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Rozprawy doktorskie na temat „Vascular endothelial growth factor”

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Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 20 lutego 2023

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1

Krishnan, Jaya. "The role of vascular endothelial growth factor receptor 3, and its ligands vascular endothelial growth factor C and vascular endothelial growth factor D in tumour metastasis and haematopoeisis". Thesis, University of London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270576.

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2

Prahst, Claudia. "Neuropilin-vascular endothelial growth factor signaling in endothelial cells". [S.l. : s.n.], 2007. http://nbn-resolving.de/urn:nbn:de:bsz:25-opus-51230.

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3

Botelho, Francisco José dos Santos. "Vascular endothelial growth factor and prostate cancer". Master's thesis, Faculdade de Medicina da Universidade do Porto, 2009. http://hdl.handle.net/10216/22291.

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Botelho, Francisco José dos Santos. "Vascular endothelial growth factor and prostate cancer". Dissertação, Faculdade de Medicina da Universidade do Porto, 2009. http://hdl.handle.net/10216/22291.

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5

Jacobsen, Jan. "Vascular endothelial growth factor in renal cell carcinoma". Doctoral thesis, Umeå : Kirurgisk och perioperativ vetenskap, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-713.

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6

Wang, Wenying. "Angiogenesis mediated by vascular endothelial growth factor (VEGF)". Thesis, University of Bristol, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419061.

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7

Roberts, Selene Karen. "Signalling via vascular endothelial growth factor receptor complexes". Thesis, University of Leicester, 2005. http://hdl.handle.net/2381/29705.

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This study sought to investigate the role of various components of VEGF receptor signalling complexes using fluorescence microscopy to complement conventional biochemical techniques. Using DsRedII-Grp1 to visualise the product of the reaction catalysed by PI3K, activation of PI3K downstream of VEGF receptor-2 is shown. There was no obvious relocalisation of p85 to phosphorylated receptors however a small amount of GFP-p85 associates with, and is phosphorylated in response to, activated VEGF receptor-2. The Shc-related adaptor ShcB/Sck was localised to the plasma membrane in stimulated endothelial cells and associated with activated VEGF receptor-2. PTB and SH2 protein domains, contained within Sck, facilitated these events. Key tyrosine amino acids found within Grb2 binding motifs of ShcA and Sck were phosphorylated in response to VEGF. Tyrosine residues 315 and 316 of Sck were phosphorylated to a greater extent when compared to the corresponding residues of ShcA. Cells expressing Sck proteins lacking tyrosine phosphorylation sites showed a reduced amount of phospho-ERK and DNA synthesis. VEGF receptor-2 was internalised and degraded in response to VEGF. This occurred, at least in part, through the conventional endocytic pathway. VEGF receptor-2 is localised in caveolin-1 and EEA-1 containing vesicles, which is suggestive of internalisation via caveolae and/or early endosomes. Nedd4 co-localises with VEGF receptor-1 at regions of the plasma membrane and this association was confirmed by co-immunoprecipitation. The over-expression of Nedd4 enhanced the degradation of VEGF receptor-1.

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8

Aase, Karin. "On vascular endothelial growth factor B and platelet-derived growth factor C : two members of the VEGF/PDGF family of growth factors /". Stockholm : Karolinska Univ. Press, 2001. http://diss.kib.ki.se/2001/91-89428-14-5/.

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9

Ng, Hoi-man, i 伍凱敏. "Regulation of vascular endothelial growth factor by ginsenoside RG1 inhuman endothelial cells". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43955915.

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10

Fearnley, Gareth William. "Vascular endothelial growth factor A isoform-specific regulation of endothelial cell function". Thesis, University of Leeds, 2015. http://etheses.whiterose.ac.uk/10721/.

