Dissertations / Theses on the topic 'Embryonic implantation'
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Henderson, Janet Katharine. "Investigations of human embryonic implantation in vitro." Thesis, University of Sheffield, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341905.
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Aghajanova, Lusine. "Endometrial, embryonic and ovarian aspects of human implantation /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-794-4/.
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Spikings, Emma Catherine. "Mitochondrial DNA replication in pre-implantation embryonic development." Thesis, University of Birmingham, 2007. http://etheses.bham.ac.uk//id/eprint/45/.
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All eukaryotic cells possess mitochondrial DNA (mtDNA), which is maternally inherited through the oocyte, its replication being regulated by nuclear-encoded replication factors. It was hypothesised that mtDNA replication is highly regulated in oocytes, pre-implantation embryos and embryonic stem cells (ESCs) and that this may be disrupted following nuclear transfer (NT). MtDNA copy number decreased between 2-cell and 8-cell staged porcine embryos and increased between the morula and expanded blastocyst stages, coinciding with increased expression of mtDNA replication factors. Competent porcine oocytes replicated their mtDNA prior to and during in vitro maturation to produce and maintain the 100000 mtDNA copies required for fertilisation. Those oocytes in which mtDNA replication was delayed had reduced developmental ability. Expression of pluripotency-associated genes decreased as murine ESCs differentiated into embryoid bodies, although expression of mtDNA replication factors did not increase until the stage equivalent to organogenesis. Cross-species NT embryos in which the donor cell-derived mtDNA was replicated produced decreased developmental outcomes compared to those in which no mtDNA replication took place. Disruption of the strict regulation of mtDNA replication that occurs during early embryogenesis, as is likely following NT, may therefore contribute to the reduced developmental ability of embryos produced using such techniques.
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Thomas, Penelope S. "Patterns of protein synthesis in early post-implantation rat embryos." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.253268.
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Pillai, Chitra Claire. "IGFPBp1 : a multifunctional role in implantation, embryonic and fetal development." Thesis, King's College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271064.
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Bagot, Catherine Nancy. "An investigation of the role of maternal hoxiao in embryonic implantation." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250192.
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Magaña, Griselda Valdez. "Crosstalk between embryonic and extraembyonic tissues in pre-implantation pig embryos." Thesis, University of Nottingham, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.662205.
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The coordinated growth of the conceptus is sustained by reciprocal signalling between the epiblast and the extraembryonic ectoderm (ExE). In mice, FGF4 produced by the epiblast promotes Cdx2 expression in the trophoblast stem cell (TSC) niche located in the ExE. Cdx2, Eomes and EIf-5 expression in the ExE constitute an auto-regulatory circuit that maintains the mouse TSC gene network. Cells in the ExE, in turn secrete BMP4, which is a critical mesoderm determinant. The ExE however, is absent in non-rodent embryos, raising the question whether the cross-talk between embryonic and extraembryonic domains is conserved in mammals. Pig embryos represent "mammotypical" embryos in that the flat epiblast is surrounded by trophectoderm (TE). The pig TE undergoes a remarkable elongation, however it is not known whether the epiblast regulates this process and whether a TSC niche supports this remarkable growth.
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Udayashankar, Ramya. "A model of trophoblast development and implantation using human embryonic stem cells." Thesis, University of Sheffield, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.505349.
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Abnormal embryo implantation may lead to poor fetal development and miscarriage, or pre-eclampsia. Due to ethical and practical restrictions, and the morphological diversity of implantation in laboratory animals, it is important to develop new in vitro models to study early events of human implantation. The aim of this study was to derive trophoblast stem cell lines from human embryonic stem cells (hESCs) through an effective repeatable protocol and to co-culture these cells together with an established endometrial cell culture system to develop and validate a model to study the molecular events of human embryo implantation. Derivation of trophoblast stem cell lines from hESC lines was established by spontaneous differentiation of embryoid bodies (EBs) and by initial measurement of human chorionic gonadotropin-{3 (hCG{3) secretion by enzyme linked immune sorbent assay (ELISA). The derived villous cytotrophoblast stem cell lines further differentiated to invasive, extra-villous cytotrophoblast cells; all cells lost their proliferative capacity and some lines acquired karyotypic changes, such as a gain in the X chromosome. Cell invasion assays confirmed that the extra-villous cytotrophoblast cells were invasive. When vesicles formed by aggregating trophoblast cells in suspension culture were co -cultured with decidualised human endometrial stromal cells in hypoxic (2% oxygen) and normoxic (20% oxygen) environments, erosion of the stromal layer in hypoxic conditions was observed similar to the embryo invasion through endometrium. To conclude, it has been possible to create trophoblast cell lines using human embryonic stem cells that differentiate and adapt in vitro and can be used as a model to study implantation in humans.
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Cha, Jeeyeon. "The role of muscle segment homeobox genes in early pregnancy events." University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1377871689.
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Huang, Tingting. "Characterization of the Visceral Endoderm Components in Early Post-Implantation Mouse Embryo Development: A Dissertation." eScholarship@UMMS, 2014. https://escholarship.umassmed.edu/gsbs_diss/694.
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Early post-implantation vertebrate embryos are shaped by complex cellular and molecular mechanisms. In mice, the visceral endoderm, an extraembryonic cell lineage that appears before gastrulation, provides several important functions such as nutrition and mechanical protection. My thesis research focused on the role of the visceral endoderm in embryo patterning, a newly discovered function for this tissue. My results showed that an interplay between two subpopulations of visceral endoderm the anterior and posterior visceral endoderm, located on the opposite sides of the developing conceptus, are critical for the establishment of the anteroposterior body axis of the embryo. I also found that senescence-associated β-galactosidase activity delineates the visceral endoderm marking apical vacuole, a lysosomal-like organelle. This however indicates the nutritional function of visceral endoderm cells rather than a senescent population. My studies highlight the fundamental role of extraembryonic tissues in patterning mammalian embryos as opposed to housekeeping roles. They also reveal important difference when conducting studies at the organismal level rather than in cells in culture.
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Huang, Tingting. "Characterization of the Visceral Endoderm Components in Early Post-Implantation Mouse Embryo Development: A Dissertation." eScholarship@UMMS, 2002. http://escholarship.umassmed.edu/gsbs_diss/694.
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Early post-implantation vertebrate embryos are shaped by complex cellular and molecular mechanisms. In mice, the visceral endoderm, an extraembryonic cell lineage that appears before gastrulation, provides several important functions such as nutrition and mechanical protection. My thesis research focused on the role of the visceral endoderm in embryo patterning, a newly discovered function for this tissue. My results showed that an interplay between two subpopulations of visceral endoderm the anterior and posterior visceral endoderm, located on the opposite sides of the developing conceptus, are critical for the establishment of the anteroposterior body axis of the embryo. I also found that senescence-associated β-galactosidase activity delineates the visceral endoderm marking apical vacuole, a lysosomal-like organelle. This however indicates the nutritional function of visceral endoderm cells rather than a senescent population. My studies highlight the fundamental role of extraembryonic tissues in patterning mammalian embryos as opposed to housekeeping roles. They also reveal important difference when conducting studies at the organismal level rather than in cells in culture.
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Loof, Gesa. "Elucidating the influence of chromatin topology on cellular identity in murine pre-implantation development." Doctoral thesis, Humboldt-Universität zu Berlin, 2021. http://dx.doi.org/10.18452/22928.
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Präzise regulierte Genexpression, ist der Schlüssel zu erfolgreicher Embryonal-entwicklung. Die Expression von Zelltyp-spezifischen Transkriptionsfaktoren kann durch räumliche Interaktionen von Promotoren und Enhancern im Nukleus kontrolliert werden, aber auch durch 3D Faltung der DNA in größere organisatorische Einheiten wie “Topologically Associating Domains” (TADs) oder “A/B compartments”.
Um die 3D Faltung in den Zelltypen des prä-implantations Embryos zu untersuchen, nutze ich ES und XEN Zellen, die stark dem Epiblast und dem primitiven Endoderm in der inneren Zellmasse des E4.5 Embryos ähneln. Um den Zusammenhang zwischen 3D DNA Faltung und zellulärer Identität zu erforschen, habe ich GAM, ATAC-seq und RNA-seq Daten von ES und XEN Zellen produziert. Um die Genom-Architektur im Embryo zu untersuchen, habe ich außerdem die GAM Methode an den Mausembryo angepasst und kann dadurch erstmals genomweit DNA-Faltung in den spezifischen Zelltypen der inneren Zellmasse des prä-implantations Embryos zeigen.
ES und XEN Zellen zeigen viele differentiell exprimierte Gene, sowie starke Veränderungen in der Chromatin-Organisation, beispielweise in der Bildung von reprimierten Chromatinnetzwerken in ESCs, die wichtige XEN Gene wie Gata6 und Lama1 enthalten, während diese nicht aktiv sind. XEN-spezifische Genexpression ist oft mit der Präsenz von XEN-spezifischen “TAD boundaries” gekoppelt. Der Sox2 Locus zeigt eine ESC-spezifische Organisation mit aktiven Genen, und Regionen die von den Transkriptionsfaktoren SOX2, NANOG und OCT4 gebunden sind.
