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Rozprawy doktorskie na temat „Endothelial cells”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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1

Holmén, Carolina. "Mechanisms of endothelial cell dysfunction in Wegener's granulomatosis /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-443-0/.

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Clayton, 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.

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Cardiovascular disease (CVD) is the leading cause of morbidity and mortality worldwide, (1, 2). Current interventions are ineffective in up to 30% of patients due to the presence of diffuse or extensive atherosclerosis, therefore the development of alternative or supplementary therapies for CVD is a high priority for medical research. Therapeutic angiogenesis, enhancing the growth of new blood vessel networks from the existing vasculature, is a promising strategy for restoring blood flow to ischaemic tissue. Stem cells have shown potential as pro-angiogenic therapies for patients with coronary

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3

Harrison, 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.

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4

Ristori, Emma. "Vascular Endothelial Growth Factors and Endothelial Cells Behaviour." Doctoral thesis, Università di Siena, 2021. http://hdl.handle.net/11365/1127960.

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L'endotelio vascolare è un importante tessuto il cui ruolo sia in fisiologia, che in patologia è stato a lungo sottovalutato. Per molti anni, l'inaccessibilità di questo tessuto ha reso difficoltoso valutarne il ruolo fisio-patologico. La disfunzione delle cellule endoteliali è alla base di molti se non tutti gli stati patologici e può manifestarsi a diversi livelli dello sviluppo vascolare: durante la vasculogenesi, durante il processo di angiogenesi oppure durante il rimodellamento vascolare. Il processo di vasculogenesi consiste nella specializzazione di precursori vascolari in arterie e v

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5

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.

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Thesis (Ph.D.)--Indiana University, 2009.<br>Title 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).

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6

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/.

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7

Altalhi, Wafa. "Biological Effects of Osteopontin on Endothelial Progenitor Cells." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/20280.

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Endothelial Progenitor Cells (EPCs) are thought to participate in the healing of injured vascular endothelium by incorporating into the defect sites to mediate endothelial recovery. Recently, osteopontin (OPN) was shown to be fundamental in accelerating estrogen-dependent healing of injured blood vessels. Here, we are investigating the effect OPN has on EPC behavior. Late outgrowth human EPCs (LEPCs) were derived from circulating monocytes isolated by leukophoresis, and grown in culture until passage six. L-EPCs were then assayed for adhesion, spreading, chemotaxis, and haptotaxis, as well as

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8

Zhu, Jing. "The role of nonmuscle myosin IIA in endothelial cell." Morgantown, W. Va. : [West Virginia University Libraries], 2010. http://hdl.handle.net/10450/11006.

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Thesis (M.S.)--West Virginia University, 2010.<br>Title from document title page. Document formatted into pages; contains viii, 37 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 33-37).

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9

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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10

Yang, Weidong. "Oxidative damage of endothelial cells." Thesis, University of Leicester, 1999. http://hdl.handle.net/2381/29603.

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This study sought to investigate the consequences of different degrees of oxidative stress on endothelial cells, using a cultured endothelial cell model; principally bovine aortic endothelial cells, subjected to oxidative stress. High concentrations of H2O2 or a superoxide generating system caused rapid endothelial cell death, as evidenced by increased membrane permeability, which could be partially protected by myoglobin. Extracellular H2O2 caused a rapid increase in intracellular peroxidation but was also eliminated by endothelial cells. However, the anti-oxidant capacity of the bovine endot

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11

Dauphinee, Shauna Marie. "Lipopolysaccharide signaling in endothelial cells." Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/23033.

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The endothelium plays a critical role in coordinating the innate immune response through the regulation of vascular tone, leukocyte recruitment and transmigration, and hemostasis. These functions are mediated, in part, by the signaling cascades initiated upon recognition of bacterial and viral products by a family of transmembrane receptors known as Toll-like receptors (TLRs). In endothelial cells, exposure to lipopolysaccharide (LPS), a major cell wall constituent of Gram negative bacteria, results in endothelial activation through TLR4. Recruitment of the adapter protein, MyD88, to the recep

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12

Zhou, Zhigang. "TNF signalling in endothelial cells." Thesis, University of East Anglia, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.435077.

