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Journal articles on the topic 'Embryonic implantation'

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Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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1

Simón, Carlos, Julio Martín, Arancha Galan, Diana Valbuena, and Antonio Pellicer. "Embryonic Regulation in Implantation." Seminars in Reproductive Medicine 17, no. 03 (September 1999): 267–74. http://dx.doi.org/10.1055/s-2007-1016234.

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2

Krüssel, Jan-S., Peter Bielfeld, Mary Lake Polan, and Carlos Simón. "Regulation of embryonic implantation." European Journal of Obstetrics & Gynecology and Reproductive Biology 110 (September 2003): S2—S9. http://dx.doi.org/10.1016/s0301-2115(03)00167-2.

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3

Barkai, Uriel, and Perry F. Kraicer. "Intrauterine Signaling and Embryonic Implantation." Neurosignals 5, no. 2 (1996): 111–21. http://dx.doi.org/10.1159/000109180.

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4

Szekeres-Bartho, Julia. "Successful Implantation from the Embryonic Aspect." American Journal of Reproductive Immunology 75, no. 3 (November 11, 2015): 382–87. http://dx.doi.org/10.1111/aji.12448.

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5

Osório, Joana. "A microRNA prevents cervical embryonic implantation." Nature Reviews Endocrinology 10, no. 8 (June 10, 2014): 445. http://dx.doi.org/10.1038/nrendo.2014.93.

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6

Artus, Jérôme, Isabelle Hue, and Hervé Acloque. "Preimplantation development in ungulates: a ‘ménage à quatre’ scenario." Reproduction 159, no. 3 (March 2020): R151—R172. http://dx.doi.org/10.1530/rep-19-0348.

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In ungulates, early embryonic development differs dramatically from that of mice and humans and is characterized by an extended period of pre- and peri-implantation development in utero. After hatching from the zona pellucida, the ungulate blastocyst will stay free in the uterus for many days before implanting within the uterine wall. During this protracted peri-implantation period, an intimate dialog between the embryo and the uterus is established through a complex series of paracrine signals. The blastocyst elongates, leading to extreme growth of extra-embryonic tissues, and at the same time, the inner cell mass moves up into the trophoblast and evolves into the embryonic disc, which is directly exposed to molecules present in the uterine fluids. In the peri-implantation period, uterine glands secrete a wide range of molecules, including enzymes, growth factors, adhesion proteins, cytokines, hormones, and nutrients like amino and fatty acids, which are collectively referred to as histotroph. The identification, role, and effects of these secretions on the biology of the conceptus are still being described; however, the studies that have been conducted to date have demonstrated that histotroph is essential for embryonic development and serves a critical function during the pre- and peri implantation periods. Here, we present an overview of current knowledge on the molecular dialogue among embryonic, extraembryonic, and maternal tissues prior to implantation. Taken together, the body of work described here demonstrates the extent to which this dialog enables the coordination of the development of the conceptus with respect to the establishment of embryonic and extra-embryonic tissues as well as in preparation for implantation.

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7

Novaro, V., E. González, A. Jawerbaum, V. Rettori, G. Canteros, and M. F. Gimeno. "Nitric oxide synthase regulation during embryonic implantation." Reproduction, Fertility and Development 9, no. 5 (1997): 557. http://dx.doi.org/10.1071/r97005.

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It has previously been demonstrated that uterine nitric oxide synthase (NOS) activity increases before embryonic implantation in rats. The aim of the present work was to investigate the regulation and the physiological relevance of the nitric oxide (NO) system in ovoimplantation. The increase in NOS activity in early pregnancy was found to be independent of the presence of embryos in the uterus. Whereas the Ca2+-dependent isoform of NOS increased gradually in the preimplantation days, the Ca2+-independent isoform increased just at the beginning of implantation (Day 5, 1800 hours); then the activity of both isoforms declined. Oestradiol, whose concentration peaks before implantation, might be regulating NOS activity in the uterus, since treatment of rats with tamoxifen, a receptor antagonist, reduces the activity of both isoforms to preimplantation levels. Intraluminal injections of L-NAME (0·5 mg kg-1), a competitive inhibitor of NOS, reduced by 50% the number of implanted embryos; this suggests that the NO system plays a role during implantation. The data suggest that oestradiol might be a modulator of NOS activity during nidation and that NO production is necessary to achieve a successful embryo implantation.

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8

Poirier, F., C. T. Chan, P. M. Timmons, E. J. Robertson, M. J. Evans, and P. W. Rigby. "The murine H19 gene is activated during embryonic stem cell differentiation in vitro and at the time of implantation in the developing embryo." Development 113, no. 4 (December 1, 1991): 1105–14. http://dx.doi.org/10.1242/dev.113.4.1105.

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The differentiation in vitro of murine embryonic stem cells to embryoid bodies mimics events that occur in vivo shortly before and after embryonic implantation. We have used this system, together with differential cDNA cloning, to identify genes the expression of which is regulated during early embryogenesis. Here we describe the isolation of several such cDNA clones, one of which corresponds to the gene H19. This gene is activated in extraembryonic cell types at the time of implantation, suggesting that it may play a role at this stage of development, and is subsequently expressed in all of the cells of the mid-gestation embryo with the striking exception of most of those of the developing central and peripheral nervous systems. After birth, expression of this gene ceases or is dramatically reduced in all tissues.

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9

Polan, M. L., C. Simon, A. Frances, B. Y. Lee, and L. E. Prichard. "Role of embryonic factors in human implantation." Human Reproduction 10, suppl 2 (December 1, 1995): 22–29. http://dx.doi.org/10.1093/humrep/10.suppl_2.22.

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10

Edwards, R. G. "New concepts in embryonic growth and implantation." Human Reproduction 13, suppl 3 (June 1, 1998): 271–82. http://dx.doi.org/10.1093/humrep/13.suppl_3.271.

