Rozprawy doktorskie na temat „Endothelial cells”
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Holmén, Carolina. "Mechanisms of endothelial cell dysfunction in Wegener's granulomatosis /". Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-443-0/.
Pełny tekst źródłaClayton, Zoe Ellen. "The pro-angiogenic properties of induced pluripotent stem cell derived endothelial cells and induced endothelial cells". Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/17300.
Pełny tekst źródłaHarrison, Vanessa Jane. "The characterisation of endothelin-converting enzyme in endothelial cells". Thesis, Queen Mary, University of London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307673.
Pełny tekst źródłaRistori, Emma. "Vascular Endothelial Growth Factors and Endothelial Cells Behaviour". Doctoral thesis, Università di Siena, 2021. http://hdl.handle.net/11365/1127960.
Pełny tekst źródłaThe vascular endothelium is an important tissue often underestimated for its role in health and disease. Endothelial cells dysfunction is at the base of many if not all diseases. The inaccessibility of this tissue made difficult its assessment for many years. Vascular dysfunction can occur at different levels of vascular development and maintenance: during initial vasculogenesis, angiogenesis and late vascular remodelling. Vasculogenesis denotes the early developmental process of artery-veins specification. Angiogenesis refers to the formation of new blood vessels from pre-existing quiescent vessels. The angiogenic process is initiated by pro-angiogenic factors that induce endothelial cell sprouting, migration and vascular anastomosis. Newly formed vascular networks undergo extensive vascular remodelling, that includes distinct processes of vascular pruning and regression of selected vascular branches, to form a functional and mature quiescent vasculature. Vascular endothelial growth factors (VEGFs) are critical players in artery specification during development, in angiogenesis and in vascular maintenance. VEGFs bind to transmembrane VEGFRs receptors to initiate the intracellular response. The VEGF-VEGFR signalling pathway activation and regulation are very complex. In fact, the binding of the ligand VEGF to the VEGFRs receptor is not the only event involved in the activation and regulation of the signalling cascade. Co-receptors, kinases, phosphatases, and other proteins involved in the intracellular trafficking of the VEGF-VEGFR complex modulate the signal specificity, amplitude and duration. Angiogenesis and vessels stability are tightly regulated physiological processes. Indeed, excessive angiogenesis and increased permeability lead to vascular dysfunction and the progression of several diseases. In the recent years, neurodegenerative diseases such as Alzheimer’s disease have been strongly associated to vascular dysfunction (Review I) and to VEGF/VEGFR2 aberrant signalling. Recent studies suggest an important role of the AD-related β-amyloid precursor protein (APP) in maintaining cellular homeostasis in the brain, however the role of this protein in endothelial cells and its interactions with the VEGF signalling is still unknown (Review II). In this thesis work, I have examined the role of APP in regulating VEGF/VEGFR2 signalling and endothelial cells stability (Paper I). Furthermore, I have investigated the in vivo role of VEGF mediated signalling in artery specification during zebrafish vascular development (Paper II). In conclusion, VEGF mediated signalling is regulated by a multifactor system and each individual regulatory mechanism leads to a specific outcome in angiogenesis and vessel stability.
Huang, Lan. "Endothelial Colony Forming Cells (ECFCs): Identification, Specification and Modulation in Cardiovascular Diseases". Thesis, Connect to resource online, 2009. http://hdl.handle.net/1805/2063.
Pełny tekst źródłaTitle from screen (viewed on February 2, 2010). Department of Biochemistry and Molecular Biology, Indiana University-Purdue University Indianapolis (IUPUI). Advisor(s): Mervin C. Yoder, Jr., David A. Ingram, Jr., Lawrence A. Quilliam, Mark D. Pescovitz. Includes vitae. Includes bibliographical references (leaves 171-194).
Leskinen, Markus. "Mast cell-mediated apoptosis of smooth muscle cells and endothelial cells". Helsinki : University of Helsinki, 2003. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/leskinen/.
Pełny tekst źródłaAltalhi, Wafa. "Biological Effects of Osteopontin on Endothelial Progenitor Cells". Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/20280.
Pełny tekst źródłaZhu, Jing. "The role of nonmuscle myosin IIA in endothelial cell". Morgantown, W. Va. : [West Virginia University Libraries], 2010. http://hdl.handle.net/10450/11006.
