Log in

Relevant bibliographies by topics / Endothelium / Dissertations / Theses

Dissertations / Theses on the topic 'Endothelium'

To see the other types of publications on this topic, follow the link: Endothelium.

Author: Grafiati

Published: 4 June 2021

Last updated: 28 July 2024

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 dissertations / theses for your research on the topic 'Endothelium.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse dissertations / theses on a wide variety of disciplines and organise your bibliography correctly.

1

Adner, Mikael. "Altered expression of contractile endothelin receptors in the vascular bed." Lund : Dept. of Internal Medicine, University of Lund, 1998. http://catalog.hathitrust.org/api/volumes/oclc/39103326.html.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Kladakis, Stephanie M. "The role of proliferation and migration in endothelial cell monolayer formation on a tissue engineered blood vessel wall model." Diss., Georgia Institute of Technology, 2002. http://hdl.handle.net/1853/16752.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Wiseman, D. M. "The vascular endothelium : Angiogenesis and lymphocyte-endothelial cell interactions." Thesis, University of Manchester, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.374797.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

5

Tidwell, Caren Diana. "Endothelial cell interactions with model surfaces : effect of surface chemistry, surface mobility, and the adsorbed protein layer /." Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/8004.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

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

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Chauhan, Sharmila Deepa. "Mechanisms of endothelium-dependant dilation : a study of EDHF and endothelial dysfunction." Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397184.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

TOPOUZIS, STAVROS. "Etudes in vitro des effets de facteurs endotheliaux sur la contraction du muscle lisse vasculaire." Université Louis Pasteur (Strasbourg) (1971-2008), 1989. http://www.theses.fr/1989STR13190.

Full text

Abstract:

L'endothelium vasculaire produit et libere plusieurs agents vasoactifs, comme le facteur relaxant endothelial (edrf) et le peptide vasocontracturant endotheline-1 (et-1). Le cotransport membranaire na#+-k#+-cl#- semble implique dans le processus de liberation de l'edrf par l'aorte isolee de rat, puisque le diuretique muzolimine, un inhibiteur de ce cotransport, inhibe selectivement les reponses relaxantes dependant de l'integrite de l'endothelium et dues a l'edrf. On considere que l'edrf agit en augmentant le taux tissulaire de gmp cyclique (gmpc). Dans l'aorte de rat, le 8-br gmpc peut produire une inhibition des contractions induites par les agonistes alpha-adrenergiques semblable a celle induite par l'endothelium. L'efficacite d'un agoniste determine l'amplitude de cette inhibition. Il y a une absence de correlation entre les augmentations du taux de gmpc et l'inhibition en resultant. L'et-1 et ses analogues structuraux, la sarafotoxine s6b, l'ala#3,11et-1 et l'ala#1,15et-1, induisent des contractions de l'aorte isolee de rat qui dependent en partie du calcium extracellulaire. Ces peptides ne semblent pourtant pas activer directement les canaux sensibles aux dihydropyridines. La presence de l'endothelium peut modifier seulement les contractions dues a l'et-1. Les differences fonctionnelles entre l'et-1 et ses analogues suggerent l'existence de sites d'action diverses ou de recepteurs differents pour ces peptides dans l'aorte de rat

APA, Harvard, Vancouver, ISO, and other styles

9

Mbanya, Dora Ngum Shu epouse. "The endothelium and hypercoagulability." Thesis, University of Newcastle Upon Tyne, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287138.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Böhm, Felix. "The importance of endothelin-1 for vascular function in patients with atherosclerosis and healthy controls /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-293-0.

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

Coleman, Sarah Elizabeth. "The development of an in vitro flow simulation device to study the effects of arterial shear stress profiles on endothelial cells." Available online, Georgia Institute of Technology, 2005, 2005. http://etd.gatech.edu/theses/available/etd-07072005-220718/.

Full text

Abstract:

Thesis (M. S.)--Biomedical Engineering, Georgia Institute of Technology, 2006.
Hanjoong Jo, Ph.D., Committee Chair ; Don P. Giddens, Ph.D., Committee Member ; W. Robert Taylor, M.D., Ph.D., Committee Member ; Ajit Yoganathan, Ph.D., Committee Member.

APA, Harvard, Vancouver, ISO, and other styles

12

McSloy, Alexandra. "Regulation of macro- and micro-vascular endothelial cell survival by leptin and thrombin: signalling mechanisms and functional relevance." Thesis, Royal Veterinary College (University of London), 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.618292.