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Vascular endothelial growth factor A (VEGF-A) binding to the receptor tyrosine kinase (RTK) vascular endothelial growth factor 2 (VEGFR2) triggers an array of downstream signal transduction pathways which modulate a multitude of endothelial cell responses, such as cell migration, proliferation, tubulogenesis and cell-cell interactions. Multiple splice isoforms of VEGF-A exist, yet it is unclear how different VEGF-A isoforms bind to the same RTK to program distinct cellular responses. The work presented in this PhD thesis evaluated VEGF-A isoforms for their ability to program VEGFR2 endocytosis, post-translational modification, proteolysis and terminal degradation. Such changes in VEGFR2 status were linked to downstream signal transduction and gene expression, with relevance to cell function and vascular physiology. VEGF-A isoforms differentially promoted VEGFR2 tyrosine transautophosphorylation and endocytosis. Different VEGFR2-VEGF-A complexes exhibit altered ubiquitination, a hallmark of trafficking through the endosome-lysosome system for subsequent terminal degradation and proteolysis. VEGF-A isoform-specific VEGFR2 phosphorylation coupled with endocytosis and delivery to early endosomes is required for isoform-specific activation of the MEK1-ERK1/2 signal transduction pathway and endothelial cell proliferation. VEGF-A isoforms also exhibited differences in their ability to stimulate arterial regeneration in a mouse hind limb ischaemia model. VEGF-A isoform-specific ERK1/2 activation was essential for the phosphorylation of activating transcription factor 2 (ATF-2) at residue T71. Differential activation of ATF-2 regulated VEGF-A isoform-specific gene transcription (e.g. VCAM-1) and endothelial cell responses, such as leukocyte recruitment. Additionally, basal ATF-2-pT71 levels are required to maintain endothelial cell cycle commitment, via repressing p53-dependent gene transcription. Furthermore, VEGF-A isoforms promoted differential PLC1 phosphorylation and a subsequent isoform-specific increase in cytosolic calcium ions. A functional consequence of this VEGF-A isoform-specific calcium ion flux, was differential dephosphorylation and subsequent nuclear translocation of the transcription factor NFATc2 (NFAT1) in order to regulate endothelial cell migration. Thus, this study provides a mechanistic framework for understanding how different ligand isoforms differentially program RTK functionality in health and disease.

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11

Grad, Sibylle. "Regulation und Expression von vascular endothelial growth factor (VEGF) /". [S.l.] : [s.n.], 1999. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=13214.

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12

Knight, Emma Lavinia. "Signalling pathways downstream of vascular endothelial growth factor receptors". Thesis, University of Leicester, 2001. http://hdl.handle.net/2381/29663.

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Vascular endothelial growth factor (VEGF) is an essential angiogenic factor for formation of the embryonic vasculature, and also has important roles in pathological conditions such as diabetic retinopthy, rheumatoid arthritis and cancer. Although the signalling pathways induced by VEGF have been well-studied, the precise molecular mechanisms remain to be determined, particularly with respect to the relative contribution of the individual receptors. Two main VEGF receptors are expressed in endothelial cells: VEGFR-1 and VEGFR-2. To identify novel effectors downstream of these receptors, their intracellular domains were used as bait to screen yeast two-hybrid cDNA libraries. The association of potential effector proteins with the VEGFRs were assessed in both yeast and mammalian cells, and the identity of the interacting residues was probed using site-directed mutagenesis and peptide competition experiments. These data revealed previously unreported interactions between VEGFRs and WW domain-containing proteins - interactions that could have important implications for the mechanisms regulating VEGF expression. Analysis of phosphorylation-dependent interactions downstream of VEGFR-1 in mammalian cells, which is generally hindered by the lack of ligand-induced receptor phosphorylation, was enabled by the development of chimeric receptors. In these constructs, the intracellular domains of the VEGFRs were fused downstream of the dimerization domain of the GyrB subunit of bacterial DNA gyrase. The chimeric receptors were significantly activated in response to ligand, thereby enabling studies of this signalling with the putative effectors PKB/Akt, PLC and ERK1.2. Both chimeric receptors were able to activate these effectors. In addition, the observed dependence of some of these effects on a specific tyrosine residue within VEGFR-2 suggested that the chimeric receptors couple to downstream effectors in a manner analogous to that of the full-length receptors.

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13

Gilmore, Louisa Jean. "Synthetic polymers for interaction with vascular endothelial growth factor". Thesis, University of Sheffield, 2010. http://etheses.whiterose.ac.uk/15109/.

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14

Grunstein, Jeremy. "The role of vascular endothelial growth factor in tumorigenesis /". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2000. http://wwwlib.umi.com/cr/ucsd/fullcit?p9981953.

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15

Brockelsby, Jeremy Charles. "Pre-eclampsia : the role of vascular endothelial growth factor and its interaction with the vascular endothelium". Thesis, University of Nottingham, 2001. http://eprints.nottingham.ac.uk/11836/.

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Hypothesis: This thesis set out to test the hypothesis first proposed by Baker et al (1995) that Vascular Endothelial Growth Factor (VEGF) may be involved in the alteration in endothelial function that is observed in the disease of pre-eclampsia. Aims: To investigate concentrations of VEGF in plasma from non-pregnant, and normal pregnant women and women with pre-eclampsia. To investigate uterine and placental expression of VEGF in non-pregnant, normal pregnant women and women with pre-eclampsia. To investigate some of the vascular adaptations that occur in pregnancy and pre-eclampsia within the uterine and systemic circulations. To investigate the effect of plasma from women with PE and VEGF on i) An in vitro endothelial cell culture model. ii) An in vitro isolated vessel model. To characterise the mechanism whereby VEGF causes any alteration in vascular function.