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Pleiotropic cytokine tumour necrosis factor a (TNF) is the archetypal member of a large super-family of ligands and associated receptors. Through its two surface presenting receptors, TNFRI and TNFR2, TNF can elicit responses such as differentiation, proliferation, and apoptosis, depending on several factors such as microenvironment, cell cycle, and cell type. Recent evidence indicated that TNF can be up-regulated in endothelial cells (EC) upon their stimulation and plays an important role in regulating EC responses which have been implicated in several cardiovascular diseases, such as heart f

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13

Vickers, James. "Endothelial cells and platelet function." Thesis, University of Nottingham, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336951.

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14

Fitchett, Caroline Jane. "Lysophosphatidate signalling in endothelial cells." Thesis, University of Wolverhampton, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252450.

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15

Philippeos, 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.

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Insulin is known to act as an anti-inflammatory agent and protect vascular endothelial cells during ischaemic damage in vivo. Although it is known that insulin signals in part through phosphatidylinositol 3-kinases (PI3Ks) and Akt, its effects on endothelial junctions and actin cytoskeleton are unknown. This study aimed to characterise endothelial responses to insulin, identify endothelial insulin-‐induced changes in protein phosphorylation and determine the roles of these changes in regulating endothelial functions. Insulin stimulation induced dose-dependent Akt activation in both primary hu

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16

McHenry, 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.

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17

Rabodzey, Aleksandr. "Flow-induced mechanotransduction in cell-cell junctions of endothelial cells." Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/41586.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Biological Engineering Division, 2006.<br>Includes bibliographical references (leaves 86-92).<br>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 o

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18

Skinner, Elizabeth Mary. "Pluripotent stem cell-derived endothelial cells for vascular regeneration." Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/15865.

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Background: Vascular endothelial dysfunction plays a major role in the pathogenesis of atherosclerosis. As such, the study of endothelial cells has sought to identify causal pathways and novel therapeutic approaches to promote vascular repair. Induced pluripotent stem (iPS) cell technology may be a particularly useful tool, and could be used to derive endothelial cells and their progenitors from individuals with endothelial dysfunction to explore these pathways and develop novel strategies for vascular regeneration. Whilst iPS cells are conventionally obtained from the reprogramming of dermal

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19

O'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.

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Much interest currently surrounds the emerging field of regenerative medicine. Cell-based therapies represent a novel therapeutic platform for the treatment of ischaemic diseases, shifting the focus clinically from the management of disease symptoms to their potential cure. Endothelial progenitor cells (EPCs) contribute to vascular repair and angiogenesis. Despite controversy surrounding the heterogeneous nature of these cells in vitro and in vivo, their vasoreparative functions suggest that EPCs have potential clinical value. The aim of this thesis is to further define the precise phenotype,

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20

Wren, 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.

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21

Bethi, Akhila. "Endothelin-1 Induced Phosphorylation of ERK1/2 in Bovine Corneal Endothelial Cells." TopSCHOLAR®, 2012. http://digitalcommons.wku.edu/theses/1191.

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The purpose of this study was to determine whether Endothelin-1 (ET-1) induced cellular responses in bovine corneal endothelial cells (BCECs) involves MAPK pathway by phosphorylating ERK1/2 protein kinase and to find out the phosphorylation patterns of ERK1/2 in confluent and sub-confluent cells. BCECs were isolated from bovine corneas and cultured in medium supplemented with 10% serum. Confluent (contact inhibited) and sub-confluent (actively growing cells) serum starved cells grown in T-75 flasks were treated with 10nM Endothelin-1. The control cells were left untreated. Total cellular prote

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22

Valdimarsdóttir, 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.

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<p>Transforming 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

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23

Millar, Christopher G. "Endothelial progenitor cells and vascular injury." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/24977.

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Endothelial progenitor cells (EPCs) are bone marrow derived cells that contribute towards neovascularisation. I have primarily used real time polymerase chain reaction (PCR), but also flow cytometry and cell culture techniques, to investigate the effect of vascular injury on the expression of the putative markers of EPCs (CD34, CD133, VEGFR-2 and VE-cadherin) and their number in peripheral blood. In the first study I investigated the effect of percutaneous coronary intervention (PCI) on EPCs in a group of patients with stable coronary disease. After PCI, EPC markers did not conclusively demons

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24

Hunter, Nikolas Ross. "In vitro studies on endothelial cells." Thesis, Heriot-Watt University, 1987. http://hdl.handle.net/10399/1040.

