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  • 2003  (3)
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  • 2003  (3)
  • 1
    Language: English
    In: European Journal of Obstetrics and Gynecology, 2003, Vol.110, pp.S10-S18
    Description: An adequate nutrient and substrate supply is essential for normal intrauterine development of the fetus. Disturbances in uterine blood supply are associated with higher perinatal morbidity and mortality caused by preterm delivery, pre-eclampsia or intrauterine growth restriction. Adaptation of the uterine vasculature to the rising needs of the fetus occurs through both vasodilation and development of new vessels. Angiogenesis is the process of neovascularization from pre-existing blood vessels in response to hypoxia or substrate demands of tissues. The endometrium, decidua and placenta are sources rich of angiogenic growth factors. In general, the angiogenic process is initiated by growth factors such as bFGF, VEGF, or placental growth factor (PlGF). Through a complex signal transduction machinery mediated by respective receptor-tyrosine kinases, an increase in the permeability of the maternal vessels is achieved to permit growth and invasion of endothelial cells. Their chemotactic migration, formation of a vessel lumen, and functional maturation of new capillaries complete the angiogenic process that involves the expression of specific adhesion receptors and extracellular matrix-degrading proteases. During vasculogenesis, endothelial progenitor cells—angioblasts—form a primitive vascular network. This process occurs mainly during fetal development, although recruitment of angioblasts from bone marrow and peripheral blood in response to ischemic insult have been described in adults. Our recent data indicate a novel function for human chorionic gonadotropin (hCG), a hormonal factor of trophoblastic origin in uterine adaptation to early pregnancy as well as in tumor invasion and underline the importance of hCG as an yet unrecognized angiogenic factor. Although there are striking similarities between, on the one hand, tumor invasion and tumor-induced vascularization and, on the other hand, trophoblast invasion and placental development, our understanding of the different molecular and functional aspects of these two different processes, in particular, the self-limitation of the trophoblastic invasion and vessels formation during gestation might allow the establishment of new therapeutic strategies for the treatment of both tumor and pregnancy related pathology.
    Keywords: Tumor ; Pregnancy ; Pathology ; Angiogenesis ; Vasculogenesis ; Hcg ; Medicine
    ISSN: 0301-2115
    E-ISSN: 1872-7654
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  • 2
    Language: English
    In: European journal of obstetrics, gynecology, and reproductive biology, 22 September 2003, Vol.110 Suppl 1, pp.S10-8
    Description: An adequate nutrient and substrate supply is essential for normal intrauterine development of the fetus. Disturbances in uterine blood supply are associated with higher perinatal morbidity and mortality caused by preterm delivery, pre-eclampsia or intrauterine growth restriction. Adaptation of the uterine vasculature to the rising needs of the fetus occurs through both vasodilation and development of new vessels. Angiogenesis is the process of neovascularization from pre-existing blood vessels in response to hypoxia or substrate demands of tissues. The endometrium, decidua and placenta are sources rich of angiogenic growth factors. In general, the angiogenic process is initiated by growth factors such as bFGF, VEGF, or placental growth factor (PlGF). Through a complex signal transduction machinery mediated by respective receptor-tyrosine kinases, an increase in the permeability of the maternal vessels is achieved to permit growth and invasion of endothelial cells. Their chemotactic migration, formation of a vessel lumen, and functional maturation of new capillaries complete the angiogenic process that involves the expression of specific adhesion receptors and extracellular matrix-degrading proteases. During vasculogenesis, endothelial progenitor cells--angioblasts--form a primitive vascular network. This process occurs mainly during fetal development, although recruitment of angioblasts from bone marrow and peripheral blood in response to ischemic insult have been described in adults. Our recent data indicate a novel function for human chorionic gonadotropin (hCG), a hormonal factor of trophoblastic origin in uterine adaptation to early pregnancy as well as in tumor invasion and underline the importance of hCG as an yet unrecognized angiogenic factor. Although there are striking similarities between, on the one hand, tumor invasion and tumor-induced vascularization and, on the other hand, trophoblast invasion and placental development, our understanding of the different molecular and functional aspects of these two different processes, in particular, the self-limitation of the trophoblastic invasion and vessels formation during gestation might allow the establishment of new therapeutic strategies for the treatment of both tumor and pregnancy related pathology.
    Keywords: Neovascularization, Physiologic ; Pregnancy -- Physiology
    ISSN: 0301-2115
    Source: MEDLINE/PubMed (U.S. National Library of Medicine)
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  • 3
    In: The Journal of Clinical Endocrinology & Metabolism, 2003, Vol.88(10), pp.4811-4817
    Description: Adaptation of the maternal uterine vasculature is essential for normal fetal and placental development in which angiogenesis is considered one of the most critical adaptive changes during pregnancy. Highly expressed in cytotrophoblasts and maternal endothelial cells during pregnancy, IGF-II promotes cell migration and regulates fetal and placental growth. We hypothesized that IGF-II regulates uterine angiogenesis during pregnancy. Both uterine vasculature and isolated uterine microvascular endothelial cells expressed high levels of IGF-II and IGF-II/mannose-6 phosphate receptor mRNA as shown by in situ hybridization. Physiological concentrations of IGF-II significantly increased vessel formation, as shown by a three-dimensional angiogenesis assay in vitro or a chicken chorionallantoic membrane assay in vivo. The angiogenic response of IGF-II could be reversed by the addition of β-galactosidase or rabbit-antihuman IGF-II/M6P receptor antiserum, whereas blocking antibodies against IGF-I receptor or insulin receptor influenced IGF-II-induced sprout formation. IGF-II promoted migration of endothelial cells (10-250 ng/ml) tested in a modified Boyden chamber, but no stimulating effect on proliferation was observed. The application of several intracellular signal transduction molecules and their inhibitors indicated that protein kinase C and Gi protein might play a role in the IGF-II-induced angiogenesis. Our results suggest an important angiogenic role of IGF-II in the vascular adaptation to pregnancy.
    Keywords: Medicine;
    ISSN: 0021-972X
    E-ISSN: 19457197
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