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11

Gómez, Eva, Maria Ruíz-Alonso, Jose Miravet, and Carlos Simón. "Human Endometrial Transcriptomics: Implications for Embryonic Implantation." Cold Spring Harbor Perspectives in Medicine 5, no. 7 (March 27, 2015): a022996. http://dx.doi.org/10.1101/cshperspect.a022996.

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12

Cioffi, Alfred. "Early Human Embryonic Development: Individuation before Implantation." Linacre Quarterly 62, no. 1 (February 1995): 70–73. http://dx.doi.org/10.1080/20508549.1995.11878294.

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13

Lee, Jong-Eun, Hyun-Ah Oh, Haengseok Song, Jin Hyun Jun, Cheong-Rae Roh, Huirong Xie, S. K. Dey, and Hyunjung Jade Lim. "Autophagy Regulates Embryonic Survival During Delayed Implantation." Endocrinology 152, no. 5 (March 1, 2011): 2067–75. http://dx.doi.org/10.1210/en.2010-1456.

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14

Cooke, I. D. "Session 18. Implantation stage of embryonic development." Human Reproduction 5, Supplement (1990): 33. http://dx.doi.org/10.1093/humrep/5.supplement.33.

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15

Gunnala, V., I. Matei, M. Toschi, A. Hoshino, L. Bojmar, C. Kenific, I. Wortzel, et al. "Characterization of human pre-implantation embryonic exosomes." Fertility and Sterility 110, no. 4 (September 2018): e81. http://dx.doi.org/10.1016/j.fertnstert.2018.07.244.

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16

Fujiwara, Hiroshi, Masanori Ono, Yukiyasu Sato, Kazuhiko Imakawa, Takashi Iizuka, Kyosuke Kagami, Tomoko Fujiwara, et al. "Promoting Roles of Embryonic Signals in Embryo Implantation and Placentation in Cooperation with Endocrine and Immune Systems." International Journal of Molecular Sciences 21, no. 5 (March 10, 2020): 1885. http://dx.doi.org/10.3390/ijms21051885.

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Embryo implantation in the uterus is an essential process for successful pregnancy in mammals. In general, the endocrine system induces sufficient embryo receptivity in the endometrium, where adhesion-promoting molecules increase and adhesion-inhibitory molecules decrease. Although the precise mechanisms remain unknown, it is widely accepted that maternal–embryo communications, including embryonic signals, improve the receptive ability of the sex steroid hormone-primed endometrium. The embryo may utilize repulsive forces produced by an Eph–ephrin system for its timely attachment to and subsequent invasion through the endometrial epithelial layer. Importantly, the embryonic signals are considered to act on maternal immune cells to induce immune tolerance. They also elicit local inflammation that promotes endometrial differentiation and maternal tissue remodeling during embryo implantation and placentation. Additional clarification of the immune control mechanisms by embryonic signals, such as human chorionic gonadotropin, pre-implantation factor, zona pellucida degradation products, and laeverin, will aid in the further development of immunotherapy to minimize implantation failure in the future.

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17

Navarro, M., C. Bluguermann, M. Von Meyeren, V. Bariani, C. Osycka, and A. Mutto. "2 Role of histone H3 lysine 9 trimethylation during bovine pre-implantation embryonic development." Reproduction, Fertility and Development 31, no. 1 (2019): 126. http://dx.doi.org/10.1071/rdv31n1ab2.

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Histones play an important role in DNA’s compaction and organisation into the cellular nucleus. Depending on which histone modification occurs, chromatin can take a conformation of heterochromatin or euchromatin, which are associated with gene repression or expression, respectively. Histone H3 lysine 9 (H3K9) trimethylation (H3K9me3) is associated with gene silencing. At least 3 methyltransferases are able to change the methylation status of H3K9: SUV39H1, SUV39H2, and SETDB1. In several mammalian species, modulation of H3K9 methylation status has been demonstrated to be necessary to achieve a successful pre-implantation embryonic development after IVF or somatic cell NT. The aim of this work was to study the role of H3K9me3 in IVF pre-implantation bovine embryos. For this purpose, immunostaining of H3K9me3 at different pre-implantation stages of development was performed. Further, the relative abundances of the methyltransferases SUV39H1 and SUV39H2 were measured by real-time PCR using luciferase transcript as an exogenous gene for normalization. Finally, to evaluate H3K9me3 involvement during pre-implantation embryonic development, we generated SUV39H1 or SUV39H2 knockout embryos by the CRISPR/Cas9 system. We designed guide RNA targeting SUV39H1 or SUV39H2 and co-injected the presumptive zygote’s cytoplasm 18h post-fertilization with Cas9 protein. At Day 8 post-fertilization, the number of blastocysts was assessed and embryos were immunostained to evaluate H3K9me3. Results were analysed using Student’s t-test or ANOVA with the post-hoc Tukey test depending on data set (P ≤ 0.05) and reported as means±standard errors of the mean. Oocytes at germinal vesicle stage and metaphase II as well as embryos at different stages of pre-implantation development (2, 4, and 8 cells, morula, and blastocyst; n=6) were immunoreactive for H3K9me3. Expression of SUV39H1 and SUV39H2 mRNA decreased significantly as embryonic development progressed, reaching undetectable levels at stages where genome activation had already occurred (morula and blastocyst; P<0.0001, n=3). When zygotes were co-injected with the guide RNA targeting SUV39H1/Cas9, embryonic production showed a significant increase compared with the control [42.26%±5.03 (28/65) v. 23.86%±3.99 (21/88), respectively; P=0.034, n=4], and H3K9me3 immunostaining was reduced in treated embryos. Editing efficiency was estimated at 66%. In contrast, no statistical differences were found in embryonic production or H3K9me3 immunostaining in embryos co-injected with the guide RNA targeting SUV39H2/Cas9 (P=0.57, n=3). In conclusion, we were able to characterise H3K9me3 and determine transcript levels of methyltransferases SUV39H1 and SUV39H2 in oocytes and different stages of pre-implantation embryonic development. We also demonstrated that SUV39H1 deletion led to an increased embryonic production, suggesting that H3K9me3 removal would allow a greater relaxation of the heterochromatin and consequently a successful activation of embryonic genes. This highlights the essential role of H3K9me3 during bovine pre-implantation embryonic development.