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25

Wood, 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.

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26

Ansari, 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.

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27

Cheluvappa, Rajkumar. "Pathophysiology of Liver Sinusoidal Endothelial Cells." Thesis, The University of Sydney, 2008. http://hdl.handle.net/2123/2802.

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Owing 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 morpho

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28

Cheluvappa, Rajkumar. "Pathophysiology of Liver Sinusoidal Endothelial Cells." University of Sydney, 2008. http://hdl.handle.net/2123/2802.

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Doctor of Philosophy(PhD)<br>Owing 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

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29

Young, Richard Steven. "Calcium entry in tumour endothelial cells." Thesis, University of Leeds, 2014. http://etheses.whiterose.ac.uk/7042/.

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Colorectal cancer liver metastases (CRLM) remain a significant cause of cancer-related mortality. There is an urgent need for novel oncological treatments to support continuing surgical advances. Tumour endothelial cells are emerging as important and unique cells that may be powerful therapeutic targets. Endothelial cell store-operated Ca2+ entry (SOCE) via Ca2+-release activated calcium (CRAC) channels underlies key angiogenic and tumourigenic processes and is the focus of this study. Normal (NEC) and tumour (TEC) endothelial cells were for the first time successfully isolated and characteris

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30

Whyte, 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.

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The differentiation of mesenchymal stem cells (MSCs) to endothelium is a critical but poorly understood feature of tissue vascularisation and considerable scepticism still remains surrounding this important differentiation event. Defining features of endothelial cells (ECs) are their ability to exist as contact-inhibited polarised monolayers that are stabilised by intercellular junctions, and the expression and activity of endothelial markers. During vasculogenesis, communication between MSCs and differentiated ECs or vascular smooth muscle cells, or between MSCs themselves is likely to influe

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31

Ng, Hoi-man, and 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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32

Maillard, 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.

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33

Waldman, 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.

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34

Baldoli, 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.

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Mg is referred to as the intracellular divalent cation par excellence. Its biological role is extremely versatile as it can serve structural functions as well as dynamic functions. Accordingly, Mg deficiency has been reported to be involved in the pathogenesis of cardiovascular diseases and, in particular, in atherogenesis. 1)Mg in macrovascular endothelial cells. In cultured macrovascular endothelial cells, low Mg increases tha adhesion of monocytes to the monolayer via upregulation of vascular cell adhesion molecule (VCAM), induces plasminogen activator inhibitor (PAI)1, augments the level

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35

Deshane, 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.

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36

Neilson, 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.

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37

Abdel-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.

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Endocardial endothelial cells (EECs) can exert a significant influence on cardiac function by releasing various factors such as nitric oxide (NO), prostanoids, endothelin-1 (ET-1) and angiotensin II (Ang II). Recently, results obtained in our laboratory demonstrated the presence of NPY and its receptors, Y[subscript 1] and Y[subscript 2], as well as ET-1 and its receptors, ET[subscript A] and ET[subscript B], at the level of endocardial endothelial cells (EECs). We have also shown that NPY induces a sustained rise in the intracellular calcium level of these cells, and that only right ventricu

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38

Shaikh, Mohsin Ahmed. "Models of coupled smooth muscleand endothelial cells." Thesis, University of Canterbury. Centre for Bioengineering, 2011. http://hdl.handle.net/10092/6190.

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Impaired mass transfer characteristics of blood borne vasoactive species such as ATP in regions such as an arterial bifurcation have been hypothesized as a prospective mechanism in the aetiology of atherosclerotic lesions. Arterial endothelial (EC) and smooth muscle cells (SMC) respond differentially to altered local hemodynamics and produce coordinated macro-scale responses via intercellular communication. Using a computationally designed arterial segment comprising large populations of mathematically modelled coupled ECs & SMCs, we investigate their response to spatial gradients of blood bor

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39

Goyal, Pankaj. "Dual function of LIMK2 in endothelial cells." Diss., lmu, 2005. http://nbn-resolving.de/urn:nbn:de:bvb:19-41291.

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Kemp, Sarah J. G. "Focal adhesion kinase signalling in endothelial cells." Thesis, University of Leicester, 2002. http://hdl.handle.net/2381/29413.