Pełny tekst źródłaTitle from document title page. Document formatted into pages; contains viii, 37 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 33-37).
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.
Pełny tekst źródłaYang, Weidong. "Oxidative damage of endothelial cells". Thesis, University of Leicester, 1999. http://hdl.handle.net/2381/29603.
Pełny tekst źródłaDauphinee, Shauna Marie. "Lipopolysaccharide signaling in endothelial cells". Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/23033.
Pełny tekst źródłaZhou, Zhigang. "TNF signalling in endothelial cells". Thesis, University of East Anglia, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.435077.
Pełny tekst źródłaVickers, James. "Endothelial cells and platelet function". Thesis, University of Nottingham, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336951.
Pełny tekst źródłaFitchett, Caroline Jane. "Lysophosphatidate signalling in endothelial cells". Thesis, University of Wolverhampton, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252450.
Pełny tekst źródłaPhilippeos, Christina. "Insulin signalling in endothelial cells". Thesis, King's College London (University of London), 2014. http://kclpure.kcl.ac.uk/portal/en/theses/insulin-signalling-in-endothelial-cells(8e35db48-dc9c-41be-b1aa-1fbe241fc356).html.
Pełny tekst źródłaMcHenry, S. M. "Synergistic interactions between osteoblast cells and endothelial cells". Thesis, Queen's University Belfast, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403243.
Pełny tekst źródłaRabodzey, Aleksandr. "Flow-induced mechanotransduction in cell-cell junctions of endothelial cells". Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/41586.
Pełny tekst źródłaIncludes bibliographical references (leaves 86-92).
Endothelial cells show an unexpected behavior shortly after the onset of laminar flow: their crawling speed decreases ~40% within the first 30 min, but only in a confluent monolayer of endothelial cells, not in subconfluent cultures, where cell-cell interactions are limited. This led us to study early shear effects on cell-cell adherens junctions. We found a 30±6% increase in the number of VE-cadherin molecules in the junctions. The strength of interactions of endothelial cells with surfaces coated with recombinant VE-cadherin protein also increased after laminar flow. These observations suggest that endothelial cell junction proteins respond to flow onset. The process of clustering may induce diffusion of monomers to the junction area, resulting in an overall increase in VE-cadherins in the junctions. To directly confirm the role of adherens junctions in the decrease in cell crawling speed, we used siRNA-knockdown technique to produce cells lacking VE-cadherin. These cells showed no decline in crawling speed under flow. Our interpretation is consistent with previous data on junction disassembly 8 hr after flow onset. The speed of endothelial cell crawling returns to the original level by that time, and junctional disassembly may explain that phenomenon. In order to understand better the change in VE-cadherin distribution under flow and during junction formation and remodelling, we developed a mathematical model of VE-cadherin redistribution in endothelial cells. This model allowed us to develop a quantitative framework for analysis of VE-cadherin redistribution and estimate the amount of protein in the junctions and on the apical surface. In addition to that, the model explains rapid junction disassembly in the leukocyte transmigration and junction formation in subconfluent cells.
(cont.) These studies show that intercellular adhesion molecules are important in the force transmission and shear stress response. Their role, however, is not limited to flow mechanotransduction. Intercellular force transmission has an important application - organ development and, specifically, angiogenesis. We studied the role of VE-cadherin in vessel development in HUVECs and showed that VE-cadherin-null cells do not form vessels in the in vitro assay. This observation confirms the important role of intercellular force transmission in response to external force caused by flow or exerted by other cells.
by Aleksandr Rabodzey.
Ph.D.
Skinner, Elizabeth Mary. "Pluripotent stem cell-derived endothelial cells for vascular regeneration". Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/15865.
Pełny tekst źródłaO'Doherty, Michelle. "Endothelial progenitor cells : development of a cell-based therapy". Thesis, Queen's University Belfast, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.602718.
Pełny tekst źródłaWren, Amanda D. "Pharmacological studies on the actions of endothelins in endothelial repair in vitro". Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363301.
Pełny tekst źródłaBethi, Akhila. "Endothelin-1 Induced Phosphorylation of ERK1/2 in Bovine Corneal Endothelial Cells". TopSCHOLAR®, 2012. http://digitalcommons.wku.edu/theses/1191.