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18

Riveiro, Alba Redó, and Joshua Mark Brickman. "From pluripotency to totipotency: an experimentalist's guide to cellular potency." Development 147, no. 16 (August 15, 2020): dev189845. http://dx.doi.org/10.1242/dev.189845.

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ABSTRACTEmbryonic stem cells (ESCs) are derived from the pre-implantation mammalian blastocyst. At this point in time, the newly formed embryo is concerned with the generation and expansion of both the embryonic lineages required to build the embryo and the extra-embryonic lineages that support development. When used in grafting experiments, embryonic cells from early developmental stages can contribute to both embryonic and extra-embryonic lineages, but it is generally accepted that ESCs can give rise to only embryonic lineages. As a result, they are referred to as pluripotent, rather than totipotent. Here, we consider the experimental potential of various ESC populations and a number of recently identified in vitro culture systems producing states beyond pluripotency and reminiscent of those observed during pre-implantation development. We also consider the nature of totipotency and the extent to which cell populations in these culture systems exhibit this property.

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19

Calle, Alexandra, Víctor Toribio, María Yáñez-Mó, and Miguel Ángel Ramírez. "Embryonic Trophectoderm Secretomics Reveals Chemotactic Migration and Intercellular Communication of Endometrial and Circulating MSCs in Embryonic Implantation." International Journal of Molecular Sciences 22, no. 11 (May 26, 2021): 5638. http://dx.doi.org/10.3390/ijms22115638.

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Embryonic implantation is a key step in the establishment of pregnancy. In the present work, we have carried out an in-depth proteomic analysis of the secretome (extracellular vesicles and soluble proteins) of two bovine blastocysts embryonic trophectoderm primary cultures (BBT), confirming different epithelial–mesenchymal transition stages in these cells. BBT-secretomes contain early pregnancy-related proteins and angiogenic proteins both as cargo in EVs and the soluble fraction. We have demonstrated the functional transfer of protein-containing secretome between embryonic trophectoderm and maternal MSC in vitro using two BBT primary cultures eight endometrial MSC (eMSC) and five peripheral blood MSC (pbMSC) lines. We observed that eMSC and pbMSC chemotax to both the soluble fraction and EVs of the BBT secretome. In addition, in a complementary direction, we found that the pattern of expression of implantation proteins in BBT-EVs changes depending on: (i) their epithelial–mesenchymal phenotype; (ii) as a result of the uptake of eMSC- or pbMSC-EV previously stimulated or not with embryonic signals (IFN-); (iii) because of the stimulation with the endometrial cytokines present in the uterine fluid in the peri-implantation period.

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20

Shufaro, Yoel, and Joseph G. Schenker. "Implantation Failure, Etiology, Diagnosis and Treatment." International Journal of Infertility & Fetal Medicine 2, no. 1 (2011): 1–7. http://dx.doi.org/10.5005/jp-journals-10016-1009.

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ABSTRACT Embryonic implantation is a complex interaction between the embryo and the endometrium. Despite great investigative effort this process is still obscure. Contrary to the great advancement in patient care, follicular recruitment, oocyte quality and aspiration, embryo quality, culture and cryopreservation, our understanding of the implantation process did not enhance as much, and the tools to intervene within this process are limited. The implantation of the transferred embryos still remains the major limiting factor in IVF. Here we will review the current literature on the maternal (uterine, hematologic, immunologic and others) and embryonic factors that are associated with repeated implantation failure (RIF) and describe the various therapeutic approaches to cope with them. In addition, we will present our conclusive recommendations on how to investigate and manage RIF based on the literature and our own experience.

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21

Hearn, John P. "Embryo implantation and embryonic stem cell development in primates." Reproduction, Fertility and Development 13, no. 8 (2001): 517. http://dx.doi.org/10.1071/rd01068.

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The endocrine dialogue that results in implantation and the successful establishment of pregnancy in primates relies on embryonic secretion of chorionic gonadotrophin (CG). This hormone is a signal of embryo viability and capacity to support the corpus luteum. The expression of CG is apparently restricted to primates. Active or passive immunization of marmoset monkeys against the beta subunit of CG prevented implantation and early pregnancy, without disrupting the ovarian cycle. Studies of individual embryos cultured in vitro showed that CG is secreted at low levels by the blastocyst from before attachment, with secretion increasing exponentially after attachment. Gonadotrophin releasing hormone (GnRH) was also secreted, from mid-blastocyst stages, before the detection of CG. The secretion of GnRH by the embryo continued through the attachment and outgrowth stages of embryonic differentiation in vitro. The hypothetical role of GnRH in regulating CG release during implantation was tested in recently completed experiments. Individual embryos cultured with GnRH, or with agonist or antagonist to GnRH, showed significant variations in their secretion of CG and in their survival in culture, suggesting a causal relationship between these hormones. Embryos cultured with natural GnRH showed enhanced growth and development. Embryonic stem cells, from the inner cell mass of marmoset and rhesus monkeys, were the first primate embryonic stem cells to be isolated and characterized, enabling the subsequent isolation of human embryonic stem cells.

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22

Kamemizu, Chizuru, and Toshihiko Fujimori. "Distinct dormancy progression depending on embryonic regions during mouse embryonic diapause†." Biology of Reproduction 100, no. 5 (February 1, 2019): 1204–14. http://dx.doi.org/10.1093/biolre/ioz017.