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16

Wendt, Astrid [Verfasser]. "Korrelation von placental growth factor, vascular endothelial growth factor und soluble vascular endothelial growth factor receptor-1 im Serum mit Tumorstadien und Prognose des hepatozellulären Karzinoms / Astrid Wendt". Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2020. http://d-nb.info/1212435109/34.

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17

Ng, Hoi-man. "Regulation of vascular endothelial growth factor by ginsenoside RG1 in human endothelial cells". Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43955915.

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18

Eriksson, Anna. "Molecular mechanisms of VEGF-family-mediated angiogenesis and vascular permeability /". Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-361-9/.

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19

Clayton, Jason Allen Faber James E. "Role of vascular endothelial growth factor-A in collateral growth and development". Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,2111.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2008.
Title from electronic title page (viewed Feb. 17, 2009). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Cell and Molecular Physiology." Discipline: Cell and Molecular Physiology; Department/School: Medicine.

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20

Kumar, Harish. "The study of vascular endothelial growth factor in colorectal cancer". Thesis, University of Hull, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.411900.

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21

Núñez, Daniel A. "Experimental estimate of the diffusivity of Vascular Endothelial Growth Factor". Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/36721.

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Thesis (S.B.)--Massachusetts Institute of Technology, Dept. of Mechanical Engineering, 2006.
Includes bibliographical references (leaf 16).
The diffusivity of Vascular Endothelial Growth Factor (VEGF) is a number that is very important in determining the transport of VEGF. The transport of VEGF determines crucial processes such as angiogenesis and vasculogenesis. This study aimed at obtaining an estimate of the diffusivity of VEGF by using a simple system consisting of an insert with a collagen membrane placed within the well of a cell culture plate. A solution of VEGF was added to the insert, and the same solution without VEGF was added to the well surrounding the insert. The VEGF diffusion was monitored by taking samples in time of both the upstream and downstream baths, and analyzing the samples with an ELISA. Modeling the diffusion as one-dimensional, it was possible to estimate the diffusivity from the change in downstream concentration with time. The diffusivity was estimated to be around 5.55e⁻⁷ cm²sec.
by Daniel A. Nunez.
S.B.

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22

Cudmore, Melissa Jane. "Novel functions of angiopoietins and vascular endothelial growth factor receptors". Thesis, University of Birmingham, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.434712.

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23

Foster, Rebecca Rachael. "The effects of vascular endothelial growth factor on podocyte biology". Thesis, University of Bristol, 2004. http://hdl.handle.net/1983/19d27014-82f5-417e-b92e-ef78b8b632a6.

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24

Plehutsa, O., A. Sydorchuk, P. Fomin, I. Sydorchuk, R. Sydorchuk, L. Sydorchuk, S. Levites i A. Vinohradskyy. "Why targeting vascular endothelial growth factor is not sufficiently effective?" Thesis, «Targeted Therapies in Hepatologu» Worshop.- Abstract Book (Hannover, Germany, January 24-25, 2013). – P.29, 2013. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/7383.

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25

Athanassiades, Andrew. "The role of vascular endothelial growth factor and placenta growth factor in human trophoblast function". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0010/MQ28535.pdf.

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26

Liisanantti, M. (Marja). "Phosphatidylethanol in lipoproteins as a regulator of vascular endothelial growth factor in vascular wall cells". Doctoral thesis, University of Oulu, 2005. http://urn.fi/urn:isbn:9514278666.

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Abstract Phosphatidylethanol (PEth) is an abnormal phospholipid formed only in the presence of ethanol. Ethanol causes changes in the concentration and composition of plasma lipoproteins and it also influences the enzymes and transfer proteins that modify lipoproteins in plasma. PEth might be one of these changes brought on by ethanol in the circulation. The present study was designed to investigate whether qualitative changes in high density lipoprotein (HDL) phospholipids caused by ethanol can mediate the beneficial effects of alcohol on atherosclerosis, and to investigate the transfer of PEth between lipoproteins and the effects of PEth on the charge of lipoprotein particles. PEth was shown to be transferred from low density lipoproteins (LDL) to HDL particles mainly by transfer proteins other than cholesteryl ester transfer protein (CETP). The transfer of PEth between lipoproteins enables the redistribution of PEth between lipoproteins in plasma. The results of this study provide evidence that PEth in HDL particles stimulates the vascular endothelial growth factor (VEGF) secretion from vascular wall cells. The increase in the secretion was mediated through protein kinase C (PKC) and mitogen-activated protein kinase (MAPK) signalling pathways. PEth-containing HDL particles were able to increase the VEGF secretion in rats in vivo. Similar effects were also observed when rats were given HDL particles isolated from the plasma of alcoholics. The PEth-induced change in the electrical charge of lipoproteins may affect the binding of lipoproteins to their receptors and binding proteins. The effects of PEth on the secretion of VEGF from the endothelial cells were shown to be mediated through HDL receptor. The changes in HDL particles caused by phosphatidylethanol may modify the metabolism of lipoproteins and lipid-mediated signalling pathways regulating VEGF in vascular wall cells.