Die starke Reorganisation der Genom-Architektur in wichtigen Loci wie Gata6 und Sox2 konnte ich mit in vivo GAM Daten bestätigen und finde ähnliche Unterschiede zwischen den beiden Zelltypen der inneren Zellmasse wie im in vitro Model. Diese Ergebnisse zeigen, wie wichtig es ist, Zelltypen getrennt zu untersuchen und, dass eine Verbindung zwischen zellulärer Identität und der Faltung des Genoms in der Embryonalentwicklung besteht.Tightly controlled gene regulation is key to functional metazoan embryonic development. The expression of cell-fate determining transcription factors orchestrates the establishment of the various lineages of the embryo. Gene expression is often regulated via specific chromatin organisation. To investigate cell type-specific differences in chromatin folding in early embryonic development, I used in vitro models of the two distinct cell populations in the blastocyst ICM. In mouse ES and XEN cells, I mapped 3D genome conformation using Genome Architecture Mapping (GAM), chromatin accessibility using ATAC-seq, and gene expression using total RNA-seq. To enable the mapping of 3D genome folding directly in the blastocyst ICM, I adapted GAM for cell type-specific selection of nuclei, by integrating immunofluorescence detection of markers, and generated the first genome-wide chromatin contact maps that distinguish ICM cell types. I report that the ES and XEN cell lineages undergo abundant large scale rearrangements of genome architecture and exhibit high numbers of differentially expressed genes. For example, extra-embryonic endoderm genes, such as Lama1 and Gata6, form silent hubs in ESCs, potentially connecting maintenance of pluripotency to 3D structure of the genome. Further, I show that the expression of XEN cell-specific genes relates to the formation of XEN cell-specific TAD boundaries. Chromatin contacts at the Sox2 locus exhibit an ESC-specific organisation around binding of pluripotency transcription factors OCT4, NANOG and SOX2, into hubs of high gene activity. The observations detected in in vitro models, were investigated in smaller GAM datasets produced using the in vivo counterparts in the ICM. Overall, in vivo data confirmed the high degree of chromatin rearrangement among the two cell types, specifically in loci of lineage driving genes. The findings from in vivo data further underscore the connection of genome topology and cellular identity.
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Barblett, Hamish. "Factors affecting the survival and implantation of human blastocysts following vitrification." Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2019. https://ro.ecu.edu.au/theses/2228.
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The increased cell numbers, presence of the blastocoel and rapid cell re-organisation have required the development of specific survival criteria post warm to effectively select the most viable blastocyst for transfer. Pre-freeze blastocyst expansion and post warm re-expansion have been shown to contribute significantly to the chances of an implantation and subsequent live birth. The aim of this study was to explore factors that influence the outcome of blastocyst transfers after vitrification and warming, and hopefully improve outcomes by further applying improvements in future cycles. Variables from 8 years of vitrified/warmed blastocysts were retrospectively compiled and analysed to determine the most significant contributors to outcome. There were 2466 transfers of either 1 or 2 vitrified/warmed blastocysts resulting in 796 (32.3%) clinical pregnancies and 751 (30.5%) live born babies. The patient/cycle specific variables of age: ≤38 years (OR: 2.01, 95% CI:1.48-2.73), transfer order: ≤ 2 (OR:1.32, 95% CI:1.10- 1.59) and cycle type: non-HRT (OR: 1.38, 95% CI:1.15-1.66) significantly influenced the live birth outcome. Blastocysts vitrified on day 5 of development had significantly improved outcomes to day 6 blastocysts (OR: 1.80, 95% CI: 1.37-2.35). A greater degree of blastocyst expansion on Day 5 further improved these outcomes (OR: 1.47, 95% CI:1.17-1.86). A grade 1 morphology rating significantly improved the outcomes of day 5 expanded blastocysts (OR: 1.51, 95% CI:1.24-1.85). The composition of the warming media and possibly the concentrations of osmotic buffer contributed to the survival of warmed blastocysts. Post warming assessment of the blastocyst showed that if the level of cell degeneration in the surviving and transferred embryo was less than 5%, this significantly influenced the outcome (OR:1.57, 95% CI:1.22-2.03). There was no significant difference if a blastocyst with ≥ 95% cell survival commenced re-expansion within 30 or 60 minutes after the warm (OR: 1.13, 95% CI:0.87-1.46). This study highlights the significance of even a small number of degenerative cells in the warmed blastocyst despite early commencement of re-expansion and warrants further prospective analysis.
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Douglas, Deborah Ann. "Luteotropic effects of prolactin on the mink, Mustela vison, ovary during embryonic diapause and early post-implantation gestation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0025/NQ29925.pdf.
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Douglas, Deborah Ann. "Luteotropic effects of prolactin on the mink (Mustela vison) ovary during embryonic diapause and early post-implantation gestation." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=42020.
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These studies were conducted to determine the mechanisms by which prolactin (PRL) exerts its luteotropic effects on the mink corpus luteum (CL). Three experimental models were developed and utilized in these studies. In the first model, the ovaries from pregnant mink were collected at regular intervals throughout gestation, half the animals were treated with the dopamine agonist 2-bromo-$ alpha$-ergocryptine (bromocryptine), to suppress their endogenous PRL levels, and half were exposed to their endogenous PRL levels. The second model consisted of treating anestrous animals with exogenous gonadotropins to induce follicular development and ovulation, half the animals were then treated with PRL while the other half were left as untreated controls. In the third model, CL were collected from mink at several stages of mink gestation. The cells were enzymatically dispersed, placed in culture and incubated with different concentrations of PRL, luteinizing hormone (LH), follicle stimulating hormone (FSH) and (Bu)$ sb2$cAMP. Using these 3 models, the effects of PRL on P450 side chain cleavage (P450scc), 3$ beta$-hydroxysteroid dehydrogenase (3$ beta$-HSD), steroidogenic acute regulatory protein (StAR), luteinizing hormone receptor (LHr) and prolactin receptor (PRLr) mRNA were determined. Messenger RNA levels for P450scc did not vary significantly over the course of mink gestation and treatment of animals with bromocryptine did not alter the abundance. In the anestrous model, treatment of mink with PRL reduced P450scc mRNA levels below that of the untreated control, while treatment of cultured mink luteal cells with increasing concentrations of PRL had no effect on the abundance of P450scc mRNA. The abundance of 3$ beta$-HSD mRNA varied over the course of mink gestation. Levels were low during embryonic diapause, increased during CL reactivation and peaked during post-implantation gestation. Treatment of mink with bromocryptine prevented the pre-implantation rise in 3$ bet
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Brimson, Christopher A. "The role of Hippo signalling in cell fate decisions in mouse embryonic stem cells and pre-implantation development." Thesis, University of Bath, 2016. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.687385.
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The Hippo signalling pathway is a conserved kinase cascade involved in the regulation of tissue growth and organ size. Activation of the Hippo pathway through multiple upstream inputs results in phosphorylation and inactivation of the transcriptional co-activator, Yes associated protein (Yap). While the role of Yap as an oncogene and an effector of the Hippo pathway is well established, its role in cellular differentiation is less well known. In this present work I have utilised quantitative immunofluorescence analysis to examine the expression of Yap in the differentiation of mouse embryonic stem cells (mESCs). I show that differentiation of mESCs is accompanied by an initial increase in nuclear Yap expression. Furthermore, I show that this increase in nuclear Yap expression is associated with differentiation towards the primitive endoderm lineage (PrE). Moreover, small molecule inhibition of Yap was able to decrease the proportion of cells differentiating towards PrE. Following on from these in vitro studies, I examine the expression of Yap in vivo in the corresponding differentiation event in mouse preimplantation embryos. I show that increased nuclear Yap expression is associated with expression of the PrE-specific transcription factor Gata6 during specification and eventual sorting of the PrE. Culturing embryos in the presence of small molecule inhibitors of Yap resulted in decreased expression of Gata6 and a reduction in trophectoderm cell number. These studies demonstrate that Yap is involved in the process of cellular differentiation and is associated with specification of the PrE lineage. Finally I attempt to create an inducible knockout of Yap in mESCs using a serial targeting strategy, with the intention of creating a model system in which to examine the role of Yap in mESCs.
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Morrish, Paul K. "A clinical and [18F]dopa PET study of the progression of Parkinson's disease and its treatment by embryonic implantation." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361927.
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Guo, Jiami. "The requirement of Smad4 in Mouse Early Embryonic Development." Kent State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=kent1343160155.
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Flores, Landaverde Luis Eduardo [Verfasser]. "Early detection of embryonic post implantation failures by ultrasound biomicroscopy and the role of the maternal immune system / Luis Eduardo Flores Landaverde." Berlin : Freie Universität Berlin, 2017. http://d-nb.info/1148426302/34.
