the administration of a high dose of testosterone, the adhesion process could well have been compromised, which ultimately would interfere with successful embryo implantation.…”

Section: Discussionmentioning

confidence: 99%

Testosterone Decreases the Number of Implanting Embryos, Expression of Pinopode and L-selectin Ligand (MECA-79) in the Endometrium of Early Pregnant Rats

Mokhtar

Giribabu

Salleh

2020

IJERPH

View full text Add to dashboard Cite

Testosterone could have adverse effect on fertility. In this study, we hypothesized that this hormone could reduce the number of embryo implantations via affecting the normal endometrium ultrastructure and expression of endometrial proteins involved in implantation. Therefore, the aims were to identify these adverse testosterone effects. Methods: Intact pregnant rats were given 250 or 500 µg/kg/day testosterone for three days, beginning from day 1 of pregnancy. Rats were euthanized either at day 4 to analyze the ultra-structural changes in the endometrium and expression and distribution of MECA-79 protein, or at day 6 to determine the number of implantation sites. Results: Administration of 500 µg/kg/day testosterone suppresses endometrial pinopodes development and down-regulates expression and distribution of MECA-79 protein in the uterus. In addition, the number of implantation sites were markedly decreased. Conclusions: Changes in endometrial ultrastructure and expression of implantation protein in the endometrium in early pregnancy period could be the reason for failure of embryo implantation under testosterone influence.

show abstract

“…The first few weeks of gestation place relatively little demand upon the mother and therefore involve little maternal investment, and so embryo quality control should occur early, with the fetal–maternal interface (i.e., the interaction between fetal ligands and maternal receptors) representing the front line in the battle between invading trophoblast and defending maternal tissues. Indeed, discussion of early fetal–maternal interactions is full of references to embryonic “invasion” of the endometrium, and the literature is full of war‐like references to “fighting lines,” “no man's land,” and the embryo as a “deceitful and treacherous enemy.” A more appropriate comparison for the very earliest stages of implantation at or soon after the initiation of embryo–maternal contact may be an interview, where the embryo seeks to make a favorable impression . The evolution of deeper implantation in placental mammals facilitated more thorough vetting of offspring, and these deeper forms of implantation may have evolved to reduce the “ease” by which a mother may reject an embryos through sloughing of superficial layers of endometrium .…”

Section: Introductionmentioning

confidence: 99%

Greater Loss of Female Embryos During Human Pregnancy: A Novel Mechanism

Mulley

2019

BioEssays

View full text Add to dashboard Cite

Given an equal sex ratio at conception, the excess of human males at birth can only be explained by greater loss of females during pregnancy. It is proposed that the bias against females during human development is the result of a greater degree of genetic and metabolic "differentness" between female embryos and maternal tissues than for similarly aged males, and that successful implantation and placentation represents a threshold dichotomy, where the acceptance threshold shifts depending on maternal condition, especially stress. Right and left ovaries are not equal, and neither are the eggs and follicular fluid that they produce, and it is further hypothesized that during times of stress, the implantation threshold is shifted sufficiently to favor survival of females, most likely those originating from the right ovary, and that this, rather than simply a greater loss of males, explains at least some of the variability in the human sex ratio at birth.

show abstract

Embryo Implantation: War in Times of Love

Cited by 158 publications

References 85 publications

Direct Cell–Cell Interactions in the Endometrium and in Endometrial Pathophysiology

Direct Cell–Cell Interactions in the Endometrium and in Endometrial Pathophysiology

Testosterone Decreases the Number of Implanting Embryos, Expression of Pinopode and L-selectin Ligand (MECA-79) in the Endometrium of Early Pregnant Rats

Greater Loss of Female Embryos During Human Pregnancy: A Novel Mechanism

Contact Info

Product

Resources

About