Pełny tekst źródłaValdimarsdóttir, Gudrun. "TGFβ Signal Transduction in Endothelial Cells". Doctoral thesis, Uppsala University, Ludwig Institute for Cancer Research, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4284.
Pełny tekst źródłaTransforming growth factor β (TGFβ) is a multifunctional cytokine that is involved in many biological effects, such as proliferation, migration, differentiation and cell survival. TGFβ regulates cellular responses by binding to a heteromeric complex of type I and type II serine/threonine kinase receptors. The type I receptor, termed activin receptor-like kinase (ALK), acts downstream of the type II receptor and propagates the signal to the nucleus by phosphorylating receptor regulated Smads (R-Smads). The activated R-Smads can associate with the common partner Smad, Smad4, and this complex translocates to the nucleus where it participates in transcriptional regulation of target genes. TGFβ plays an important role in vascular morphogenesis. The aim of this study was to obtain more insight into the mechanisms by which TGFβ can act as an inhibitor or stimulator of angiogenesis Our findings show that in endothelial cells (ECs), TGFβ can activate two distinct type I receptor/Smad signalling pathways with opposite cellular responses. In most cell types, TGFβ signals via the TGFβ type I receptor, ALK5. However, ECs express a predominant endothelial type I receptor, named ALK1. Whereas the TGFβ/ALK1 signalling leads to activation, the TGFβ/ALK5 pathway results in an inhibition of the activation state. This suggests that TGFβ regulates the activation state of the endothelium via a fine balance between these two pathways. We identified genes that are specifically induced by TGFβ mediated ALK1 or ALK5 activation. Id1 was found to be the target gene of the ALK1/Smad1/5 pathway while induction of plasminogen activator inhibitor-1 was activated only by ALK5/Smad2 pathway. Furthermore, ALK1 activated ECs are highly invasive but this property is lost if Id1 expression is specifically knocked-down. ECs invasiveness is highly dependent on αv integrin binding to its extracellular matrix (ECM) protein partner and the invasion requires proteolytic cleavage of the ECM by metalloproteases (MMPs). Hence, TGFβ/ALK1/Id1 pathway may promote invasion by modulating the expression or activity of integrins and MMPs that are well known components of the ECM. Timing and duration of TGFβ signalling are important specificity determinants for its effect on cellular behaviour. After binding to ALK1, TGFβ induces a transient phosphorylation of Smad1/5 but a stable phosphorylation of Smad2 via ALK5. Our studies indicate that Smad7 is potently induced by ALK1 signalling and may recruit a PP1α/TIMAP phosphatase complex to ALK1 to dephosphorylate the receptor and thereby turning off phosphorylation resulting in a temporal activation of TGFβ/ALK1-induced Smad1/5 pathway. This mechanism enables an efficient and tightly temporally controlled activation resulting in the dominance of ALK5 upon prolonged exposure to TGFβ. Bone morphogenetic protein (BMP) is a member of the TGFβ superfamily and signals through Smad1/5. The BMP/Smad1/5 pathway was found to potently activate the endothelium. Id1 was identified as an important BMP target gene in ECs and was sufficient and necessary for BMP-induced EC migration. These studies not only provide new insights into possible molecular mechanisms that underlie activation and quiescence of ECs during physiological angiogenesis but may also explain the vascular phenotypes observed in mice and humans with perturbed TGFβ signalling pathways.
Millar, Christopher G. "Endothelial progenitor cells and vascular injury". Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/24977.
Pełny tekst źródłaHunter, Nikolas Ross. "In vitro studies on endothelial cells". Thesis, Heriot-Watt University, 1987. http://hdl.handle.net/10399/1040.
Pełny tekst źródłaWood, Peter G. "Intracellular calcium mobilization in endothelial cells". Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.310032.
Pełny tekst źródłaAnsari, Abdul-Haq. "Targeting statins to the endothelial cells". Thesis, University of Newcastle Upon Tyne, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.438361.
Pełny tekst źródłaCheluvappa, Rajkumar. "Pathophysiology of Liver Sinusoidal Endothelial Cells". Thesis, The University of Sydney, 2008. http://hdl.handle.net/2123/2802.