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Abstract Many mammalian species undergo embryonic diapause and suspend development at the blastocyst stage before implantation, which is also known as delayed implantation. We studied the process of how mouse embryos enter a dormancy status at a cellular level. Immunofluorescent analysis of differentiation markers for epiblast, primitive endoderm, and trophectoderm suggested that cell differentiation status was maintained during 7 days in diapause. To understand the progression of cellular dormancy during diapause, we examined the expression of a transgenic cell cycle marker Fucci2 and Ki67 by antibody staining, in addition to direct counting of nuclei in embryos. From these analyses, embryos during diapause were categorized into four stages by cell number and cell cycle. Cell cycle arrest occurred from the ab-embryonic region and from the trophectoderm to the ICM in the embryonic side. We also observed cell cycle transition by live imaging of Fucci2 embryos during the reactivation in culture from dormant status. Cell cycle was initially recovered from the embryonic side of embryos and eventually spread throughout the whole embryo. We also found that embryos in later stages of diapause required a longer period of time for reactivation. From these observations, it was shown that entrance into and exit from dormant status varied depending on cell types and location of cells in an embryo. These results suggest that embryonic diapause includes multiple steps and the mechanisms involved in cellular dormancy may be distinct between embryonic regions.

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23

Boroviak, Thorsten, and Jennifer Nichols. "The birth of embryonic pluripotency." Philosophical Transactions of the Royal Society B: Biological Sciences 369, no. 1657 (December 5, 2014): 20130541. http://dx.doi.org/10.1098/rstb.2013.0541.

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Formation of a eutherian mammal requires concurrent establishment of embryonic and extraembryonic lineages. The functions of the trophectoderm and primitive endoderm are to enable implantation in the maternal uterus, axis specification and delivery of nutrients. The pluripotent epiblast represents the founding cell population of the embryo proper, which is protected from ectopic and premature differentiation until it is required to respond to inductive cues to form the fetus. While positional information plays a major role in specifying the trophoblast lineage, segregation of primitive endoderm from epiblast depends upon gradual acquisition of transcriptional identity, directed but not initiated by fibroblast growth factor (FGF) signalling. Following early cleavage divisions and formation of the blastocyst, cells of the inner cell mass lose totipotency. Developing epiblast cells transiently attain the state of naive pluripotency and competence to self-renew in vitro as embryonic stem cells and in vivo by means of diapause. This property is lost after implantation as the epiblast epithelializes and becomes primed in preparation for gastrulation and subsequent organogenesis.

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24

Vitiello, Danielle, and Pasquale Patrizio. "Implantation and Early Embryonic Development: Implications for Pregnancy." Seminars in Perinatology 31, no. 4 (August 2007): 204–7. http://dx.doi.org/10.1053/j.semperi.2007.05.006.

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25

Soares, Michael J. "Embryo implantation - coordination of maternal and embryonic adaptations." International Journal of Developmental Biology 58, no. 2-3-4 (2014): 71–74. http://dx.doi.org/10.1387/ijdb.140086ms.

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26

Suginami, Hiroshi. "Endocrine Regulation of Early Embryonic Development and Implantation." Hormone Research 44, no. 2 (1995): 1–3. http://dx.doi.org/10.1159/000184652.

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27

Simón, Carlos. "CLINICAL IMPACT OF MATERNAL-EMBRYONIC COMMUNICATION AT IMPLANTATION." Reproductive BioMedicine Online 39 (August 2019): e6-e7. http://dx.doi.org/10.1016/j.rbmo.2019.04.024.

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28

BULLETTI, C., V. POLLI, F. LICASTRO, and R. PARMEGGIANI. "Endometrial and Embryonic Factors Involved in Successful Implantation." Annals of the New York Academy of Sciences 734, no. 1 The Human End (September 1994): 221–31. http://dx.doi.org/10.1111/j.1749-6632.1994.tb21750.x.

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29

Gandolfi, F., T. A. L. Brevini, S. Modina, and L. Passoni. "Early embryonic signals: embryo-maternal interactions before implantation." Animal Reproduction Science 28, no. 1-4 (July 1992): 269–76. http://dx.doi.org/10.1016/0378-4320(92)90113-r.

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30

Jaiswal, Yogesh Kumar, Madan Mohan Chaturvedi, and Kaushik Deb. "Effect of Bacterial Endotoxins on Superovulated Mouse Embryos In Vivo: Is CSF-1 Involved in Endotoxin-Induced Pregnancy Loss?" Infectious Diseases in Obstetrics and Gynecology 2006 (2006): 1–9. http://dx.doi.org/10.1155/idog/2006/32050.

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Mammalian embryonic development is regulated by several cytokines and growth factors from embryonic or maternal origins. Since CSF-1 plays important role in embryonic development and implantation, we investigated its role in gram-negative bacterial LPS-induced implantation failure. The effect of LPS on normal (nonsuperovulated) and superovulated in vivo-produced embryos was assessed by signs of morphological degeneration. A significantly similar number of morphologically degenerated embryos recovered from both nonsuperovulated and superovulated LPS treated animals on day 2.5 of pregnancy onwards were morphologically and developmentally abnormal as compared to their respective controls (P<.001. Normal CSF-1 expression level and pattern were also altered through the preimplantation period in the mouse embryos and uterine horns after LPS treatment. This deviation from the normal pattern and level of CSF-1 expression in the preimplantation embryos and uterine tissues suggest a role for CSF-1 in LPS-induced implantation failure.

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31

Suemori, H., S. Hashimoto, and N. Nakatsuji. "Presence of the adenovirus E1A-like activity in preimplantation stage mouse embryos." Molecular and Cellular Biology 8, no. 8 (August 1988): 3553–55. http://dx.doi.org/10.1128/mcb.8.8.3553-3555.1988.

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The presence of the adenovirus E1A-like activity in embryonal carcinoma stem cells has been reported. We now show that preimplantation stage mouse embryonic cells allow transcription of the E1A-dependent E2A gene when infected with E1A-deleted mutant dl312, indicating the presence of the E1A-like activity in morulae and blastocysts. Moreover, such activity seems to decrease or disappear at about the time of implantation.