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27

Rubins, Leigh Ruth. "Recombinant antibody fragments to vascular associated targets of human tumours". Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.369066.

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Chen, Jing. "Mechanism of induction of vascular endothelial growth factor (vegf) in osteoarthritis". Diss., Columbia, Mo. : University of Missouri-Columbia, 2006. http://hdl.handle.net/10355/4616.

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Thesis (M.S.)--University of Missouri-Columbia, 2006.
"December 2006" The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Includes bibliographical references.

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張毅 i Ngai Cheung. "Expression of vascular endothelial growth factor and its receptors in tumours". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31220587.

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30

McElhinney, B. R. "Vascular endothelial growth factor and the ovarian response to iatrogenic stimulation". Thesis, Queen's University Belfast, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.395369.

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Cheung, Ngai. "Expression of vascular endothelial growth factor and its receptors in tumours /". Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B20720981.

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Logan, Patrick. "Vascular endothelial growth factor-A expression and role in uveal melanoma". Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=119440.

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Introduction: Uveal melanoma (UM) is an intraocular tumor that affects 4-6 people per million in the United States, 40% of which will develop liver metastasis within five years. Vascular endothelial growth factor A (VEGF-A) has been extensively studied in cancer due to the requirement for additional vasculature in tumors. Bevacizumab is a humanized monoclonal antibody that binds VEGF-A and is approved for the treatment of various malignancies. Herein, we investigated the expression of VEGF-A in three UM cell lines and the effects of inhibiting VEGF-A on their functional abilities. We also determined if positive VEGF-A expression can predict metastasis in a UM model and in patients. Materials and Methods: VEGF-A secretion was evaluated in three UM cell lines using sandwich ELISA. Proliferation, migration, and invasion assays were performed before and after the administration of bevacizumab and cytokine expression was assessed by ELISA. One cytokine that was upregulated following bevacizumab treatment (CCL3) was knocked down using siRNA, and the functional assays were repeated using CCL3 siRNA and combination treatments. Uveal melanoma tumors (n = 27) from an animal model and tumors from human patients (n = 29) were immunostained for VEGF-A. Two different custom immunostaining quantification algorithms implemented with ImageJ software were used to automatically count positive cells and positive staining area. Binary logistic regression was performed to determine if positive staining could predict metastases. P < 0.05 was considered significant. Results: All three UM cell lines produced and secreted VEGF-A and expressed VEGF-R2. Bevacizumab usurped VEGF-A and reduced phosphorylated-VEGF-R2. Proliferation and migration were reduced following bevacizumab treatment (p < 0.05 for one cell line, and p < 0.05 for two cell lines, respectively). Both CCL3 and MMP-9 were significantly upregulated after bevacizumab treatment in all cell lines (p < 0.05). Proliferation was significantly reduced in all three cell lines following CCL3 siRNA and combination treatments (p < 0.05). Migration was significantly reduced in all three cell lines after combination treatment (p < 0.05) and invasion was significantly reduced in two cell lines following siRNA (p < 0.05). In general, combination therapy was more effective than bevacizumab monotherapy for inhibiting UM functional abilities. In both rabbit and human tissue, VEGF-A positivity could be used to significantly predict metastasis (p > 0.05). Conclusions: Auto and paracrine VEGF-A signalling is abundant in UM cell lines, but inhibiting VEGF-A has only moderate effects on their functional abilities. This is attributable to compensatory effects, including the upregulation of CCL3. In addition, VEGF-A staining correlated with metastatic development in our patient cohort. VEGF-A is a powerful cytokine that may play a role in UM development and progression. However, compensatory effects induced by bevacizumab suggest that dual or multiple therapies may be required to effectively treat this tumor.