Pełny tekst źródłaCheluvappa, Rajkumar. "Pathophysiology of Liver Sinusoidal Endothelial Cells". University of Sydney, 2008. http://hdl.handle.net/2123/2802.
Pełny tekst źródłaOwing to its strategic position in the liver sinusoid, pathologic and morphologic alterations of the Liver Sinusoidal Endothelial Cell (LSEC) have far-reaching repercussions for the whole liver and systemic metabolism. LSECs are perforated with fenestrations, which are pores that facilitate the transfer of lipoproteins and macromolecules between blood and hepatocytes. Loss of LSEC porosity is termed defenestration, which can result from loss of fenestrations and/ or decreases in fenestration diameter. Gram negative bacterial endotoxin (Lipopolysaccharide, LPS) has marked effects on LSEC morphology, including induction LSEC defenestration. Sepsis is associated with hyperlipidemia, and proposed mechanisms include inhibition of tissue lipoprotein lipase and increased triglyceride production by the liver. The LSEC has an increasingly recognized role in hyperlipidemia. Conditions associated with reduced numbers of fenestrations such as ageing and bacterial infections are associated with impaired lipoprotein and chylomicron remnant uptake by the liver and consequent hyperlipidemia. Given the role of the LSEC in liver allograft rejection and hyperlipidemia, changes in the LSEC induced by LPS may have significant clinical implications. In this thesis, the following major hypotheses are explored: 1. The Pseudomonas aeruginosa toxin pyocyanin induces defenestration of the LSEC both in vitro and in vivo 2. The effects of pyocyanin on the LSEC are mediated by oxidative stress 3. Defenestration induced by old age and poloxamer 407 causes intrahepatocytic hypoxia and upregulation of hypoxia-related responses 4. Defenestration of the LSEC seen in old age can be exacerbated by diabetes mellitus and prevented or ameliorated by caloric restriction commencing early in life
Young, Richard Steven. "Calcium entry in tumour endothelial cells". Thesis, University of Leeds, 2014. http://etheses.whiterose.ac.uk/7042/.
Pełny tekst źródłaWhyte, Jemima Lois. "Density dependent differentiation of mesenchymal stem cells to endothelial cells". Thesis, University of Manchester, 2010. https://www.research.manchester.ac.uk/portal/en/theses/density-dependent-differentiation-of-mesenchymal-stem-cells-to-endothelial-cells(d839ac9d-3bda-46fb-8e8e-556a85772db9).html.
Pełny tekst źródłaNg, 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.
Pełny tekst źródłaMaillard, Marjorie. "The effects of hyperglycaemia on endothelial barrier function in human endothelial cells". Thesis, University of Nottingham, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.395604.
Pełny tekst źródłaWaldman, W. James. "Preservation of natural endothelial cytopathogenicity of cytomegalovirus by propagation in endothelial cells /". The Ohio State University, 1990. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487681788253941.
Pełny tekst źródłaBaldoli, E. "MAGNESIUM AND ENDOTHELIAL FUNCTION: COMPARATIVE STUDIES IN MACRO AND MICROVASCULAR ENDOTHELIAL CELLS". Doctoral thesis, Università degli Studi di Milano, 2010. http://hdl.handle.net/2434/150045.
Pełny tekst źródłaDeshane, Jessy S. "Regulation of HO-1 and its role in angiogenesis". Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2009r/deshane.pdf.
Pełny tekst źródłaNeilson, Kirstie Jane. "Differentiation of mouse embryonic stem cells into endothelial progenitor cells". Thesis, University of Sheffield, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.500200.
Pełny tekst źródłaAbdel-Samad, Dima. "Regulation of human endocardial endothelial cells' secretion of endothelin-1 by neuropeptide Y". Thèse, Université de Sherbrooke, 2008. http://savoirs.usherbrooke.ca/handle/11143/4271.
Pełny tekst źródłaShaikh, Mohsin Ahmed. "Models of coupled smooth muscleand endothelial cells". Thesis, University of Canterbury. Centre for Bioengineering, 2011. http://hdl.handle.net/10092/6190.
Pełny tekst źródłaGoyal, Pankaj. "Dual function of LIMK2 in endothelial cells". Diss., lmu, 2005. http://nbn-resolving.de/urn:nbn:de:bvb:19-41291.