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Bloomfield, Kelly Louise, and n/a. "Investigation of the Role of Thioredoxin in the Invasive Phenotype and its Interaction with the Transcription Factor Sp1." Griffith University. School of Biomolecular and Biomedical Science, 2003. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20031021.120018.
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Thioredoxin is a small ubiquitous oxido-reductase found in all species. The highly conserved active site, which facilitates thioredoxins redox activity, contains two redox active cysteine residues. Thioredoxin has numerous protein substrates to which it donates H+ ions and it can also function as a free radical scavenger. Through these activities thioredoxin is able to influence the redox state of not only its protein targets, but also the entire cellular environment. Thioredoxin has been implicated in many biological functions, and one mechanism by which it influences these functions is through interactions with a number of transcription factors including NF-kappa-B and p53. Thioredoxin also has numerous extracellular biological roles. It has been shown that thioredoxin is actively secreted from a number of normal and transformed cell lines including fibroblasts and activated B and T cells. This study investigates the role of thioredoxin in embryonic implantation and cancer cell metastasis, two physiological functions which rely on the same basic processes. Thioredoxin expression has previously been shown to be increased in many cancers. However it has not yet been established whether this increase is a causative or a side effect of the cancerous phenotype. Similarly thioredoxin expression has previously been shown to be increased during different phases of the oestrus cycle and pregnancy. This thesis describes the role of thioredoxin in embryonic implantation using a marmoset model. A thioredoxin cDNA was isolated and subsequently sequenced. Preliminary antibody experiments indicated that the anti human thioredoxin monoclonal antibodies available in our laboratory would recognise marmoset thioredoxin. Subsequently immunocytochemistry using anti human thioredoxin antibodies was carried out on sectioned marmoset uterus and embryonic tissue. The results indicated that thioredoxin is expressed by cells at the embryonic-maternal interface of early implantation sites. Further studies demonstrated that thioredoxin is also expressed and secreted by cultured blastocysts in vitro. This thesis also describes the role of thioredoxin in cancer cell metastasis. Results of this study indicate that thioredoxin is actively involved in facilitating the invasive phenotype of breast cancer cells. The two cell lines utilised were MCF-7, a well differentiated, relatively non-invasive breast cancer cell line; and MDA-MB-231, a poorly differentiated, highly invasive breast cancer cell line. The cell lines were transfected with thioredoxin sense, antisense and 1SS (encodes thioredoxin with both active cysteine residues mutated to serine residues and is thus redox inactive) constructs. The results demonstrate that when endogenous thioredoxin levels are increased, i.e. transfected with a sense thioredoxin construct, the invasive breast cancer cell line MDA-MB-231 becomes more invasive, conversely when endogenous levels are decreased, i.e. transfected with antisense or 1SS constructs, the invasive capacity of these cells decreases. However, when the endogenous level of thioredoxin was manipulated in the relatively non-invasive cell line MCF-7 very little effect was observed. Results also indicate that thioredoxin has the ability to act as a chemoattractant for actively invading breast cancer cells. Both of these functions appear to be dependent on thioredoxin's redox activity. Additional studies described in this thesis have shown that thioredoxin is involved in the regulation of Sp1 in vitro. Sp1 is a transcription factor known to regulate the transcription of a number of genes whose products are intimately involved in the invasive phenotype. The results in this study suggest that Sp1 DNA binding is regulated by thioredoxin such that when reduced by the enzyme its binding to DNA is facilitated. Results also indicate that Sp1 may regulate the transcription of thioredoxin by binding to Sp1 sites within the thioredoxin promoter.
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Bloomfield, Kelly Louise. "Investigation of the Role of Thioredoxin in the Invasive Phenotype and its Interaction with the Transcription Factor Sp1." Thesis, Griffith University, 2003. http://hdl.handle.net/10072/366170.
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Thioredoxin is a small ubiquitous oxido-reductase found in all species. The highly conserved active site, which facilitates thioredoxins redox activity, contains two redox active cysteine residues. Thioredoxin has numerous protein substrates to which it donates H+ ions and it can also function as a free radical scavenger. Through these activities thioredoxin is able to influence the redox state of not only its protein targets, but also the entire cellular environment. Thioredoxin has been implicated in many biological functions, and one mechanism by which it influences these functions is through interactions with a number of transcription factors including NF-_B and p53. Thioredoxin also has numerous extracellular biological roles. It has been shown that thioredoxin is actively secreted from a number of normal and transformed cell lines including fibroblasts and activated B and T cells. This study investigates the role of thioredoxin in embryonic implantation and cancer cell metastasis, two physiological functions which rely on the same basic processes. Thioredoxin expression has previously been shown to be increased in many cancers. However it has not yet been established whether this increase is a causative or a side effect of the cancerous phenotype. Similarly thioredoxin expression has previously been shown to be increased during different phases of the oestrus cycle and pregnancy. This thesis describes the role of thioredoxin in embryonic implantation using a marmoset model. A thioredoxin cDNA was isolated and subsequently sequenced. Preliminary antibody experiments indicated that the anti human thioredoxin monoclonal antibodies available in our laboratory would recognise marmoset thioredoxin. Subsequently immunocytochemistry using anti human thioredoxin antibodies was carried out on sectioned marmoset uterus and embryonic tissue. The results indicated that thioredoxin is expressed by cells at the embryonic-maternal interface of early implantation sites. Further studies demonstrated that thioredoxin is also expressed and secreted by cultured blastocysts in vitro. This thesis also describes the role of thioredoxin in cancer cell metastasis. Results of this study indicate that thioredoxin is actively involved in facilitating the invasive phenotype of breast cancer cells. The two cell lines utilised were MCF-7, a well differentiated, relatively non-invasive breast cancer cell line; and MDA-MB-231, a poorly differentiated, highly invasive breast cancer cell line. The cell lines were transfected with thioredoxin sense, antisense and 1SS (encodes thioredoxin with both active cysteine residues mutated to serine residues and is thus redox inactive) constructs. The results demonstrate that when endogenous thioredoxin levels are increased, i.e. transfected with a sense thioredoxin construct, the invasive breast cancer cell line MDA-MB-231 becomes more invasive, conversely when endogenous levels are decreased, i.e. transfected with antisense or 1SS constructs, the invasive capacity of these cells decreases. However, when the endogenous level of thioredoxin was manipulated in the relatively non-invasive cell line MCF-7 very little effect was observed. Results also indicate that thioredoxin has the ability to act as a chemoattractant for actively invading breast cancer cells. Both of these functions appear to be dependent on thioredoxin's redox activity. Additional studies described in this thesis have shown that thioredoxin is involved in the regulation of Sp1 in vitro. Sp1 is a transcription factor known to regulate the transcription of a number of genes whose products are intimately involved in the invasive phenotype. The results in this study suggest that Sp1 DNA binding is regulated by thioredoxin such that when reduced by the enzyme its binding to DNA is facilitated. Results also indicate that Sp1 may regulate the transcription of thioredoxin by binding to Sp1 sites within the thioredoxin promoter.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
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Castro, Karla Ribeiro de. "Efeitos da exposição crônica à poluição atmosférica urbana sobre a receptividade uterina: estudo morfo-funcional do remodelamento celular do endométrio e expressão de fatores envolvidos na preparação para implantação embrionária." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5160/tde-05112013-155805/.