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32

Suemori, H., S. Hashimoto, and N. Nakatsuji. "Presence of the adenovirus E1A-like activity in preimplantation stage mouse embryos." Molecular and Cellular Biology 8, no. 8 (August 1988): 3553–55. http://dx.doi.org/10.1128/mcb.8.8.3553.

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The presence of the adenovirus E1A-like activity in embryonal carcinoma stem cells has been reported. We now show that preimplantation stage mouse embryonic cells allow transcription of the E1A-dependent E2A gene when infected with E1A-deleted mutant dl312, indicating the presence of the E1A-like activity in morulae and blastocysts. Moreover, such activity seems to decrease or disappear at about the time of implantation.

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33

Shen, Ying, and Aiping Qin. "Regulation of Embryonic Signal on Talin1 in Mouse Endometrium." Reproductive Sciences 26, no. 9 (December 20, 2018): 1277–86. http://dx.doi.org/10.1177/1933719118815584.

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Embryonic signals can affect the spatiotemporal-specific expression of the uterus to establish a successful pregnancy. Our previous study has found that talin1 underwent dynamic changes in the mouse endometrium during peri-implantation period. However, whether talin1 is affected by the embryo signals is not clear. In order to investigate the effect of embryonic signals, especially human chorionic gonadotropin (HCG) on talin1, we have designed mouse models of pseudopregnancy, delayed implantation and activation, and HCG treatment. Using these models, the expression of talin1 in the mouse endometrium was determined by immunohistochemistry and Western blotting. In the pseudopregnancy model, an increased expression of talin1 was found from day 3 to day 5, whereas the talin1 protein was decreased on day 5 in the normal pregnant mice. In the delayed implantation model, a strong cytoplasmic staining of talin1 was found, especially in stromal cells. However, after activation of the implantation, the expression of talin1 decreased ( P < .05). Furthermore, a significantly lower expression of talin1 was found at the implantation site when compared to the interimplantation sites ( P < .05). In the HCG treatment model, an intrauterine perfusion of 10u HCG significantly reduced the expression of talin1 in both stromal and epithelial cells in pseudopregnant mice ( P < .05), although further increase in the HCG concentration did not have additional effect on expression of talin1. Taken together, our data suggest that the presence of embryos can affect expression of talin1 in the mouse endometrium, and a certain concentration of HCG can regulate its expression.

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34

van Mourik, M. S. M., N. S. Macklon, and C. J. Heijnen. "Embryonic implantation: cytokines, adhesion molecules, and immune cells in establishing an implantation environment." Journal of Leukocyte Biology 85, no. 1 (October 23, 2008): 4–19. http://dx.doi.org/10.1189/jlb.0708395.

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35

Yonaha, Hitoshi, Hiroyuki Minoura, Toshimichi Yoshida, Shigeto Takeuchi, Naomi Noda, Keisuke Tanaka, Rika Nishiura, Hiroaki Kawato, and Nagayasu Toyoda. "Expression of neuropeptide Y is increased in murine endometrial epithelium during the peri-implantation period under regulation by sex steroids." Reproduction, Fertility and Development 16, no. 3 (2004): 355. http://dx.doi.org/10.1071/rd02088.

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Oligopeptide hormones are involved in cell–cell interaction during embryonal implantation and neuropeptide Y (NPY) is expressed in the human placenta and decidual cells in the third trimester of pregnancy. However, there is no report regarding the intrauterine localisation and the functions of NPY during the peri-implantation period. In the present study, the spatiotemporal changes in NPY expression in the murine uterus during the peri-implantation period were investigated using reverse transcription–polymerase chain reaction (RT-PCR), quantitative RT-PCR and immunohistochemical techniques, as were the effects of sex steroids on NPY mRNA expression in primary cultured murine uterine epithelial cells. Neuropeptide Y mRNA was increased in the pregnant murine uterus, as well as in the pseudopregnant murine uterus, during the peri-implantation period. Immunohistochemical analysis revealed increases in NPY expression in luminal and glandular epithelial cells and decidualised stromal cells. Neuropeptide Y mRNA expression was strongly induced in cultured epithelial cells in response to sex steroids. The data suggest that NPY is involved in cell–cell interactions during embryonic implantation.

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36

He, Bo, Hangxiao Zhang, Jianqi Wang, Mengying Liu, Yang Sun, Chuanhui Guo, Jinhua Lu, Haibin Wang, and Shuangbo Kong. "Blastocyst activation engenders transcriptome reprogram affecting X-chromosome reactivation and inflammatory trigger of implantation." Proceedings of the National Academy of Sciences 116, no. 33 (July 25, 2019): 16621–30. http://dx.doi.org/10.1073/pnas.1900401116.

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Implantation of the blastocyst into the uterus is the gateway for further embryonic development in mammals. Programming of blastocyst to an implantation-competent state known as blastocyst activation is the determining factor for implantation into the receptive uterus. However, it remains largely unclear how the blastocyst is globally programmed for implantation. Employing a delayed implantation mouse model, we show here that the blastocyst undergoes extensive programming essential for implantation. By analyzing the transcriptional profile of blastocysts with different implantation competency, we reveal the dynamic change in the biosynthesis, metabolism, and proliferation during blastocyst reactivation from diapause. We also demonstrate that reactivation of the X chromosome, one of the most important events during periimplantation of female embryonic development, is not completed even in blastocysts under conditions of dormancy, despite long term suspension in the uterus. Moreover, the mural trophectoderm (TE), but not the polar TE, differentiates to be more invasive through the weakened cell-cell tight junctions and extracellular matrices (ECMs). By analyzing the differentially expressed profile of secretory proteins, we further demonstrate that the blastocyst functions as a proinflammatory body to secrete proinflammatory signals, such as TNFα and S100A9, thereby triggering embryo-uterine attachment reaction during implantation. Collectively, our data systematically and comprehensively disclose the programming of blastocyst reactivation from diapause for implantation and uncover previously undefined roles of blastocyst during implantation.