Pełny tekst źródłaKemp, Sarah J. G. "Focal adhesion kinase signalling in endothelial cells". Thesis, University of Leicester, 2002. http://hdl.handle.net/2381/29413.
Pełny tekst źródłaChan, Giulia. "Regulation of viability in corneal endothelial cells". Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1444592/.
Pełny tekst źródłaJalilian, E. "Characterization of progenitors of endothelial cells (PECs)". Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/1560479/.
Pełny tekst źródłaFranses, Joseph W. (Joseph Wang). "Regulatory roles of endothelial cells in cancer". Thesis, Massachusetts Institute of Technology, 2011. http://hdl.handle.net/1721.1/65518.
Pełny tekst źródła"May 2011." Cataloged from PDF version of thesis.
Includes bibliographical references (p. 109-121).
This thesis describes the biochemical regulatory impact of endothelial cells, the cells that line all blood vessels, in cancer. Our work draws from concepts in vascular repair and tissue engineering and extends the view of tumor vessels from perfusing tubes to delivery platforms lined with potent paracrine regulatory cells. We focus on how the endothelial cells themselves regulate tumor biology in a state-dependent fashion. We found that healthy endothelial cells inhibit cancer cell proliferation, invasiveness, and inflammatory signaling and that a defined perturbation of the healthy endothelial cell state - silencing of the gene encoding perlecan - causes loss of the invasion-inhibitory capabilities of endothelial cells by transcriptional upregulation of IL-6. The use of matrixembedded endothelial implants enabled the effects in cell culture to be expanded and validated in animal models. Moreover, endothelial cells exposed to a pathologically activating and inflammatory culture environment, similar to endothelial cells exposed to the atherosclerotic milieu, were leaky and inflamed, with dysregulated proliferative and leukocyte binding properties. Unlike healthy endothelial cells, which suppress cancer cell proliferation and metastasis, these dysfunctional endothelial cells instead aggressively stimulated cancer cell inflammatory signaling and invasiveness, which correlated with stimulation of spontaneous metastasis when implanted as matrixembedded cell implants adjacent to tumors. Fascinatingly we were able to identify markers of endothelial dysfunction, including reduction of endothelial perlecan expression, in human non-small cell lung carcinoma specimens. The state-dependent impact of endothelial cells on cancer biology adds another element to stromal regulation of cancer and brings together a range of disciplines and disparate findings regarding vascular control of tumors. That healthy endothelial cells suppress and dysfunctional cells promote tumor aggression may help to explain undesired effects of therapies that target tumor blood vessels. The harnessing of tissue engineering to regulate vascular and cancer biology may motivate the development of innovative pharmacologic and cell-based therapies for cancer.
by Joseph W. Franses.
Ph.D.
May, Michael Jonathan. "Cytokine-induced signal transduction in endothelial cells". Thesis, King's College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.339150.
Pełny tekst źródłaPrasad, Raju. "Endothelial progenitor cells, vascular function, and exercise". Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 59 p, 2009. http://proquest.umi.com/pqdweb?did=1654501181&sid=4&Fmt=2&clientId=8331&RQT=309&VName=PQD.
Pełny tekst źródłaMancardi, Sabrina. "Characterization of endothelial cells of lymphatic vessels". Thesis, Open University, 2001. http://oro.open.ac.uk/54568/.
Pełny tekst źródłaKim, Sung Kyu. "Endothelial cell interaction with collagen". Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709002.
Pełny tekst źródłaPlatt, Manu Omar. "Role of Shear Stress in the Differential Regulation of Endothelial Cathepsins and Cystatin C". Diss., Georgia Institute of Technology, 2006. http://hdl.handle.net/1853/11635.
Pełny tekst źródłaKono, Tomoya. "Differentiation of lymphatic endothelial cells from embryonic stem cells on OP9 stromal cells". Kyoto University, 2008. http://hdl.handle.net/2433/135863.
Pełny tekst źródłaJohansson, Magnus. "Role of Islet Endothelial Cells in β-cell Function and Growth". Doctoral thesis, Uppsala universitet, Institutionen för medicinsk cellbiologi, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6801.
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