Introduction: Le mélanome uvéal (MU) est une tumeur intra-oculaire qui affecte 4 à 6 personnes par million aux États-Unis, dont 40% développeront des métastases du foie dans les cinq ans. Le facteur de croissance vasculaire endothélial A (VEGF-A) a été largement étudié sur le cancer en raison de l'exigence de la vascularisation des tumeurs supplémentaires. Le bevacizumab est un anticorps monoclonal humanisé qui se lie au VEGF-A et il est approuvé pour le traitement de diverses tumeurs malignes. Ici, nous avons étudié l'expression du VEGF-A dans trois lignées cellulaires du MU et les effets de l'inhibition du VEGF-A sur leurs capacités fonctionnelles. Nous avons également déterminé si VEGF-A positif d'expression ne peut prédire les métastases dans un modèle UM et chez les patients. Matériaux et méthodes: VEGF-A sécrétion a été évaluée dans trois lignées cellulaires du MU en utilisant ELISA en sandwich. Des tests de prolifération, la migration et l'invasion ont été réalisés avant et après l'administration de l'expression des cytokines et bevacizumab a été évaluée par ELISA. Une cytokine qui a été régulée à la hausse après le traitement bevacizumab (CCL3) a été renversée à l'aide de siRNA, et les tests fonctionnels ont été répétés en utilisant CCL3 siRNA et des traitements combinés. Des tumeurs de MU (n = 27) provenant d'un modèle animal et des tumeurs provenant de patients humains énucléés (n = 29) ont été immunocolorées pour le VEGF-A. Deux différents algorithmes de quantification immunomarquage mis en œuvre avec le logiciel ImageJ ont été utilisés pour compter automatiquement des cellules positives pour la région et une coloration positive. La régression logistique binaire a été effectuée pour déterminer si une coloration positive pouvait prédire les métastases. P <0,05 était considérée comme significative. Résultats: Les trois lignées cellulaires de MU ont produites et sécrétées du VEGF-A et ont exprimées du VEGF-R2. Le bevacizumab usurpé VEGF-A et réduit phosphorylée-VEGF-R2. La prolifération et la migration ont été réduites à la suite du traitement par le bevacizumab (p <0,05 pour une lignée cellulaire, et p <0,05 pour les deux lignées cellulaires, respectivement). Les deux CCL3 et MMP-9 étaient significativement augmentés à la hausse après le traitement par le bevacizumab dans toutes les lignées cellulaires (p <0,05). La prolifération a été réduite de façon significative dans les trois lignées cellulaires à la suite CCL3 siRNA et des traitements combinés (p <0,05). La migration a été significativement réduite dans les trois lignées cellulaires après le traitement combiné (p <0,05) et l'invasion a été considérablement réduite dans les deux lignées cellulaires suivantes siRNA (p <0,05). En général, la thérapie combinée était plus efficace que la monothérapie bevacizumab pour inhiber les capacités fonctionnelles du MU.Dans les deux lapins et les tissus humains, la présence du VEGF-A pourrait être utilisée pour prédire de façon significative des métastases (p> 0,05). Conclusions: La signalisation autocrine et paracrine du VEGF-A est abondante dans les lignées cellulaires du MU, mais l'inhibition du VEGF-A n'a que des effets modérés sur ses capacités fonctionnelles. Cette situation est attribuable à des effets compensatoires, y compris la régulation positive du CCL3. En outre, le VEGF-A coloration peuvent être utilisées pour identifier les patients prédisposés au développement métastatique. Le VEGF-A est une cytokine puissante qui peut jouer un rôle dans le développement et la progression du MU. Cependant, les effets compensatoires induits par le bevacizumab suggèrent que les thérapies doubles ou multiples peuvent être nécessaires pour traiter efficacement ce type de tumeur.

