Vasculogenesis
Mostrando 1-12 de 51 artigos, teses e dissertações.
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1. Congenital hemangioma in spondylocostal dysostosis: a novel association
Abstract Congenital hemangioma is a benign tumor caused by dysfunction in embryogenesis and vasculogenesis, which progresses during fetal life to manifest as fully developed at birth. Although hemangiomas are the most common tumor of infancy, rapidly involuting congenital hemangioma has not been described in spondylocostal dysostosis. I report the novel asso
An. Bras. Dermatol.. Publicado em: 2016-10
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2. Bone marrow mesenchymal stem cells overexpressing human basic fibroblast growth factor increase vasculogenesis in ischemic rats
Administration or expression of growth factors, as well as implantation of autologous bone marrow cells, promote in vivo angiogenesis. This study investigated the angiogenic potential of combining both approaches through the allogenic transplantation of bone marrow-derived mesenchymal stem cells (MSCs) expressing human basic fibroblast growth factor (hbFGF).
Braz J Med Biol Res. Publicado em: 08/08/2014
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3. Análise fractal da vascularização da membrana corioalantóide de embriões de codornas japonesas (Coturnix japonica submetidas a campo eletromagnético de 60 Hz.
The formation of vascular network is governed mainly by two processes, vasculogenesis and angiogenesis. In vasculogenesis, the angioblastic which are the precursors of endothelial cells arising in germ layer (mesoderm) of the yolk sac (outside the embryo body). These angioblastic organize themselves to form blood islands, differing in blood vessels where the
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 30/06/2010
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4. Effects of ethnicity on the distribution of genetic polymorphisms and haplotypes in vascular endothelial growth factor / Efeitos da etnicidade sobre a distribuição de polimorfismos geneticos e haplotipos do fator de crescimento endotelial vascular
Vascular Endothelial Growth Factor (VEGF, or also known as VEGF-A) is a homodimeric glycoprotein of 45kDa produced mostly in endothelial cells in hypoxic conditions. VEGF leads to proliferation, migration and survival of endothelial cells, plays an important role in regulating vascular permeability and angiogenesis, both physiological and pathophysiological
Publicado em: 2009
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5. Transplantation of genetically modified cardiac fibroblasts to induce angiogenesis and vasculogenesis in ischemic myocardium / Fibroblastos geneticamente modificados para estimular angiogênese e vasculogênese em miocárdio isquêmico
Este trabalho avaliou o efeito de fibroblastos cardíacos (FC) modificados geneticamente para produzir VEGF (vascular endothelial growth factor) e/ou em conjunto com IGF-1(insulin -like growth factor) associados a um biopolímero de fibrina na indução de angiogênese, vasculogênese e melhora de função em miocárdio isquêmico. Em experimentos preliminar
Publicado em: 2008
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6. Immunolocalization of VEGF, bFGF and their receptors in the bovine placenta and influence of these growth factors on progesterone production from placental cells in culture / Imunolocalização do VEGF, bFGF e seus receptores na placenta bovina e influência destes fatores sobre a produção de progesterona pelas células placentárias em cultura
Placental establishment and function are dependent on intense vascularization. Placental vasculogenesis and angiogenesis are modulated by several factors, including VEGF (vascular endothelial growth factor) and bFGF (basic fibroblast growth factor). Although the role of VEGF and bFGF during vascularization is already well established, some studies have indic
Publicado em: 2005
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7. Angiogenesis and vasculogenesis as therapeutic strategies for postnatal neovascularization
American Society for Clinical Investigation.
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8. Identification of Novel Roles of the Cytochrome P450 System in Early Embryogenesis: Effects on Vasculogenesis and Retinoic Acid Homeostasis
The cytochrome P450-dependent monooxygenase system catalyzes the metabolism of xenobiotics and endogenous compounds, including hormones and retinoic acid. In order to establish the role of these enzymes in embryogenesis, we have inactivated the system through the deletion of the gene for the electron donor to all microsomal P450 proteins, cytochrome P450 red
American Society for Microbiology.
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9. Defective placental vasculogenesis causes embryonic lethality in VHL-deficient mice
Inheritance of an inactivated form of the VHL tumor suppressor gene predisposes patients to develop von Hippel–Lindau disease, and somatic VHL inactivation is an early genetic event leading to the development of sporadic renal cell carcinoma. The VHL gene was disrupted by targeted homologous recombination in murine embryonic stem cells, and a mouse line co
National Academy of Sciences.
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10. Placental Failure and Impaired Vasculogenesis Result in Embryonic Lethality for Neuropathy Target Esterase-Deficient Mice
Age-dependent neurodegeneration resulting from widespread apoptosis of neurons and glia characterize the Drosophila Swiss Cheese (SWS) mutant. Neuropathy target esterase (NTE), the vertebrate homologue of SWS, reacts with organophosphates which initiate a syndrome of axonal degeneration. NTE is expressed in neurons and a variety of nonneuronal cell types in
American Society for Microbiology.
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11. Inhibition of endothelial progenitor cell differentiation by VEGI
Endothelial progenitor cells (EPCs) play a critical role in postnatal and tumor vasculogenesis. Vascular endothelial growth inhibitor (VEGI; TNFSF15) has been shown to inhibit endothelial cell proliferation by inducing apoptosis. We report here that VEGI inhibits the differentiation of EPCs from mouse bone marrow–derived Sca1+ mononuclear cells. Analysis o
American Society of Hematology.
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12. c-Myc is essential for vasculogenesis and angiogenesis during development and tumor progression
c-Myc promotes cell growth and transformation by ill-defined mechanisms. c-myc−/− mice die by embryonic day 10.5 (E10.5) with defects in growth and in cardiac and neural development. Here we report that the lethality of c-myc−/− embryos is also associated with profound defects in vasculogenesis and primitive erythropoiesis. Furthermore, c-myc−/−
Cold Spring Harbor Laboratory Press.