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Moreno-Moya, J. M., N. A. Franchi, S. Martínez-Escribano, J. A. Martínez-Conejero, S. Bocca, S. Oehninger, and J. A. Horcajadas. "Transcriptome of early embryonic invasion at implantation sites in a murine model." Reproduction, Fertility and Development 28, no. 10 (2016): 1487. http://dx.doi.org/10.1071/rd14166.

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Successful implantation relies on the interaction between a competent embryo and a receptive endometrium. The aim of the present study was to investigate genes differentially expressed in early invasive embryonic tissue versus decidual tissue in mice. Samples were obtained from the ectoplacental cone, the immediately surrounding deciduas and from deciduas from interimplantation sites. Microarray analysis showed that 817 genes were differentially expressed between extra-embryonic tissue and the surrounding decidua and that 360 genes were differentially expressed between the different deciduas, with a high representation of developmental processes. Genes differentially expressed in the maternal compartment included chemokines, lipoproteins, growth factors and transcription factors, whereas the embryonic invasive tissue expressed genes commonly observed in invasive tumour-like processes. These results provide information about genes involved in early embryonic invasion and the control exerted by the surrounding decidua. This information may be useful to find targets involved in pathologies associated with implantation failure and early pregnancy loss.

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Golos, Thaddeus G., M. Giakoumopoulos, and M. A. Garthwaite. "Embryonic stem cells as models of trophoblast differentiation: progress, opportunities, and limitations." REPRODUCTION 140, no. 1 (July 2010): 3–9. http://dx.doi.org/10.1530/rep-09-0544.

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While the determination of the trophoblast lineage and the facilitation of placental morphogenesis by trophoblast interactions with other cells of the placenta are crucial components for the establishment of pregnancy, these processes are not tractable at the time of human implantation. Embryonic stem cells (ESCs) provide an embryonic surrogate to derive insights into these processes. In this review, we will summarize current paradigms which promote trophoblast differentiation from ESCs, and potential opportunities for their use to further define signals directing morphogenesis of the placenta following implantation of the embryo into the endometrium.

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Murray, P., and D. Edgar. "Regulation of the differentiation and behaviour of extra-embryonic endodermal cells by basement membranes." Journal of Cell Science 114, no. 5 (March 1, 2001): 931–39. http://dx.doi.org/10.1242/jcs.114.5.931.

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Both the extracellular matrix and parathyroid hormone-related peptide (PTHrP) have been implicated in the differentiation and migration of extra-embryonic endodermal cells in the pre-implantation mammalian blastocyst. In order to define the individual roles and interactions between these factors in endodermal differentiation, we have used embryoid bodies derived from Lamc1(-/-) embryonic stem cells that lack basement membranes. The results show that in the absence of basement membranes, increased numbers of both visceral and parietal endodermal cells differentiate, but they fail to form organised epithelia. Furthermore, although parietal endodermal cells only migrate away from control embryoid bodies in the presence of PTHrP, they readily migrate from Lamc1(-/-) embryoid bodies in the absence of PTHrP, and this migration is unaffected by PTHrP. Thus, the basement membrane between epiblast and extra-embryonic endoderm is required for the proper organisation of visceral and parietal endodermal cells and also restricts their differentiation to maintain the population of primitive endodermal stem cells. Moreover, this basement membrane inhibits migration of parietal endodermal cells, the role of PTHrP being to stimulate delamination of parietal endodermal cells from the basement membrane rather than promoting migration per se.

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Rinkenberger, Julie L., Susan Horning, Barbara Klocke, Kevin Roth, and Stanley J. Korsmeyer. "Mcl-1 deficiency results in peri-implantation embryonic lethality." Genes & Development 14, no. 1 (January 1, 2000): 23–27. http://dx.doi.org/10.1101/gad.14.1.23.

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We disrupted the Mcl-1 locus in murine ES cells to determine the developmental roles of this Bcl-2 family member. Deletion of Mcl-1 resulted in peri-implantation embryonic lethality. Mcl-1−/− embryos do not implant in utero, but could be recovered at E3.5–4.0. Null blastocysts failed to hatch or attach in vitro, indicating a trophectoderm defect, although the inner cell mass could grow in culture. Of note, Mcl-1−/−blastocysts showed no evidence of increased apoptosis, but exhibited a delay in maturation beyond the precompaction stage. This model indicates that Mcl-1 is essential for preimplantation development and implantation, and suggests that it has a function beyond regulating apoptosis.

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Bedzhov, Ivan, Sarah J. L. Graham, Chuen Yan Leung, and Magdalena Zernicka-Goetz. "Developmental plasticity, cell fate specification and morphogenesis in the early mouse embryo." Philosophical Transactions of the Royal Society B: Biological Sciences 369, no. 1657 (December 5, 2014): 20130538. http://dx.doi.org/10.1098/rstb.2013.0538.

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A critical point in mammalian development is when the early embryo implants into its mother's uterus. This event has historically been difficult to study due to the fact that it occurs within the maternal tissue and therefore is hidden from view. In this review, we discuss how the mouse embryo is prepared for implantation and the molecular mechanisms involved in directing and coordinating this crucial event. Prior to implantation, the cells of the embryo are specified as precursors of future embryonic and extra-embryonic lineages. These preimplantation cell fate decisions rely on a combination of factors including cell polarity, position and cell–cell signalling and are influenced by the heterogeneity between early embryo cells. At the point of implantation, signalling events between the embryo and mother, and between the embryonic and extraembryonic compartments of the embryo itself, orchestrate a total reorganization of the embryo, coupled with a burst of cell proliferation. New developments in embryo culture and imaging techniques have recently revealed the growth and morphogenesis of the embryo at the time of implantation, leading to a new model for the blastocyst to egg cylinder transition. In this model, pluripotent cells that will give rise to the fetus self-organize into a polarized three-dimensional rosette-like structure that initiates egg cylinder formation.