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Anderl, Jeffrey Neil. "PLGA microsphere formulations for sustained local delivery of vascular endothelial growth factor : considerations for therapeutic angiogenesis of infarcted myocardium /". Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/8110.

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Roche, Rebecca I. "Role of RNA Processing Factors in the Expression of Flt-1 and its Secreted Variant, sFlt-1". Diss., Virginia Tech, 2005. http://hdl.handle.net/10919/29632.

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Vascular endothelial growth factor (VEGF) is an endothelial cell mitogen involved in angiogenesis, the formation of new blood vessels. sFlt-1, a secreted form of the signal-transducing VEGF receptor Flt-1, can inhibit cellular responses to VEGF both in vitro and in vivo. sFlt-1 is generated by alternative pre-mRNA processing; removal of Flt-1 intron 13 by splicing produces the mRNA for transmembrane Flt-1, whereas cleavage/polyadenylation within this intron, preserving the exon 13/intron 13 junction, yields sFlt-1 mRNA. Despite the likely importance of sFlt-1 in VEGF signaling, little is known about the regulation of its expression. Previous studies using an Flt-1 minigene (pFIN13) revealed that intronic cleavage/polyadenylation signals can affect Flt-1 expression, and, conversely, that 3' intronic splice signals can affect sFlt-1 expression. The goal of present work was to test the hypothesis that splicing and cleavage/polyadenylation factors compete functionally on Flt-1 transcripts, by 1) assessing the influence of exon 13/14 splicing determinants on expression of Flt-1 RNA processing variants in a transfected cell model system; 2) determining the effects of altering the relative abundance of proteins principally involved in splicing or cleavage/polyadenylation; and 3) characterizing a previously-unknown splice variant, predicted to encode a novel sFlt-1 protein isoform, in cells overexpressing the spliceosomal RNA binding protein U2AF65. When the upstream exon in pFIN13 was decreased from 2135 to 309 bp, the sFlt-1:Flt-1 mRNA ratio decreased 8.9-fold and an aberrant 5'UTR/exon 14 splice decreased 60-fold, indicating that "exon definition" is a key parameter of successful Flt-1 RNA processing. Mutation of 5' or 3' intronic splice signals had little effect on Long sFlt-1:Total sFlt-1 mRNA ratio, suggesting that splicing and cleavage/polyadenylation factors may not compete physically for Flt-1 transcripts. Although co-transfection with RNA processing factor cDNAs did not generally produce the predicted pattern of effects on sFlt-1:Flt-1 mRNA ratio, a cryptic exon within intron 13 was revealed in cells overexpressing U2AF65. sFlt-1 protein apparently can be encoded by mRNAs either cleaved/polyadenylated within intron 13 or, surprisingly, by splicing of the cryptic exon "13b." Thus, the cellular decision to produce sFlt-1 or Flt-1 from a nascent RNA can no longer be viewed as a simple choice between cleavage/polyadenylation and splicing.
Ph. D.

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35

Jehle, Mirjam. "Die Bedeutung des Vaskular-Endothelialen Wachstumsfaktor (VEGF) in der Heilung von Frakturen unter Weichteilschaden und Schock". [S.l. : s.n.], 2006. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-56057.

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Leucht, Frank Martin. "Untersuchungen zur VEGF und PlGF induzierten Chemotaxis multipotenter Stromazellen des Knochenmarks". [S.l. : s.n.], 2008. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-64417.

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王, 英泰. "Hypoxia and vascular endothelial growth factor selectively upregulate angiopoietin-2 in bovine microvascular endothelial cells". Kyoto University, 2001. http://hdl.handle.net/2433/150200.

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Poon, Tung-ping Ronnie. "Prognostic significance of circulating vascular endothlial [sic] growth factor in patients with hepatocellular carcinoma". Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36922249.

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Yan, Qi. "Regulation of retinal endothelial cells and pericytes by VEGF, TGF-beta1, and SPARC /". Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/5686.

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Wan, Wai-chong. "Identification and characterization of vascular endothelial growth factor (VEGF) in rat testis /". Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B20668120.

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溫慧莊 i Wai-chong Wan. "Identification and characterization of vascular endothelial growth factor (VEGF) in rat testis". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31221841.

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Sipola, A. (Annina). "Effects of vascular endothelial growth factor (VEGF-A) and endostatin on bone". Doctoral thesis, University of Oulu, 2009. http://urn.fi/urn:isbn:9789514293184.

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Abstract Angiogenesis is essential for the replacement of cartilage by bone during skeletal growth and regeneration. Vascular endothelial growth factor-A (VEGF-A) is a key regulator of angiogenesis whereas endostatin, a potent inhibitor of endothelial cell proliferation and migration, is a natural antagonist of VEGF-A. The regulatory roles of these peptides in angiogenesis, bone formation and bone cells were investigated in this study. In the present work we studied the effects of VEGF-A, delivered with an adenoviral vector, on the recovery of bone drilling defects in rat femur. Our data confirm the important role of VEGF in bone healing and that adenoviral VEGF gene transfer may modify bone defect healing in a rodent model. We studied the effects of VEGF-A and endostatin on bone resorption activity. It was found that VEGF-A is a potent stimulator of bone resorption and osteoclast differentiation in vitro and endostatin can antagonize this stimulatory effect when acting directly on bone cells. This suggests that endostatin is indeed a regulator of bone resorption, but not a critical one. In the present study we induced ectopic bone formation in the hamstring muscles of adult mice. The effects of VEGF-A and endostatin in the ectopic bone formation assay were evaluated by the simultaneous delivery of both peptides with recombinant adenoviral vectors. It was found that endostatin retards the cartilage phase in endochondral ossification that subsequently reduces bone formation. We conclude that bone growth and healing, which share features with ectopic bone formation, may be regulated by endostatin. To confirm in vivo effects on bone formation we further investigated the effects of endostatin and VEGF-A on mouse pre-osteoblastic cells in vitro. Finally the effects of endostatin on bone were studied in transgenic mouse lines overexpressing endostatin, and mice lacking collagen XVIII.

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Aldridge, S. E. "Vascular endothelial growth factor and osteoclastogenesis : a role in metastasis to bone". Thesis, University of Newcastle upon Tyne, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405067.