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Evidências epidemiológicas associam diferentes fatores ambientais, tais como poluição e ingestão de alimentos contaminados, com desfechos gestacionais negativos e fertilidade diminuída em humanos. Não há duvidas de que a poluição do ar nos grandes centros urbanos é capaz de provocar desfechos negativos sobre a gestação: baixo peso ao nascer, prematuridade, perda gestacional, entre outros. Entretanto, poucos estudos foram conduzidos para avaliar um possível efeito da exposição à poluição ambiental particulada do ar sobre a saúde reprodutiva feminina. O objetivo deste trabalho foi avaliar se a exposição subcrônica a poluição atmosférica particulada da cidade de São Paulo é capaz de alterar a receptividade uterina à implantação embrionária. Para tanto, foram avaliados 3 grupos de fêmeas de camundongos (n=10), expostas cronicamente desde o período de desmame (PND21) até atingirem a idade reprodutiva (PND60) à duas concentrações de MP2,5 (600?g/m3 ou 1200ug/m3) ou ar filtrado. Diferentes parâmetros relacionados à fertilidade e a receptividade uterina foram avaliados. Nossos achados mostram que a exposição ao material particulado de origem veicular provoca alterações na ciclicidade estral prévia ao acasalamento, bem como um aumento no peso dos ovários. Avaliação da reserva folicular indica que há um aumento na quantidade de folículos médios associado à exposição a menor concentração de MP (p=0,04). A avaliação histopatológica do tecido uterino revelou que há aumentos na fração de volume das glândulas uterinas (600ug/m3; p=0,01); o epitélio glandular (p=0,001) e luminal (p=0,03) estão espessados e o diâmetro médio das glândulas uterinas foi maior nos grupos expostos ao MP (p=0,004). A análise qualitativa da distribuição de pinopódios no epitélio luminal por microscopia eletrônica de varredura e transmissão indica que há uma redução na presença destas estruturas. A avaliação da expressão de LIF por imunomarcação mostrou-se reduzida no epitélio luminal (p<0,001), nas glândulas (p<0,001) e estroma (p=0,004) nas fêmeas expostas ao MP, porém nenhuma diferença foi observada na expressão de MUC-1 (mucina). Entretanto quando avaliadas a expressão gênica de MUC-1 e LIF no tecido uterino e os níveis de IL-1beta e IL-6 no fluído uterino nenhuma diferença foi observada entre os grupos. Com base em nossos achados conclui-se que a exposição à poluição particulada do ar de origem veicular pode estar envolvida no aumento das perdas gestacionais e/ou implantacionais pelo comprometimento da receptividade uterina provavelmente pelo prejuízo do remodelamento uterino necessário a implantaçãoEpidemiological evidences have shown that environmental factors, such as environmental pollution and ingestion of contaminated food, are associated with negative gestational outcomes and decreased fertility in human. There is no doubt that exposure to air pollution in large urban areas are capable of impairing health (e.g. hypertension) and of aggravating preexisting diseases (e.g asthma). However, the effects of air pollution exposures on female reproductive health are lesser known. Previous experimental studies have shown that low birth weights are reduced and embryonic implantational index are reduced in animals exposed to ambient levels of air pollution. The aim of this study was to evaluate if sub chronic exposures to particulate air pollution before pregnancy and during the initial stages is capable to alter the uterine receptivity of mice. To test this, 3 groups of female mice were continually exposed from 21st to 60th postnatal day to either filtered or two different doses of concentrated ambient particles (MP2,5 - 600ug/m3 or 1200ug/m3) with the aid of a Ambient Particle Concentrator and different parameters associated with fertility and uterine receptivity were evaluated. Or data have shown that exposures to particulate air pollution from vehicular origin are associated to changes in estrous ciclicity, cycles are shorter and the number of days in estrous reduced. Evaluation of the follicular reserve also indicates that animals exposed to MP present an increased number of ovarian medium follicles (p=0.04). Histopathological evaluation of the uterine tissue revealed increases in the volume fraction of uterine glands (p= 0.01) of those animals exposed to 600ug/m3. The luminal (p= 0.03) and glandular epithelium (p= 0,001) are thicker and the uterine glands diameters (p=0,004) were greater in exposed animals. Qualitative analysis by transmission and scanning electron microscopy indicates that there is a reduction in the presence of pinopódios in the luminal epithelium of PM exposed females. The expressions of LIF assessed by immunohistochemistry in those females exposed to PM were reduced in the luminal epithelium (p<0,001), and in the glandular (p<0,001) and stromal compartments as well. However no differences in the expression of MUC-1 were seen. Gene expression of LIF and MUC-1 in the whole endometrium (qPCR) and the expression of IL-6 and IL-1beta in the uterine fluid did not show significant difference between the groups tested. In conclusion, our data have shown that exposures to ambient air particulate pollution can be associated with increased rates of implantational losses due to changes in the uterine receptivity related to factors involved in uterine remodeling for pregnancy
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Sun, Congshan. "Effect of pre-implantation maternal low protein diet on embryos and embryoid bodies." Thesis, University of Southampton, 2014. https://eprints.soton.ac.uk/363661/.
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Previous studies have shown that poor maternal nutrition during pregnancy may induce metabolic syndrome in adults. In this study, we explored the mechanisms of how maternal low protein diet during the first 3.5 days of pregnancy, programs embryo development and embryonic stem cell function. Our results showed that mouse maternal low protein diet (9% casein; Emb-LPD) enhanced both Clathrin dependent and independent endocytosis in both in vivo blastocysts and in vitro differentiated embryoid bodies (EB day 5) compared with maternal normal protein diet (18% casein; NPD) controls. This increase in endocytosis was accompanied by an increase in lysosome volume per cell. This was done by confocal microscopy and 3D image analysis. To determine whether this effect on the lysosome system was due to autophagy or simply due to increased endocytosis, we studied the expression of LC3 protein, Clathrin, Megalin (also named as low density lipoprotein receptor 2 (LRP2)) and Cubilin. Immunostaining and Western blot analysis revealed Megalin and Cubilin were significantly up-regulated in Emb-LPD embryos and EBs, whilst Clathrin protein level was marginally increased and LC3 protein unaltered. This enhanced nutrient uptake ability was maintained even after cells or embryos were re-introduced into a normal environment in vitro. Thus, stimulated nutrient uptake in day 5.5 EB showed compensatory growth, known to associate with long-term disease symptoms. To understand the mechanisms involved, we investigated elements of the mTOR pathway. In vitro culture of early embryos in the presence of reduced levels of the three branched-chain amino acids (Lecine, Valine and Isoleucine) as occurring in Emb-LPD uterine fluid resulted in stimulated endocytosis of Trophectoderm (TE). In addition, we found although mTORC1 was partially suppressed, mTORC2 downstream RhoA-Actin interaction was stimulated in blastocysts by observing more actin and RhoA protein in Emb-LPD blastocysts as well as that inhibiting RhoA function abolished the enhanced endocytosis by Emb-LPD. We also investigated epigenetic changes induced by Histone deacetylase 3 (Hdac3) in terms of regulation of genes involved in Extraembronic Endoderm (XEN) differentiation and cardiomyocyte differentiation. We found that Emb-LPD EBs expressed reduced Gata6 and exhibited increased histone deacetylation at promoter of Gata6, together with increased Hdac3 expression. Our results reveal for the first time at the cellular level how early embryos respond to poor nutrition environment and reprogram to protect fetal growth. This further helps us to understand the mechanism of how adult metabolic syndrome can be originated from environment which early embryos were exposed to.
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Piger, Veronika. "Einfluss immunologischer Mechanismen bei der Implantation von Embryonen und deren therapeutischer Nutzen im Rahmen des IVF-Programms." Doctoral thesis, [S.l.] : [s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=963988859.
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Lindgren, Karin E. "The Histidine-rich Glycoprotein in Reproduction." Doctoral thesis, Uppsala universitet, Institutionen för kvinnors och barns hälsa, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-300769.
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Infertility affects 15% of reproductive-aged couples. The milieu surrounding the growing embryo is of outmost importance, and should be optimised during in vitro fertilisation (IVF). Many biological processes, such as angiogenesis, coagulation, and immune processes need to be well regulated for a pregnancy to occur and progress normally. Histidine-rich glycoprotein (HRG) is a plasma protein that regulates components of these systems by building complexes with various ligands. A single nucleotide polymorphism (SNP) in HRG, denoted HRG C633T, seem to be of importance for IVF treatment outcomes. The aim of this thesis was to further investigate the proposed human fertility effects of the HRG C633T SNP. According to the findings of this thesis, the HRG C633T genotype is associated with primary recurrent miscarriage. Male HRG C633T genotype is associated with semen characteristics in infertile men, and pregnancy rates following IVF. However, the distribution of the HRG C633T SNP does not differ between infertile and fertile couples. We further examined the role of the region surrounding the HRG C633T SNP for regulation of endometrial angiogenesis and human embryo development. The region affects primary endometrial endothelial cell migration, proliferation and tube-formation in vitro but does not appear to affect human embryo development. No effect of the HRG peptide was noted on the secretome of human embryos. However, early embryos secrete proteins into the surrounding culture media and the level of secretion of VEGF-A, IL-6, EMMPRIN and PlGF is greater in embryos of higher developmental stages. In conclusion, the HRG C633T genotype appears to play a role only if infertility is established. The region surrounding HRG C633T SNP is of relevance in vitro for regulation of human endometrial endothelial cell angiogenesis. To predict which embryos to transfer in IVF, we have highlighted a number of proteins of interest for further investigation.
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Gurchenkov, Vasily. "The functional study of the asymmetric specific element of the Nodal gene during the early mouse development." Paris 6, 2009. http://www.theses.fr/2009PA066056.