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Nie, Li, You-bo Zhao, Dan Zhao, Yun Long, Yi Lei, Min Liu, Yi-cheng Wang, et al. "Progesterone-induced miR-152 interferes with embryonic implantation by downregulating GLUT3 in endometrial epithelium." American Journal of Physiology-Endocrinology and Metabolism 316, no. 4 (April 1, 2019): E557—E567. http://dx.doi.org/10.1152/ajpendo.00245.2018.

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To investigate the role of progesterone-induced micro-RNA (miR)-152 in early embryonic development and implantation by regulating GLUT3 in endometrial epithelium, qRT-PCR was used to detect the expression of miR-152, GLUT1, and GLUT3 in the endometrial epithelial cells of female mice. GLUT1 and GLUT3 proteins were detected by immunohistochemical staining in the mouse endometrial epithelium. Bioinformatics prediction associated with a luciferase assay was performed to determine whether GLUT1 and GLUT3 are target genes of miR-152. Specific miR-152 mimics or inhibitors were transfected into the endometrial epithelial cells to, respectively, overexpress or downregulate miR-152. Next, the glucose concentration of uterine fluid was measured by conducting high-performance liquid chromatography in vivo, and the glucose uptake of the endometrial epithelial cells was observed using a fluorometric assay in vitro. Early embryonic development and implantation were also observed after the miR-152 mimics or inhibitors had been transfected. Embryo transfer was observed after the miR-152 mimic transfection. miR-152 was found to directly target and thereby downregulate GLUT3 expression. The expressions of both miR-152 and GLUT3 in the mouse endometrial epithelium had spatiotemporal characteristics on days 1–4 of pregnancy. miR-152 affected the glucose concentration of uterine fluid and the glucose uptake of endometrial epithelial cells. The transfection of specific miR-152 mimics led to impaired embryonic development and implantation. To conclude, in endometrial epithelial cells, progesterone-induced miR-152 downregulates GLUT3 at the posttranscriptional level to maintain a proper glucose concentration in the uterine fluid, which is necessary for early embryonic development and implantation.

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Novaro, V., A. Jawerbaum, A. Faletti, M. A. F. Gimeno, and E. T. González. "Uterine nitric oxide and prostaglandin E during embryonic implantation in non-insulin-dependent diabetic rats." Reproduction, Fertility and Development 10, no. 3 (1998): 217. http://dx.doi.org/10.1071/r98027.

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In the process of embryo implantation in the rat, both nitric oxide and prostaglandins act as vascular and myometrial regulators. The aim of the present work was to evaluate the effect of diabetes on the synthesis of both agents during embryo implantation. In diabetic rats, uterine activity of the enzyme nitric oxide synthase and prostaglandin E production were increased during peri-implantation compared to the control group (P < 0·05 and P < 0·001, respectively). Both parameters showed a prolonged increase in temporal profile during peri-implantation days. Local production of nitric oxide and prostaglandin E in the implantation sites was higher in diabetic rats (P < 0·05), but the intersite : site ratio was similar to that of the control group. On the other hand, the implantation rate and the timing of the beginning of this process were not altered in the diabetic group. These results suggest that the vasoactive modulators of the implantation process, nitric oxide and prostaglandins, are increased in this diabetic pathology, and that this increase is probably functioning as a compensatory mechanism, so as to allow an unaltered rate of embryo implantation in this model. Extra keyword: diabetes mellitus.

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Fukuda, A. I., and K. F. Breuel. "Implantation: Effect of platelet activating factor on embryonic development and implantation in the mouse." Human Reproduction 11, no. 12 (December 1, 1996): 2746–49. http://dx.doi.org/10.1093/oxfordjournals.humrep.a019202.

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Irollo, Alfonso Maria, Maria Francesca Gangale, Gennaro Calabrese, Ezio Stortini, Sara Zanconi, Raffaele Aiello, Catella Criscuolo, et al. "H.A.R.O.T. Human assisted reproduction ozone therapy: the use of Oxygen-Ozone therapy as an adjunct in the therapy of couple sterility." Ozone Therapy 4, no. 3 (December 31, 2019): 64–67. http://dx.doi.org/10.4081/ozone.2019.8700.

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The increase in couple sterility and the average increase in the age of women seeking pregnancy has placed the scientific community in front of the need to improve the quality of oocytes and the percentage of the embryonic implantation. The oxygen- ozone therapy seems to be able to help in this research thanks to its modes of action. A therapeutic protocol, identified with the acronym H.A.R.O.T (Human assisted reproduction ozone therapy) has been developed, the first results of which seem to be considerably encouraging in order to obtain a greater number and quality of oocytes and improve the percentage of embryonic implantation.

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Plaks, Vicki, Eran Gershon, Amit Zeisel, Jasmine Jacob-Hirsch, Michal Neeman, Elke Winterhager, Gideon Rechavi, Eytan Domany, and Nava Dekel. "Blastocyst implantation failure relates to impaired translational machinery gene expression." REPRODUCTION 148, no. 1 (July 2014): 87–98. http://dx.doi.org/10.1530/rep-13-0395.