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The angiogenic factor vascular endothelial growth factor (VEGF) induces migration and cytoskeletal changes in endothelial cells. The mechanism by which VEGF signals was not known but it was possible an adhesion associated protein such as focal adhesion kinase (FAK) was involved. Further investigation revealed VEGF caused a marked activation of tyrosine phosphorylation of FAK in HUVE cells, which was time and concentration dependent. The PI3K inhibitor wortmannin partially inhibited VEGF stimulated FAK phosphorylation and it inhibited phosphorylation in response to lysophosphatidic acid and VEG

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41

Chan, Giulia. "Regulation of viability in corneal endothelial cells." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1444592/.

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The major cause of corneal opacity and resultant visual loss is a critical decrease in corneal endothelial cell density. Due to the fact that corneal endothelial cells do not generally proliferate, cell densities gradually decrease in the corneal endothelium with age. Before we can begin to aid patients with decreasing endothelial cell densities, by inhibiting cell death or stimulating cell proliferation, it is necessary to understand the basic cell signalling that underlies these processes. As human tissue is difficult to obtain, a representative animal model of corneal endothelium was devise

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42

Jalilian, E. "Characterization of progenitors of endothelial cells (PECs)." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/1560479/.

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There are a number of different stem cell sources that have the potential to be used as therapeutics in vascular degenerative diseases such as diabetic retinopathy. On the one hand, there are so called endothelial progenitor cells (EPCs), which are typically derived from adult blood. They carry the marker CD34, but the true nature and definition of EPCs is still controversial. On the other hand, there are embryonic precursors of endothelial cells (PECs), which also express CD34, and which can be differentiated from embryonic stem cells (ESCs) or induced pluripotent stem cells (iPSCs) in vitro.

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Franses, Joseph W. (Joseph Wang). "Regulatory roles of endothelial cells in cancer." Thesis, Massachusetts Institute of Technology, 2011. http://hdl.handle.net/1721.1/65518.

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Thesis (Ph. D.)--Harvard-MIT Division of Health Sciences and Technology, June 2011.<br>"May 2011." Cataloged from PDF version of thesis.<br>Includes bibliographical references (p. 109-121).<br>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 stat

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44

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.

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45

Prasad, 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.

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46

Mancardi, Sabrina. "Characterization of endothelial cells of lymphatic vessels." Thesis, Open University, 2001. http://oro.open.ac.uk/54568/.

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Endothelial cells form the inner lining of blood and lymphatic vessels. In mice only tumours of the blood vessel endothelium (haemangiomas) have been thus far reported. In the first part of this thesis is described a highly reproducible method for the induction of benign tumours of the lymphatic endothelial cells (lymphangioma) in mice, by intraperitoneal injection of incomplete Freund's adjuvant. Different criteria have been used in order to establish the nature of the induced lesion. Morphological and histophatological studies of the tumour developed in the peritoneal cavity revealed the pre

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47

Kim, Sung Kyu. "Endothelial cell interaction with collagen." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709002.

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48

Platt, 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.

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The importance of shear stress in vascular biology and pathophysiology has been highlighted by the focal development patterns of atherosclerosis, abdominal aortic aneurysms, and heart valve disease in regions exposed to disturbed flow leading to low or oscillatory shear stress at the wall of the blood vessel or the surface of the valve leaflet. The novel and significant finding of this study is that mouse aortic endothelial cell exposure to pro-atherogenic oscillatory shear stress (OS) (+/- 5 dynes/cm2) increased their production of cathepsins, the family of lysosomal cysteine proteases that a

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49

Kono, Tomoya. "Differentiation of lymphatic endothelial cells from embryonic stem cells on OP9 stromal cells." Kyoto University, 2008. http://hdl.handle.net/2433/135863.

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Johansson, 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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The pancreatic islets are collections of endocrine cells, dispersed throughout the pancreas. In adult islets, endocrine cells are closely associated with capillary endothelial cells and receive a high blood perfusion. Transplanted pancreatic islets, on the other hand, have a vascular disturbance, manifested as decreased blood vessel density. Besides impaired islet blood perfusion and oxygenation, this means that the normal close proximity between endothelial cells and β-cell in adult islets is interrupted. The aim of the thesis was to investigate if, and to what extent, β-cells and islet endot

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