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Le travail décrit dans ce manuscrit est une étude du fonctionnement de la voie de signalisation du facteur de type TGF-beta Nodal pendant l’embryogenèse précoce de la souris. Ce travail est centré sur l’analyse de l’activité de l’ASE, une séquence régulatrice du gène Nodal. Cette séquence est une cible de la voie de signalisation Smad2,3, qui transduit le signal Nodal, et permet donc au gène Nodal d’amplifier sa propre expression. Des lignées transgéniques où l’expression de protéines fluorescentes est placée sous le contrôle de l’ASE avaient été générées au laboratoire. La caractérisation de ces lignées et leur comparaison avec d’autres lignées transgéniques a permis de les valider en tant que lignées rapportrices de l’activité de =l’élément régulateur ASE. Une lignée ASE-YFP a été retenue pour la suite de l’étude. L’analyse du profil d’expression du transgène a révélé qu’il est actif dès les stades pré-implantatoires. Ceci a suggéré implication de l’ASE dans l’initiation de l’expression de Nodal. Entre E3,5 et E4,5, nous avons observé que l’expansion de l’activité du transgène passe par des périodes alternées de relative stabilité et d’accroissement rapide. Deux courtes périodes de propagation rapide de l’activité de l’ASE semblent correspondre à la différenciation de l’endoderme primitif et à l’implantation, deux événements majeurs du développement embryonnaire à ces stades. L’observation que le transgène ASE-YFP à E3,5 est exprimé façon poivre et sel dans les cellules de l’ICM a soulevé une interrogation quand aux destins relatifs des deux populations de cellules ainsi identifiées au sein de ce tissu pluripotent. Des études de co-marquage ont permis de montrer que l’activité du transgène ASE-YFP marque indifféremment aussi bien des précurseurs de l’épiblaste, qui expriment le facteur de pluripotence Nanog, que des précurseurs de l’endoderme primitif, qui expriment Gata4. Cependant, les co-marquages réalisés après la formation de l’endoderme primitif indiquent qu’au sein de l’épiblaste l’expansion du nombre de cellules exprimant le transgène ASE-YFP est concomitante d’une diminution du nombre de cellules exprimant Nanog. De façon intéressante, le pool des cellules co-exprimant Nanog et le transgène ASE-YFP décroît plus lentement que la population des cellules exprimant Nanog seul. Ceci apporte un éclairage nouveau aux données impliquant la signalisation Nodal dans le maintien de la pluripotence, et suggère que l’activité de la voie de signalisation de Nodal et le facteur Nanog, pourraient être liés via l’ASE au sein d’une même boucle de régulation. Enfin, la régulation de l’ASE aux stades pré et péri-implantatoires a été étudiée par une approche combinant génétique et inhibition pharmacologique. L’utilisation d’un inhibiteur spécifique des récepteurs ALK4, 5, 7 qui normalement participent à l’activation de Smad2,3, a permis de démontrer que l’activation du transgène est bien dépendante de cette voie de signalisation à ces stades. Cependant, le maintien de l’activité du transgène ASE-YFP en contexte mutant pour Nodal indique qu’un autre ligand que Nodal contribue alors à l’activité de la voie. De même, le maintien de l’activité du transgène en contexte mutant pour Foxh1, l’effecteur classique de Smad2,3 dans l’épiblaste, confirme que d’autres acteurs que ceux déjà identifiés sont impliqués dans l’activité de la voie Smad2,3 à ces stades. Il est à noter que l’extinction du transgène par l’inhibiteur pharmacologique ne s’accompagne pour les embryons traités d’aucun effet visible sur leur croissance ou leur physiologie. L’ensemble de ces travaux précise la façon dont Nodal est exprimé et régulé aux stades pré et péri-implantatoires mais pose in fine la question du rôle de cette molécule et de sa voie de signalisation à ces stades.
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Boudjenah, Radia. "Impact des polymorphismes génétiques sur les chances individuelles des patientes prises en charge en AMP." Versailles-St Quentin en Yvelines, 2012. http://www.theses.fr/2012VERS0037.
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L’aide médicale à la procréation constitue aujourd’hui le premier traitement pour les infertilités, mais malgré de nombreux progrès enregistrés, les taux de succès restent autour de 30% par cycle. La réponse ovarienne aux gonadotrophines et l’implantation embryonnaire demeurent très variables entre les patientes et très difficile à prévoir. Notre travail a porté sur l’étude de l’impact des polymorphismes génétiques sur la réponse ovarienne et sur l’implantation embryonnaire. Sur les 13 polymorphismes génétiques analysés, le résultat de la stimulation ovarienne, objectivés par le nombre d’ovocytes recueillis, varie en fonction du génotype de 4 polymorphismes : FSHR-Asn680Ser, p53-Arg72Pro, ESR2+1730-G/A et AMH-Ile49Ser. Les taux d’implantation embryonnaire et de grossesse varient quand à eux en fonction du génotype de 2 polymorphismes : VEGF+405-G/C et TNFα-308-GA individuellement ou associés. A coté de l’approche gène candidat, nous avons réalisé une étude whole génome sur l’impact des CNPs sur l’implantation embryonnaire. Des résultats préliminaires montrent l’impact de 2 CNV sur l’implantation embryonnaire contenant 2 gènes BTNL3 etGSTT1. Au total, nos résultats montrent que l’étude des facteurs génétiques de prédisposition àl’infertilité pourrait nous permettre d’adapter la prise en charge des patientes en AMPMedical assistance for procreation is now the first treatment for infertility, but in spite of various advances, success rates remain around 30% per cycle. Ovarian response to gonadotropins and embryo implantation are variable between patients and very difficult to predict. Our work focused on studying the influence of genetic polymorphisms on ovarian response and embryo implantation. Of the 13 polymorphisms analyzed, the result of ovarian stimulation, objectified by the number of oocytes collected, varies with the genotype 4 polymorphisms: FSHR-Asn680Ser, p53-Arg72Pro, ESR2 +1730- G / A and AMH-Ile49Ser. Rates of embryo implantation and pregnancy vary with the genotype of two polymorphisms : VEGF+405-G/C and TNFα-308-GA individually or combined. Besides the candidate gene approach, we performed a whole genome study on the impact of CNPs on embryo implantation. Preliminary results show the impact of two CNVs on two genes containing embryo implantation BTNL3 andGSTT1. Altogether, our results show that the study of genetic factors predisposing to infertility could allow us to tailor the care of patients in AMP
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Déchaud, Hervé. "Développement et évaluation de la falloposcopie : application à la compréhension des stérilités tubaires et de leurs conséquences." Montpellier 1, 1998. http://www.theses.fr/1998MON1T023.
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Vitorino, Carvalho Anaïs. "Contribution à la caractérisation de l’expression, de la régulation et des rôles biologiques de STAT1 dans l’endomètre bovin au cours de la gestation précoce." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA11T067.
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Au cours de la gestation précoce, la régulation de la physiologie endométriale est cruciale au bon déroulement de l’implantation. Chez les mammifères, une famille de facteurs de transcription est fortement impliquée dans la régulation de la physiologie endométriale, les facteurs STAT. Chez la vache, des analyses haut-débit ont révélé que l’expression endométriale de STAT1 est régulée au cours de la période préimplantatoire. Le but de cette thèse est donc d’apporter de nouvelles données sur l’expression et la régulation endométriales de STAT1 mais également sur ses fonctions biologiques au cours de la gestation précoce chez la vache.Grâce à différents modèles physiologiques et expérimentaux, l’impact de la progestérone, de l’IFNT (signal majeur de reconnaissance maternelle de la gestation chez les ruminants) et de la gestation sur l’expression et la régulation de STAT1 (y compris sa phosphorylation) a été analysé dans l’endomètre bovin et sur des cultures primaires de cellules endométriales. Ainsi, l’expression de STAT1 (transcrit et protéine) ainsi que sa phosphorylation sont augmentés en présence du conceptus et de l’IFNT, indépendamment du taux circulant de progestérone à l’implantation chez la vache. Pour avoir une meilleure connaissance des rôles de STAT1, l’identification de ses gènes cibles a été entreprise : d’abord avec une approche gènes candidats (avec la famille des gènes SOCS), puis par une approche exploratoire.Les facteurs SOCS sont connus pour être des régulateurs négatifs de la voie de signalisation des cytokines. L’utilisation des différents modèles physiologiques et expérimentaux évoqués plus haut a permis l’analyse de l’expression et de la régulation des huit membres de la famille des gènes SOCS au cours de la gestation précoce chez la vache. L’application d’un protocole d’immunoprécipitation de la chromatine sur des cultures primaires de cellules stromales bovines montre le recrutement rapide de STAT1 par l’IFNT sur les promoteurs des gènes SOCS IFNT-dépendants. D’autre part, l’identification systématique des gènes cibles de STAT1 a été entreprise via l’élaboration d’un protocole d’immunoprécipitation de la chromatine suivit de séquençage haut-débit, appliqué à des échantillons d’endomètre bovin. L’ensemble de ces travaux suggèrent l’implication de STAT1 dans la signalisation endométriale de l’IFNT, dans la régulation du système immunitaire maternel et également dans le contôle des phénomènes d’apposition et d’adhérence, fonctions cruciales à l’implantation chez la vacheDuring the early stage of the pregnancy, the regulation of the endometrial physiology is crucial to the right establishment of the implantation. In mammals, a transcription factor family is highly involved in the regulation of endometrial physiology, the STAT family. In cattle, high-throughput analyses light up the regulation of endometrial STAT1 expression during the pre-implantation period. Thus, the aim of this work is to bring new insights about endometrial STAT1 expression and regulation but also on its biological functions during the early pregnancy in cattle. Using physiological and experimental models, the impact of progesterone, IFNT (major signal of the maternal recognition of pregnancy in ruminants) and pregnancy on the expression and the regulation of STAT1 transcript and protein (including its phosphorylation status) have been analyzed in the bovine endometrium and endometrial cells. Thus, STAT1 (transcript, protein and phosphorylation) is up-regulated by the presence of the conceptus and by IFNT but independent of progesterone level at implantation in cattle. To better understand endometrial STAT1 functions, the identification of STAT1 target genes has been initiated: first, on a candidate genes family, SOCS genes, and secondly, with an explorative approach.The proteins SOCS are known to be negative regulator of cytokine signalling pathway. Using physiological and experimental models previously quoted, the eight members of SOCS genes expression and regulation were analyzed during the early pregnancy in cattle. Chromatin immunoprecipitation protocol applied on stromal cells show the recruitment of STAT1 on SOCS promoters by a rapid treatment of IFNT. Moreover, the exhaustive identification of STAT1 target gene has been initiated, using a chromatin immunoprecipitation followed by high-throughput sequencing on bovine endometrium samples. Collectively, this data suggests the involvement of STAT1 in IFNT signalling pathway but also in the regulation of maternal immune system and the apposition/adhesion process, all that being crucial for the implantation in cattle
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Duval, Fabien. "Rôles de l'adiponectine à l'interface foeto-maternelle humaine au cours du premier trimestre de grossesse." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLV070/document.