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Oocyte quality is a well-established determinant of embryonic fate. However, the molecular participants and biological markers that affect and may predict adequate embryonic development are largely elusive. Our aim was to identify the components of the oocyte molecular machinery that part take in the production of a healthy embryo. For this purpose, we used an animal model, generated by us previously, the oocytes of which do not express Cx43 (Cx43del/del). In these mice, oogenesis appears normal, fertilisation does occur, early embryonic development is successful but implantation fails. We used magnetic resonance imaging analysis combined with histological examination to characterise the embryonic developmental incompetence. Reciprocal embryo transfer confirmed that the blastocyst evolved from the Cx43del/deloocyte is responsible for the implantation disorder. In order to unveil the genes, the impaired expression of which brings about the development of defective embryos, we carried out a genomic screening of both the oocytes and the resulting blastocysts. This microarray analysis revealed a low expression ofEgr1,Rpl21andEif4a1in Cx43del/deloocytes and downregulation ofRpl15andEif4g2in the resulting blastocysts. We propose that global deficiencies in genes related to the expression of ribosomal proteins and translation initiation factors in apparently normal oocytes bring about accumulation of defects, which significantly compromise their developmental capacity. The blastocysts resulting from such oocytes, which grow within a confined space until implantation, may be unable to generate enough biological mass to allow their expansion. This information could be implicated to diagnosis and treatment of infertility, particularly to IVF.

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Sherer, D. M., and O. Abulafia. "Angiogenesis during Implantation, and Placental and Early Embryonic Development." Placenta 22, no. 1 (January 2001): 1–13. http://dx.doi.org/10.1053/plac.2000.0588.

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Hartshorne, Geraldine M., and Robert G. Edwards. "9 Role of embryonic factors in implantation: Recent developments." Baillière's Clinical Obstetrics and Gynaecology 5, no. 1 (March 1991): 133–58. http://dx.doi.org/10.1016/s0950-3552(05)80075-6.

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Boyd, I. L. "Environmental and physiological factors controlling the reproductive cycles of pinnipeds." Canadian Journal of Zoology 69, no. 5 (May 1, 1991): 1135–48. http://dx.doi.org/10.1139/z91-162.

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The reproductive pattern of pinnipeds is characterised by embryonic diapause, annual reproduction, and synchronous breeding cycles. Active gestation lasts about 8 months in most species, but the duration of embryonic diapause varies indirectly with the length of the postpartum oestrous cycle. Data on reproductive endocrinology are limited to a few species, owing to difficulties involved in obtaining serial samples from individuals. The postpartum oestrus is marked by elevated oestradiol concentrations followed by a rise in progesterone levels after ovulation. An infertile cycle may lead to pseudo-pregnancy, although on rare occasions there may be a further period of oestrus. Progesterone concentrations remain elevated for the duration of pregnancy and chorionic gonadotrophin concentration in the placenta increases early in postimplantation. Sex steroids do not appear to be directly involved in blastocyst reactivation. The environmental factors influencing implantation appear to be the most significant proximate factors in timing pinniped reproductive cycles. In most species, implantation occurs when day length is declining, and a photoperiod of about 12 h may provide the signal for implantation in some species. Other proximate factors may include sea temperature, at least for grey seals. Pinnipeds have reproductive cycles with an active and an inactive phase. The inactive phase may be equivalent to the period of embryonic diapause. Transition from the inactive to the active phase and reactivation of embryonic growth are probably controlled by the same environmental cues.

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Hernández-Vargas, Purificación, Manuel Muñoz, and Francisco Domínguez. "Identifying biomarkers for predicting successful embryo implantation: applying single to multi-OMICs to improve reproductive outcomes." Human Reproduction Update 26, no. 2 (February 25, 2020): 264–301. http://dx.doi.org/10.1093/humupd/dmz042.

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Abstract BACKGROUND Successful embryo implantation is a complex process that requires the coordination of a series of events, involving both the embryo and the maternal endometrium. Key to this process is the intricate cascade of molecular mechanisms regulated by endocrine, paracrine and autocrine modulators of embryonic and maternal origin. Despite significant progress in ART, implantation failure still affects numerous infertile couples worldwide and fewer than 10% of embryos successfully implant. Improved selection of both the viable embryos and the optimal endometrial phenotype for transfer remains crucial to enhancing implantation chances. However, both classical morphological embryo selection and new strategies incorporated into clinical practice, such as embryonic genetic analysis, morphokinetics or ultrasound endometrial dating, remain insufficient to predict successful implantation. Additionally, no techniques are widely applied to analyse molecular signals involved in the embryo–uterine interaction. More reliable biological markers to predict embryo and uterine reproductive competence are needed to improve pregnancy outcomes. Recent years have seen a trend towards ‘omics’ methods, which enable the assessment of complete endometrial and embryonic molecular profiles during implantation. Omics have advanced our knowledge of the implantation process, identifying potential but rarely implemented biomarkers of successful implantation. OBJECTIVE AND RATIONALE Differences between the findings of published omics studies, and perhaps because embryonic and endometrial molecular signatures were often not investigated jointly, have prevented firm conclusions being reached. A timely review summarizing omics studies on the molecular determinants of human implantation in both the embryo and the endometrium will help facilitate integrative and reliable omics approaches to enhance ART outcomes. SEARCH METHODS In order to provide a comprehensive review of the literature published up to September 2019, Medline databases were searched using keywords pertaining to omics, including ‘transcriptome’, ‘proteome’, ‘secretome’, ‘metabolome’ and ‘expression profiles’, combined with terms related to implantation, such as ‘endometrial receptivity’, ‘embryo viability’ and ‘embryo implantation’. No language restrictions were imposed. References from articles were also used for additional literature. OUTCOMES Here we provide a complete summary of the major achievements in human implantation research supplied by omics approaches, highlighting their potential to improve reproductive outcomes while fully elucidating the implantation mechanism. The review highlights the existence of discrepancies among the postulated biomarkers from studies on embryo viability or endometrial receptivity, even using the same omic analysis. WIDER IMPLICATIONS Despite the huge amount of biomarker information provided by omics, we still do not have enough evidence to link data from all omics with an implantation outcome. However, in the foreseeable future, application of minimally or non-invasive omics tools, together with a more integrative interpretation of uniformly collected data, will help to overcome the difficulties for clinical implementation of omics tools. Omics assays of the embryo and endometrium are being proposed or already being used as diagnostic tools for personalised single-embryo transfer in the most favourable endometrial environment, avoiding the risk of multiple pregnancies and ensuring better pregnancy rates.

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