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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

Cellular characteristics of canine trophoblasts

Sahlfeld, Laura 18 May 2012 (has links)
This research investigated the development of a novel canine model to study preeclampsia. Normal canine placental development has morphologic and histologic similarities to the shallow trophoblast invasion occurring with preeclampsia in humans, which makes the dog a particularly good choice for modeling this disease and will be an improvement on existing animal models. Preeclampsia is a pregnancy-specific syndrome, occurring in mild (late onset) and severe (early onset) forms. Severe preeclampsia is a major cause of maternal, fetal, and neonatal morbidity and mortality worldwide. It affects 0.35-1.40% of human pregnancies. Despite intense investigation, the cause (and therefore the prevention or treatment) of shallow trophoblast invasion in preeclampsia remains largely unknown. In a normal human pregnancy, trophoblasts invade the endometrium and myometrium as well as the maternal blood vessels (hemochorial placentation). In preeclampsia, trophoblast invasion is shallow and vascular transformation incomplete. In contrast to the normal human placenta, trophoblasts within the canine placenta only invade to the level of the endothelial cells within the maternal blood vessels (endotheliochorial). In this way, normal canine placental development is similar to preeclampsia. The hypothesis of this research was that isolated canine trophoblasts will express similar proteins as human preeclamptic trophoblasts. The objectives of the research were to (1) isolate canine trophoblasts from fresh and cryogenically frozen placenta and (2) perform immunocytochemistry and immunohistochemistry on canine trophoblasts for proteins expressed in human preeclamptic trophoblasts. Cellular morphology was similar to that reported for trophoblasts. More than 97% of the cells cultured expressed cytokeratin-7. Although both matrix metalloproteinases (MMPs) were immunolocalized to the cytoplasm, MMP2 was found in large, coalescing granules, whereas MMP9 was more diffusely expressed throughout the cell. More cultured canine trophoblasts expressed MMP9 (54.7±3.4%) compared to MMP2 (40.3±1.8%) (p=0.02). Cryopreserving placental tissue prior to primary cell culture had no effect on cell proliferation (p=0.37). Relaxin, vascular endothelial growth factor, and tissue inhibitor of metalloproteinase 2 were positively expressed in primary canine trophoblasts. Immunohistochemical results revealed CK-7, MMP9, TIMP2 and relaxin was expressed in trophoblasts along the villous margin with MMP9, TIMP2 and relaxin extending towards the basement membrane. S100A4 was minimally expressed in the basement membrane. MMP2 was strongly expressed within the basement membrane. CK-7, MMP2, MMP9 & TIMP2 were all immunolocalized to the same cells in canine placental sections as previously described in human preeclamptic placental sections. These results have demonstrated the cellular similarities in protein expression between normal canine and human preeclamptic trophoblasts thereby confirming this model is suitable for further studies. / Graduation date: 2012
2

Human trophoblast invasion

Oefner, Carolin Melati January 2015 (has links)
No description available.
3

Glycodelin-A as a modulator of trophoblast invasion

Lam, Ka-wai, 林嘉維 January 2010 (has links)
published_or_final_version / Obstetrics and Gynaecology / Doctoral / Doctor of Philosophy
4