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L’implantation embryonnaire repose sur une synchronisation spatio-temporelle entre un placenta fonctionnel et un endomètre réceptif. La réceptivité endométriale requiert la différenciation des cellules stromales en cellules déciduales sous l’effet des hormones ovariennes (œstrogènes et progestérone). Le placenta est un organe transitoire constitué de deux types cellulaires. Le cytotrophoblaste villeux est responsable des échanges fœtaux maternels et de la fonction endocrine du placenta. Le cytotrophoblaste extravilleux présente des propriétés invasives et assure ainsi l’ancrage du placenta dans l’endomètre maternel. Un dialogue paracrine complexe entre les cellules placentaires et endométriales s’établit au cours des premières étapes de l’implantation.L’adiponectine est une adipokine produite majoritairement par le tissu adipeux. Elle contrôle le métabolisme glucido-lipidique et joue le rôle d’hormone insulino-sensibilisatrice. Dans de nombreux tissus, l’adiponectine exerce des effets anti-prolifératifs, pro-invasifs et pro-différenciants. L’adiponectine et ses récepteurs ADIPOR1 et ADIPOR2 sont présents à l’interface fœto-maternelle. Le placenta et l’endomètre sont donc des tissus cibles de l’adiponectine.Au cours de ce travail, nous nous sommes intéressés aux effets directs de l’adiponectine à l’interface foeto-maternelle au cours du premier trimestre de grossesse.Dans une première partie, nous avons observé que l’adiponectine exerce des effets anti-différenciants et anti-invasifs dans les cellules stromales endométriales.Dans un second temps, nous avons démontré que l’adiponectine favorise la production de glycogène dans les cellules déciduales. Inversement, l’adiponectine semble limiter l’entrée du glycogène dans les cellules placentaires. Ces résultats démontrent que l’adiponectine pourrait contrôler la nutrition histiotrophe du foetus.Dans une dernière partie, nous avons observé que l’adiponectine diminue l’expression des transporteurs de nutriments et exerce une action pro-apoptotique dans le trophoblaste villeux. Ces derniers résultats pourraient permettre de mieux comprendre le rôle de l’adiponectine dans les pathologies placentaires telles que le retard de croissance intra-utérin qui se caractérise par une diminution du poids foetal et une augmentation de l’apoptose des cellules trophoblastiques.L’ensemble de ces résultats montre que l’adiponectine est un acteur clé du dialogue foeto-maternel au cours de la grossesse précoce en contrôlant la maturation d’un endomètre fonctionnel et en régulant les échanges nutritifs transplacentairesEmbryo implantation requires a spatiotemporal synchronization between a functional placenta and a receptive endometrium. Endometrium receptivity based on the differentiation of stromal cells into decidual cells, under the influence of ovarian hormones (estrogens and progesterone). The placenta is a transient organ composed of two cell types. Villous trophoblast ensures fetal-maternal exchanges and the endocrine functions. Extravillous trophoblast acquire an invasive phenotype resulting in the placenta anchoring in the endometrium. Then, a complexe paracrine dialog between placental cells and endometrial cells is established during the first stages of the embryo implantation.Adiponectin is an adipokine predominantly produced by the adipose tissue. This cytokine has an important role in the control of energy metabolism and displays an insulin-sensitizing action. In some cell types, adiponectin limits proliferation, but promotes invasion and differentiation. Adiponectin and its receptors ADIPOR1 and ADIPOR2, are expressed at the fetal-maternal interface. Thus, endometrium and placenta are adiponectin targets.In this work, we aimed to determine adiponectin direct effects at the human fetal maternal interface during the first trimester of pregnancy.In a first part, we observed that adiponectin limits differentiation and invasion in endometrial stromal cells.In a second part, we showed that adiponectin promotes glycogen production by decidual cells. Conversely, adiponectin seems to limit glycogen uptake by placental cells. These results demonstrate that adiponectin could regulate histiotrophic nutrition to the fetus.In a last part, we demonstrated that adiponectin down-regulates the expression of nutrient transporters and promotes apoptosis in villous trophoblast. These last results could help to better understand the adiponectin roles in some placental pathologies, as intrauterine growth restriction, characterized by a decreased fetal weight and a enhanced trophoblastic apoptosis. Altogether, these results demonstrate that adiponectin is a key regulator of the fetal-maternal dialog by controlling the differentiation of a functional endometrium and by regulating transplacental nutrient exchanges
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Rahmati, Mona. "Granulocyte-Colony Stimulating Factor and Embryo Implantation Process : Effects on Human Endometrium and on Murine Abortion Prone Model CBA/J x DBA/2." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA11T048/document.
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L’immunologie de la reproduction englobe les principes de l’immunologie générale et les aspects spécifiques de la reproduction et du développement. Les Colony Stimulating Factors (CSFs) sont une illustration de l'application médicale de ce domaine. Dans la famille des CSFs, le Granulocyte-Colony Stimulating Factor (G-CSF) apparaît aujourd'hui comme une thérapie innovante dans divers cas d'échec de la reproduction, bien que ses cibles et ses effets ne soient pas encore clairement établis. Dans ce travail, à travers une revue sur les CSFs dans la reproduction, une étude consacrée aux gènes cibles du G-CSF dans l'endomètre humain, et une étude consacrée aux effets de la supplémentation systémique en G-CSF sur l’implantation embryonnaire murine, nous avons essayé d'approcher certains mécanismes d'action possibles pour cette cytokine. Dans les modèles murins fertiles et pro-abortifs, la supplémentation systémique en G-CSF, ciblant spécifiquement l’endomètre préimplantatoire, modifie les taux d’implantation embryonnaire. Dans l’endomètre humain, certaines dérégulations préimplantatoires de gènes cibles du G-CSF ont également été observées chez les patients infertiles. L'influence du G-CSF sur ces gènes cibles a été également illustrée dans un modèle ex-vivo de culture endométriale. Ces cibles dont l’expression est influencée par le G-CSF sont décrites comme des molécules clés dans le processus implantatoire, intervenant sur l’adhésion embryonnaire, la migration cellulaire, le remodelage des tissus et l'angiogenèse locale. Ces données suggèrent des possibilités de diagnostic préventif et pré-conceptionnel de certains échecs de reproduction, considérés jusqu’à maintenant comme idiopathiques, et de thérapies innovantes orientées, afin d’optimiser la réceptivité du biosenseur endométrial afin de permettre une implantation embryonnaire harmonieuse et une grossesse évolutiveReproductive Immunology involves general immunology principles and special aspects of reproduction and development. Colony Stimulating Factors (CSFs) are an illustration of the medical application of this domain. In the CSF family, Granulocyte-Colony Stimulating Factor (G-CSF) appears today as a promising therapy in various cases of reproductive failure although its targets and effects are not clearly established. In this work, through a review on CSFs in reproduction, a study dedicated to human endometrial targets of G-CSF, and a study dedicated to systemic G-CSF supplementation effects on murine embryo implantation, we tried to approach some possible mechanisms of action of this cytokine. In the considered non-abortive and abortion-prone murine models, the timed systemic G-CSF supplementation, targeting specifically the pre implantation endometrium, influenced the embryo implantation process. Some pre conceptual human endometrial dysregulations of G-CSF target genes were also observed in infertile patients. The endometrial influence of G-CSF on these target genes was also illustrated in an ex-vivo model. These molecules under G-CSF influence are described as critically involved in embryo implantation process, by influencing embryo adhesion, cell migration, tissue remodelling and angiogenesis. These data suggest possible pre-conceptual preventive diagnosis of such reproductive failures and future orientated therapies to optimise the endometrial biosensor and the further embryo implantation and ongoing pregnancy
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Hsu, Wen-Ling, and 徐玟鈴. "Physiological role of the embryonic progesterone receptor in the implantation and post-implantation development." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/b3aw3j.