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Caires, Kyle Cody. "Investigating the role of vascular endothelial growth factor in bovine testis development". Online access for everyone, 2007. http://www.dissertations.wsu.edu/Thesis/Spring2007/k_caires_050207.pdf.

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Hunter, A. J. "Studies into the role of vascular endothelial growth factor in pre-eclampsia". Thesis, Queen's University Belfast, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368545.

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Thickett, D. R. "The role of vascular endothelial growth factor in the pathogenesis of ARDS". Thesis, University of London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393645.

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McFee, Renee Marie. "The role of vascular endothelial growth factor isoforms in early follicle development". Thesis, Kansas State University, 2012. http://hdl.handle.net/2097/13525.

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Master of Science
Department of Animal Sciences and Industry
Timothy G. Rozell
Since vascularization of the theca layer increases as follicles progress in size through preantral and antral stages, the principal angiogenic factor, vascular endothelial growth factor A (VEGFA), may influence follicle growth via regulation of angiogenesis. However, VEGFA may also influence follicular development through nonangiogenic mechanisms since its expression has been localized to nonvascular follicles and cells. Alternative mRNA splicing of 8 exons from the VEGFA gene results in the formation of different VEGFA isoforms. Each isoform has unique properties and is identified by the number of amino acids within the mature protein. Proangiogenic isoforms are encoded by exon 8a while a sister set of isoforms with antiangiogenic properties are encoded by exon 8b. The antiangiogenic isoforms comprise the majority of VEGFA expressed in most tissues while expression of the proangiogenic VEGFA isoforms is upregulated in tissues undergoing active angiogenesis. The Vegfa angiogenic isoforms (Vegfa_120, Vegfa_164, and Vegfa_188) were detected in developing rat ovaries, and quantitative RT-PCR determined that Vegfa_120 and Vegfa_164 mRNA was more abundant after birth, while Vegfa_188 mRNA was highest at embryonic day 16. The antiangiogenic isoforms, Vegfa_165b and Vegfa_189b, were amplified and sequenced from rat ovaries and quantitative RT-PCR determined that Vegfa_165b mRNA was more abundant around embryonic day 18, but Vegfa_189b lacked a distinct pattern of abundance. VEGFA and its receptors were localized to pregranulosa and granulosa cells of all follicle stages and to theca cells of advanced-stage follicles. Antiangiogenic VEGFA isoforms were localized to pregranulosa and granulosa cells of all follicle stages and to theca cells of advanced-stage follicles. To determine the role of VEGFA in developing ovaries, postnatal day 3/4 rat ovaries were cultured with VEGFR-TKI, a tyrosine kinase inhibitor that blocks signaling through the VEGFA receptors, FLT1 and KDR. Ovaries treated with VEGFR-TKI had vascular development reduced by 94%. In addition, treated ovaries had more primordial follicles, fewer early primary, transitional, and secondary follicles, and greater total follicle numbers compared with control ovaries. This suggests that VEGFA promotes follicle recruitment and early follicular development. These effects may be dependent upon increased ovarian vascularization or they may be mediated by nonvascular mechanisms.

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Peyromaure, Debord Broca Michaël. "Rôle du vascular endothelial growth factor (VEGF) dans le cancer prostatique localisé". Paris 5, 2006. http://www.theses.fr/2006PA05A001.

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Dans la première étude, nous avons mesuré le taux sérique de VEGF-A chez 47 patients ayant une suspicion clinique et/ou biologique de cancer prostatique. Tous les patients ont eu des biopsies prostatiques. Il n’y avait pas d’association entre le taux sérique de VEGF-A et la présence de cancer sur les biopsies prostatiques (p=0,55). En analyse logistique, le taux sérique de VEGF-A n’était pas prédictif de cancer prostatique après ajustement sur les autres paramètres. Ces résultats suggèrent que le VEGF-A, lorsqu’il est mesuré dans le sérum des patients, n’a pas de valeur dans la détection du cancer prostatique. Dans la deuxième étude, nous avons mesuré le taux plasmatique de VEGF-A chez 100 patients opérés par prostatectomie radicale pour un cancer prostatique cliniquement localisé. Nous avons également mesuré par technique ELISA l’expression tissulaire du VEGF-A sur les pièces opératoires.

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Nock, Sarah. "Prostate cancer expression of vascular endothelial growth factor splice forms in hypoxia". Kent State University Honors College / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ksuhonors1430770359.

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Heathcote, Helen Rachel. "The regulation of AMP-activated protein kinase by vascular endothelial growth factor". Thesis, University of Glasgow, 2016. http://theses.gla.ac.uk/7375/.