Adrenomedullin as a modulator of human trophoblast invasion

Wong, Siu-tak., 黃兆德. January 2012 (has links)
During placental development, human trophoblasts differentiate along two pathways leading to the formation of the extravillous cytotrophoblasts (EVCT) and the villous cytotrophoblasts. EVCTis responsible for trophoblast invasion, which is an important process for successfulplacentation in early pregnancy.Dysregulation of the process is associated with a wide range of pregnancy complications, including intrauterine growth restriction, preeclampsia and choriocarcinoma. EVCTsproducematrix metalloproteinase and urokinase plasminogen activator(uPA)that degrade the extracellular matrix of the endometrium for the invasion process. Adrenomedullin is a 52-amino acid polypeptide belonging to the calcitonin/calcitoningene-related peptide/amylin peptide family. The expression of adrenomedullin in trophoblasts is most abundant in the first-trimester human placentas, consistent with the involvement of the molecule in early placentation. Most of the studies on adrenomedullin concentrate on its vasodilatory activity. Studies on the action of adrenomedullin in human trophoblast functions are limited. Therefore the role of adrenomedullin in early placentation is not known. The hypothesis of this project is that adrenomedullin regulates the invasion of human EVCT. Two human EVCT cell lines, JEG-3 and TEV-1 were used as study models in this project. The functions of adrenomedullin aremediated through a receptor system composedof two transmembrane components, the calcitonin receptor-likereceptor and receptor activity-modifying protein(RAMP). Adrenomedullin binds to calcitoninreceptor-likereceptorwhen coupled with RAMP2 or RAMP3. Immunostaining, western blotting and RT-PCR demonstrated the presence of these components on EVCT cell lines. Adrenomedullin treatment significantly enhanced invasiveness, migration, but not proliferation in EVCT as demonstrated by transwell invasion assay, transwell migration assay and cell proliferation assayrespectively. The adrenomedullin antagonist, adrenomedullin22-52, blocked the effects of adrenomedullin on EVCT cell lines, confirming adrenomedullin exerted its biological effects through its classical receptors. RT-PCR results further demonstrated that while adrenomedullin treatment had no effect on matrix metalloproteinase-2 expression, it up-regulated uPA expression and activity. Silencingof uPA by siRNA transfection abolished the stimulatory effect of adrenomedullin, suggesting uPA is the key mediator for adrenomedullin-induced invasion. Adrenomedullin increased nitric oxide synthase expression and nitric oxide (NO) production in JEG-3 cells. The involvement of NO in adrenomedullin-induced EVCT invasion and biosynthesis of uPAwas confirmed bypharmacologicalstudy using nitric oxide synthase inhibitorsor NO donors.Protein kinase G was shown to be one of the downstream regulator of NO that mediated the adrenomedullin-induced EVCT invasion. By using a biotin-switch based method to purify theS-nitrosylated proteins, adrenomedullin was further demonstrate to up-regulate the NO-dependent S-nitrosylation in EVCTs.Interestingly, S-nitrosylation of uPA in vitro induced a higher proteinaseactivitywhich may be responsiblefor the stimulatory action of adrenomedullin. In conclusion, thisstudyhas provided evidence that adrenomedullin modulates EVCT invasion by regulating the uPA expression andactivity through NO signaling pathway. Abnormal trophoblast invasion can lead to a range of major pregnancy complications. The outcome of this project enhanced our understanding of the mechanisms that regulate trophoblast invasion. These data could constitute the basis for new therapeutic strategies of the diseases in the future. / published_or_final_version / Obstetrics and Gynaecology / Doctoral / Doctor of Philosophy
5

ROLE OF ACTIVATED MACROPHAGES AND PRO-INFLAMMATORY CYTOKINES IN PLACENTAL TROPHOBLAST INVASION AND FETAL OUTCOME

Renaud, STEPHEN 30 September 2008 (has links)
The invasion of trophoblast cells into the uterine wall is an essential component of normal human pregnancy. These trophoblast cells transform the uterine spiral arterioles into high-flow, low-resistance vessels that supply the placenta to support fetal growth and development. Inadequate trophoblast invasion and spiral arteriole remodelling may result in excessive placental pathology leading to pre-eclampsia and intra-uterine growth restriction (IUGR), which are major causes of maternal and fetal morbidity and mortality. These pregnancy complications have also been linked to an increased presence of pro-inflammatory cytokine-secreting (activated) macrophages at the fetal-maternal interface. In particular, increased production of tumour necrosis factor-alpha (TNF) by activated macrophages has been implicated as a causative factor mediating various pregnancy complications. Results from this thesis showed that macrophage-derived TNF decreased the invasiveness of trophoblast cells, primarily by affecting the urokinase system of plasminogen activators, a network of proteases that promotes cellular invasion. TNF also stimulated the production of macrophage chemoattractants by trophoblast cells, providing a putative mechanism for the aberrant recruitment and localization of macrophages in complicated pregnancies. Administration of lipopolysaccharide (LPS), a potent stimulator of macrophage activation and TNF production, to pregnant rats resulted in IUGR and fetal death correlating with significant placental pathology, including displaced endovascular trophoblast cells and increased fibrinoid and macrophage accumulation at the fetal-maternal interface. The immunoregulatory cytokine interleukin-10, which inhibited TNF production from macrophages after LPS-exposure, completely prevented the adverse effects of TNF in vitro and in vivo. Collectively, these findings show that the aberrant presence and localization of TNF-secreting macrophages may be involved in the etiology and pathophysiology of various pregnancy-related complications. / Thesis (Ph.D, Anatomy & Cell Biology) -- Queen's University, 2008-09-29 16:32:00.845
6

Characterisation of the possible trophoblast progenitor niches in first trimester human placentas

Lee, Qin En Cheryl January 2014 (has links)
No description available.
7

MHC class I expression on human trophoblast

Ellis, Shirley A. January 1990 (has links)
No description available.
8

The quantification of nitric oxide production in pregnant and non-pregnant women

Ramsay, Bruce January 1997 (has links)
No description available.
9

Zelluläre Interaktionen während der plazentaren Vaskularisation : Modell der plazentaren Vaskulogenese unter besonderer Berücksichtigung der Rolle des Trophoblasten /

Baal, Nelli. January 2007 (has links)
Zugl.: Giessen, Universiẗat, Diss., 2007.
10

Zelluläre Interaktionen während der plazentaren Vaskularisation Modell der plazentaren Vaskulogenese unter besonderer Berücksichtigung der Rolle des Trophoblasten /

Baal, Nelli. January 2007 (has links) (PDF)
Zugl.: Giessen, Universiẗat, Diss., 2007.

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