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碩士國立屏東科技大學
生物科技系所
105
Progesterone, a steroid hormone plays an important role in gestation, female menstrual cycle and implantation. Must be P4 and progesterone receptor combination can trigger action. If P4 and PR antagonist-RU486 binding will cause P4 can not its function. Previous studies have focused more on the effect of progesterone on the endometrium of uterus rather than on embryo development. In this study, we investigated the roles of progesterone in mouse embryo development and implantation. We examined the effects of RU486 (2x10-9 to 2x10-5M) on mouse embryonic cell growth and blastocyst outgrowth in vitro. Expression of PR on embryo was examined by immunofluorescence staining. We found that expression of PR was detected on the stages of preimplantation embryo from zygotes to blastocysts. The presence of progesterone in reproductive tract was determined by Radioimmunoassay (RIA). The progesterone level could be found in the serum, fallopian tube and uterine cavity. Our results showed that RU486-pretreated blastocysts with human cord serum (hCS) or treatment 48 hours a significant reduction the number of cells (P <0.001 ). The RU486-pretreated 48 hours or 8 days blastocysts were allowed to implant in vitro, significantly fewer embryos were able to reach a later stage of embryo development (P <0.05/ P <0.001 ). Our results suggested that the expression of PR on preimplantation embryos was involved in the physiological roles in the embryo development in the time of or after implantation.
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Landrock, Danilo. "Acyl CoA Binding Protein (ACBP) Gene Ablation Induces Pre-Implantation Embryonic Lethality in Mice." Thesis, 2010. http://hdl.handle.net/1969.1/ETD-TAMU-2010-12-9003.
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Unique among the intracellular lipid binding proteins, acyl CoA binding protein (ACBP)
exclusively binds long chain fatty acyl CoAs (LCFA-CoAs). To test if ACBP is an
essential protein in mammals, the ACBP gene was ablated by homologous
recombination in mice. While ACBP heterozygotes appeared phenotypically normal,
intercrossing of the heterozygotes did not result in any live homozygous deficient (null)
ACBP^(-/-) pups. Heterozygous and wild type embryos were detected at all
postimplantation stages, but no homozygous ACBP null embryos were obtained–
suggesting that an embryonic lethality occurred at a preimplantation stage of
development, or that embryos never formed. While ACBP null embryos were not
detected at any blastocyst stage, ACBP null embryos were detected at the morula (8-
cell), cleavage (2-cell), and zygote (1-cell) preimplantation stages. Two other LCFACoA
binding proteins, sterol carrier protein-2 (SCP-2) and sterol carrier protein-x (SCPx)
were significantly upregulated at these stages. These findings demonstrate for the first
time that ACBP is an essential protein required for embryonic development and its loss
of function may be initially compensated by concomitant upregulation of two other LCFA-CoA binding proteins only at the earliest preimplantation stages. The fact that
ACBP is the first known intracellular lipid binding protein whose deletion results in
embryonic lethality suggests its vital importance in mammals.
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Llerena, Evelyn M. "Embryonic and Uterine Characteristics of Diapause." Thèse, 2011. http://hdl.handle.net/1866/6952.
Full textAbstract:
L’implantation retardée ou diapause embryonnaire décrit l'arrêt ou le retardement pendant l'embryogenèse. Chez le vison, la diapause est corrélée avec une sécrétion pituitaire insuffisante de la prolactine, ayant pour résultat la différentiation incomplète du corpus luteum et réduction de la progestérone. Des études antérieures suggèrent que le blastocyste de vison en diapause demeure dans un état de quiescence ou se développe lentement. Pour élucider ceci, la réplication de l'ADN a été étudiée. Les résultats démontrent synthèse de l’ADN et prolifération cellulaire dans les embryons au stade de morula, avant la diapause et dans les blastocystes après la réactivation. La réplication de l'ADN a été également détectée dans des blastocystes en diapause et en diapause prolongée. L'implantation est considérée comme une interaction bidirectionnelle entre le blastocyste et l'utérus. Il a été montré que les prostaglandines sont importantes pour la vascularisation de l’utérus au moment de l’implantation et peuvent réactiver l'utérus des visons après la diapause. La concentration protéinique et la localisation de la phospholipase citosolique A2 (CPLA2) et de la cyclooxygenase 2 (COX2) ont été étudiées dans l'utérus de vison. L’expression de la CPLA2 et COX2 étaient sur-régulées au moment de l'implantation. Il est connu que la prolactine active les corpus luteum des visons. L'idée de un lien entre la prolactine et la voie de signalisation des prostaglandines a été testée en mesurant les récepteurs de prolactine. Les résultats montrent une augmentation de l’expression des récepteurs de prolactine à l'implantation suggérant que la prolactine pourrait activer la voie de prostaglandine à l'utérus par son propre récepteur. La conclusion, les embryons pendant la diapause ne sont pas arrêtées complètement et les protéines liées à la voie de prostaglandine sont implique dans la réactivation de l'utérus.Delayed implantation or diapause describes arrest or retardation during embryogenesis. In mink, diapause is related to insufficient pituitary prolactin secretion, resulting in incomplete differentiation of the corpus luteum with reduced progesterone concentration. The mink blastocyst at diapause was believed to be totally quiescent or expanding at a low rate. To explore this, DNA replication was studied. Results showed synthesis of DNA, and thus cell proliferation at the morulae stage before diapause and at the blastocyst following activation. DNA replication was detected not only at diapause but also at extended diapause. Furthermore, implantation is considered as a two-way interaction between the blastocyst and the uterus. It has been shown that prostaglandins are important for vascularization of the uterus and products of the prostaglandin pathway could reactivate the mink uterus following diapause. Protein concentration and localization was studied for cytosolic phospholipase A2 (CPLA2) and cyclooxygenase 2 (COX2) in mink uterus. Expression of CPLA2 and COX2 was up regulated at implantation. It is know that prolactin is the factor that activates the mink corpus luteum. The idea of a link between prolactin and prostaglandin pathway was investigated by quantifying the prolactin receptors in the uterus. Results showed an increase of prolactin receptors at implantation suggesting that prolactin could activate the prostaglandin pathway at the uterus through its own receptor. In conclusion, embryos during diapause are not completely arrested, and proteins related to the prostaglandin pathway are implicated in reactivation of the uterus.
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Huang, Tzu-Wei, and 黃子瑋. "Effects and regulatory mechanisms of berberine on mouse embryonic development in both pre- and post-implantation stages." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/zdwk86.
Full textAbstract:
碩士中原大學
生物科技研究所
99
Berberine is an alkaloid isolated from Coptis Chinensis, Phellodendron and other plant extracts. Berberine is a traditional Chinese medicine in China which has been applied for a long time. Berberine has been evaluated as anti-diarrhea, anti-bacterial, anti-arrhythmic, anti-vascular smooth muscle proliferation and cholesterol-lowering. Berberine also performs a wide range of applications in the cardiovascular system and nervous system diseases. Several studies have demonstrated that berberine is able to induce apoptosis process in cancer cells. However, a study regarding the embryonic toxicity of berberine has not yet been done. In this study, mouse embryos were used to study the effects of berberine on embryonic development and proliferation. The study results showed that blastocysts treated with 5 or 10 μM of berberine that resulted a significant dose-dependent increase in apoptosis and inhibited cell proliferation. To evaluate the alteration of inner cell mass (ICM) and trophoblast cell (TE) of mouse blastocysts, we used differential staining and TUNEL assay. Statistics showed, TE subject to more damage than ICM. Furthermore, the immunofluorescence staining, revealed that berberine induced apoptosis in mouse blastocysts by reducing expression of anti-apoptotic Bcl-2 protein and increasing expression of the pro-apoptotic Bax protein, which increases the ratio of Bax/Bcl-2. Conclusion, berberine induced embryo cell apoptosis and caused hazardous effects on embryonic development.
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Liao, Chen-Yi, and 廖珍頤. "The role of ECM in the migration of embryonic stem cells and trophoblast cells: implication in early embryo development and embryo implantation." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/30430593392166353822.