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The function of the vascular endothelium is to maintain vascular homeostasis, by providing an anti-thrombotic, anti-inflammatory and vasodilatory interface between circulating blood and the vessel wall, meanwhile facilitating the selective passage of blood components such as signaling molecules and immune cells. Dysfunction of the vascular endothelium is implicated in a number of pathological states including atherosclerosis and hypertension, and is thought to precede atherogenesis by a number of years. Vascular endothelial growth factor A (VEGF) is a crucial mitogenic signaling molecule, not only essential for embryonic development, but also in the adult for regulating both physiological and pathological angiogenesis. Previous studies by our laboratory have demonstrated that VEGF-A activates AMP-activated protein kinase (AMPK), the downstream component of a signaling cascade important in the regulation of whole body and cellular energy status. Furthermore, studies in our laboratory have indicated that AMPK is essential for VEGF-A-stimulated vascular endothelial cell proliferation. AMPK activation typically stimulates anabolic processes and inhibits catabolic processes including cell proliferation, with the ultimate aim of redressing energy imbalance, and as such is an attractive therapeutic target for the treatment of obesity, metabolic syndromes, and type 2 diabetes. Metabolic diseases are associated with adverse cardiovascular outcomes and AMPK activation is reported to have beneficial effects on the vascular endothelium. The mechanism by which VEGF-A stimulates AMPK, and the functional consequences of VEGF-A-stimulated AMPK activation remain uncertain. The present study therefore aimed to identify the specific mechanism(s) by which VEGF-A regulates the activity of AMPK in endothelial cells, and how this might differ from the activation of AMPK by other agents. Furthermore, the role of AMPK in the pro-proliferative actions of VEGF-A was further examined. Human aortic and umbilical vein endothelial cells were therefore used as a model system to characterise the specific effect(s) of VEGF-A stimulation on AMPK activation. The present study reports that AMPK α1 containing AMPK complexes account for the vast majority of both basal and VEGF-A-stimulated AMPK activity. Furthermore, AMPK α1 is localized to the endoplasmic reticulum when sub-confluent, but translocated to the Golgi apparatus when cells are cultured to confluence. AMPK α2 appears to be associated with a structural cellular component, but neither α1 nor α2 complexes appear to translocate in response to VEGF-A stimulation. The present study confirms previous reports that when measured using the MTS cell proliferation assay, AMPK is required for VEGF-A-stimulated endothelial cell proliferation. However, parallel experiments measuring cell proliferation using the Real-Time Cell Analyzer xCELLigence system, do not agree with these previous reports, suggesting that AMPK may in fact be required for an aspect of mitochondrial metabolism which is enhanced by VEGF-A. Studies into the mitochondrial activity of endothelial cells have proved inconclusive at this time, but further studies into this are warranted. During previous studies in our laboratory, it was suggested that VEGF-A-stimulated AMPK activation may be mediated via the diacylglycerol (DAG)-sensitive transient receptor potential cation channel (TRPCs -3, -6 or -7) family of ion channels. The present study can neither confirm, nor exclude the expression of TRPCs in vascular endothelial cells, nor rule out their involvement in VEGF-A-stimulated AMPK activation; more specific investigative tools are required in order to characterise their involvement. Furthermore, nicotinic acid adenine dinucleotide phosphate (NAADP)-stimulated Ca2+ release from acidic intracellular organelles is not required for AMPK activation by VEGF-A. Despite what is known about the mechanisms by which AMPK is activated, far less is known concerning the downregulation of AMPK activity, as observed in human and animal models of metabolic disease. Phosphorylation of AMPK α1 Ser485 (α2 Ser491) has recently been characterised as a mechanism by which the activity of AMPK is negatively regulated. We report here for the first time that VEGF-A stimulates AMPK α1 Ser485 phosphorylation independently of the previously reported AMPK α1 Ser485 kinases Akt (protein kinase B) and ERK1/2 (extracellular signal-regulated kinase 1/2). Furthermore, inhibition of protein kinase C (PKC), the activity of which is reported to be elevated in metabolic disease, attenuates VEGF-A- and phorbol 12-myristate 13-acetate (PMA)-stimulated AMPK α1 Ser485 phosphorylation, and increases basal AMPK activity. In contrast to this, PKC activation reduces AMPK activity in human vascular endothelial cells. Attempts to identify the PKC isoform responsible for inhibiting AMPK activity suggest that it is one (or more) of the Ca2+-regulated DAG-sensitive isoforms of PKC, however cross regulation of PKC isoform expression has limited the present study. Furthermore, AMPK α1 Ser485 phosphorylation was inversely correlated with human muscle insulin sensitivity. As such, enhanced AMPK α1 Ser485 phosphorylation, potentially mediated by increased PKC activation may help explain some of the reduced AMPK activity observed in metabolic disease.

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