Full textAbstract:
碩士國立陽明大學
解剖暨細胞生物學研究所
96
Extracellular matrix (ECM) plays an important role in embryo implantation and embryogenesis, since previous studies have shown that functional blockade of ECM receptors results in implantation failure and deficiency in ECM proteins causes embryonic lethality. Interaction between ECM proteins and their receptors, integrins, promotes cellular migration, which is critical for embryo implantation and development. In this study, we compared the effects of various ECM proteins on the migration of embryonic stem (ES) cells and trophoblast cells of the blastocysts, followed by examination of the underlying mechanisms. We found that collagen IV, fibronectin and laminin were expressed in the inner cell mass (ICM) and trophoectoderm of the mouse blastocysts. Using a mouse ES cell line, ESC26GJ, embryoid bodies (EB) were generated to mimic the ICM and cultured on surfaces coated with or without collagen IV, fibronectin, laminin, collagen I and matrigel. Among the various ECM proteins, collagen IV maximally stimulated EB expansion, even under mitomycin C inhibition of proliferation. ES cells expressed ��2 and ��1 integrin subunits, but not ��1 integrin. The promoting effect of collagen IV on EB expansion was prevented by the RGD peptide and blocking antibodies against ��2 and ��1 integrins. Cytochalasin D, a reagent disrupting actin cytoskeleton that links to integrins, also blocked the enhancing effect of collagen IV on EB expansion. Interestingly, we found that the expression of two epithelial-mesenchymal transition (EMT) markers, fibronectin and vimentin, was up-regulated in ES cells when culturing on collagen IV. In addition, among various ECM proteins, collagen IV also had the greatest stimulatory effect on trophoblast outgrowth of the mouse blastocysts. The enhancing effect of collagen IV on trophoblast outgrowth could be blocked by cytochalasin D. Our results demonstrated that collagen IV maximally stimulated migration of ES cells and trophoblast cells of the blastocysts and the collagen IV-promoted ES cell migration was mediated by signaling through ��2/��1 integrin and actin cytoskeleton. Our findings may help improve the successful rate of stem cell transplantation and assisted reproductive technology
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Shen, Jin-Te, and 沈金德. "The Roles of Intracellular Calcium Fluxes and Signaling in the Spreading of Trophoblast Cells on Endometrial Epithelium during Embryonic Implantation – an In Vitro Model System." Thesis, 2004. http://ndltd.ncl.edu.tw/handle/68241036816432251550.
Full textAbstract:
碩士國立陽明大學
解剖暨細胞生物學研究所
92
The Ca2+ ion as a secondary messenger, mediated many signaling pathway, including cytochrome c release, tight junction formation and cell migration ability. During implantation, complex embryo-endometrium interaction result in blastocyst adhesion. At the implantation site, the Ca2+ ion play an important role to mediate the interaction between trophoblast and endometrial epithelial cells, the function is still unclear. To role out the function of Ca2+ mediated the trophoblast and endometrial epithelial cells at the implantation stage. RL95-2 cells grow to confluent monolayers of a EEC line, using as the matrices, trophoblast spheroid were dispensed into 96-wells plates containing the monolayers and incubated for 24 hours. Prevention of Ca2+ influx by EDTA, EGTA, verapamil or nifedipine significantly inhibited the trophoblast spheroids outgrowth, whereas prevention of Ca2+ mobilization with BAPTA-AM also had the inhibition of trophoblast spheroid outgrowth area in a dose-dependent manner. The uterine secretion of calcitonin, a 32-amino acid peptide hormone involved in calcium homeostasis, peaks on day 4 of pregnancy in rat to mediated implantation successful. In our co-culture system, removed Ca2+ ions from the medium by EDTA, EGTA, verapamil or nifedipine respectily, prevention of Ca2+ mobilization by BAPTA-AM was due to make the decrease of [Ca2+]i, all of above experiments showed the reduced the area of trophoblast spheroid outgrowth. On the other hand, we treated calcitonin which well to know increase [Ca2+]i, shown increase of the area. In BeWo and RL95-2 cells, increase [Ca2+]i was induced by calcitonin using calcium image system in a dose-dependent manner. The increase [Ca2+]i was induced by calcitonin could be depressed by pretreated EDTA, EGTA and BAPTA-AM, or at the calcium free environment. The calcitonin induced calcium influx could be depressed in RL95-2 cells by verapamil and nifedipine, the specific L-type calcium channel blocker, partly effect in BeWo cells. Concluding above data, we suggested that the area of trophoblast outgrowth was mediated by intracellular calcium signaling. The calcium influx was induced by calcitonin, mainly across by L-type calcium channel in RL95-2 cells, but in BeWo cells were not. Interaction between trophoblast and EEC, Ca2+ play an important role to stimulate the downstream signaling pathway, involved PKC activation. In previous studies, the cytoskeleton rearrangement and migration ability was induced by PKC activation. We treated PKC inhibitor, staurosporine and verapamil, shown the decrease of the area of trophoblast spheroid outgrowth. We suggested that PKC pathway involved in trophoblast outgrowth on EEC monolayers. Pretreated with staurosporine and calphostin C could depress the expansion area of trophoblast spheroid outgrowth. We speculated that calcitonin elicited calcium influx to activate PKC pathway.
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Piger, Veronika [Verfasser]. "Einfluß immunologischer Mechanismen bei der Implantation von Embryonen und deren therapeutischer Nutzen im Rahmen des IVF-Programms / vorgelegt von Veronika Piger." 2001. http://d-nb.info/963988859/34.
Full text
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Desmarais, Joëlle. "Les interactions foeto-maternelles et l'implantation embryonnaire chez le vison." Thèse, 2007. http://hdl.handle.net/1866/18029.
Full text
40
Yang, Chun-Ru, and 楊淳茹. "The embryoid body as a model system to study the effect of heat stress on post-implantation development of mammalian embryos." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/2d654s.
Full textAbstract:
碩士國立中興大學
動物科學系所
101
The odjectives of this study were to establish an in vitro system to determine the effect of heat shock on germ layer differentiation, heat shock protein (hsp70) expression and apoptosis markers of mouse and rabbit embryoid bodies (EB). In Exp. 1, 5.5-8.5 day-old mouse fetuses and 1-7 day-old mouse EBs were collected to examine their gene expressions of the three germ layers. Results showed that Days 3 and 6 EBs are retrospectively associated with the Days 6.5 and 7.5 fetuses, respectively, in terms of the germ layer gene expressions. In Exp. 2.1, mouse EBs were subjected to heat shock and randomly allocated to one of the eight treatment groups, i.e., incubation at 37℃ for 12 h or 24 h, heat-shock at 39℃ for 12 h or 24 h, heat-shock at 41℃ for 12 h or 24 h, incubation at 37℃ for 12 h following 39℃ or 41℃ (12 h) of heat-shock treatment. TUNEL and LIVE/DEAD assays were used to inspect apoptosis of EB and western blotting for the expressions of heat shock proteins (Hsc70 and Hsp72). Our observations showed that the peripheral cell layer of EBs started to degenerate and significantly increased the apoptotic cells after heat-shock at 41℃ for 12 h or 24 h (P ＜ 0.05). When resumed to a normal culture temperature (37℃), EBs morphologically recovered from the damages progressively during further culture. The changes of gene expression in the germ layers after various treatments, namely, timing for the expressions of mesoderm marker Brachyury and the endoderm markers, α-fetoprotein (AFP) and Transthyretin (TTR), were set back for 1-2 days in the heat-shocked groups compared to the control group. In another experiment (Exp. 2.2), we determinated whether a mild heat shock could enhance thermotolerance of mEB when followed by another more severe heat shock. Mouse EBs were randomly allocated to one of the eight treatment groups, i.e., heat-shock at 39℃ for 12 h (M12) or 24 h (M24), heat-shock at 41℃ for 12 h (H12) or 24 h (H24), incubation for 12 h at 39℃ and heat-shock at 41℃for 12 h (M12H12) or 24 h (M12H24), and incubation for 24 h at 39 ℃ and heat-shock at 41 ℃ for 12 h (M24H12) or 24 h (M24H24). Results showed the expression of Casepase3 and Hsp70 were significantly decreased in the M24H24 group (P＜0.05). In Exp. 3., we tested the effect of heat shock on the germ layer differentiation of rabbit EB,apoptosis cells and Hsp72 expression. Similar results were also observed as that in mouse EB, where the peripheral cellular layer started to degenerate and significant increased apoptosis cells after heat shock (P＜0.05). Hsp72 expression significantly increased with the increases of temperatures and treatment duration. Timing for the expressions of mesoderm marker Desmin and BMP4 were also set back for 1-2 days in the heat-shocked groups (41℃) compared to the control group, but ectoderm marker Pax6 expressed 1-2 days earlier in the 39℃ heated group than the control group. Based on our current observation, we conclude that EB are similar to in vivo developing embryos in terms of their germ layer marker expression. They can be a potential model system for the study of various environmental insults to post-implantation embryos. In general, in vitro heat shock delays the expressions of germ layer marker genes of EBs, but enhances Hsp72 expressions in both mouse and rabbit systems. Further in vivo studies are required to confirm the physiologic alterations of embryo/fetus in response to the elevation of ambient temperatures.