Full text

APA, Harvard, Vancouver, ISO, and other styles

13

Dignat-George, Françoise. "Apport de l'immuno-technologie a l'etude des cellules endotheliales : mise en evidence d'un marqueur antigenique et application a l'exploration de l'endotheliemie." Aix-Marseille 2, 1992. http://www.theses.fr/1992AIX22954.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Kelland, Nicholas. "The role of the endothelial cell endothelin B receptor in cardiovascular function." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/1899.

Full text

Abstract:

Endothelin-1 (ET-1) binds to endothelin A (ETA) and B (ETB) receptors on vascular smooth muscle cells, resulting in profound vasoconstriction and cellular proliferation. In contrast, activation of endothelial cell (EC) ETB receptors releases nitric oxide (NO) and prostacyclin (PGI2), which are anti-mitotic and mediate vasodilatation. ETB receptors are also responsible for the clearance of ET-1 from the circulation and renal ETB receptors contribute to sodium and water balance. Pharmacological blockade and genetic models featuring total ETB ablation, demonstrate salt sensitive hypertension. However, these do not allow the role of the EC ETB in cardiovascular homeostasis to be determined. Mice featuring loxP sites flanking exons 3 and 4 of the ETB gene (floxed ETB mice: FF/--) were crossed with Tie2-Cre mice (WW/Tie2-Cre), in which the expression of a Cre recombinase cDNA transgene is limited to EC, to generate EC-specific ETB down-regulated mice (FF/Tie2-Cre). Having demonstrated EC-specific down-regulation of ETB receptors using autoradiography, the role and relative contribution of the EC ETB to the regulation of systemic BP, to the clearance of ET-1 from the plasma, as well as to the development of pulmonary arterial hypertension were investigated. Autoradiography revealed significant down-regulation of ETB in EC-rich tissues such as lung of FF/Tie2-Cre animals (8 ± 3 amol.mm-2) compared to controls (80 ± 21 amol.mm-2) (n=4; p<0.05). Levels of ETA expression were preserved despite higher concentrations of plasma ET-1 in the FF/Tie2-Cre samples (12.4 ± 3.0 pg.ml-1) compared to controls (3.0 ± 0.8 pg.ml-1) (n=6; p<0.001). Using radiotelemetry, mean arterial blood pressure of FF/Tie2 mice was not significantly different to that of FF/- controls on low salt (FF/Tie2-Cre: 122.7 ± 1.52 mmHg, n=10; FF/--: 125.7 ± 0.58 mmHg, n=12), normal salt (FF/Tie2-Cre: 133.8 ± 4.0 mmHg, n=10; FF/--: 131.5 ± 3.33 mmHg, n=12) or high salt diet (FF/Tie2-Cre: 149.2 ± 2.71 mmHg, n=10; FF/--: 143.9 ± 2.97 mmHg, n=12). Similarly no differences in SBP, DBP or HR were seen between genotypes. The clearance of an intravenous bolus of radiolabelled ET-1 was significantly impaired in FF/Tie2-Cre mice (0.054 ± 0.006 ml.sec-1) compared to control mice (0.175 ± 0.032 ml.sec-1) (n=5; p<0.01). ETB blockade of control mice reduced ET-1 clearance to that of untreated FF/Tie2-Cre animals (n=4). Two weeks of hypobaric hypoxia induced an exaggerated increase in systolic right ventricular pressure in FF/Tie2-Cre mice (34.4 ± 1.2 mmHg, n=10) compared with FF/-- mice (24.6 ± 1.4mmHg, n=10; p<0.05), associated with an increased right ventricular/ left ventricular + septum ratio in FF/Tie2-Cre mice (normoxia: 0.224 ± 0.009; hypoxia: 0.285 ± 0.017; p<0.01), but not in FF/-- mice. Hypoxia increased the percentage of remodeled vessels in FF/-- mice (normoxia: 5.6 ± 0.6%; hypoxia: 11.4 ± 0.6%; n=6; p<0.001), and this was augmented in FF/Tie2-Cre mice (normoxia: 7.1 ± 0.5%; hypoxia: 18.5 ± 1.2%; n=6; p<0.001). The EC ETB receptor does not play a significant role in the BP response to salt, suggesting that ETB signalling on other cell types is responsible for ETB mediated natriuresis. However, the EC ETB receptor is crucial to the elimination of ET-1 from the circulation and is protective against the development of pulmonary arterial hypertension, most likely by preventing remodeling of small pulmonary arteries.

APA, Harvard, Vancouver, ISO, and other styles

15

Steer, Peter. "Lipids and Endothelium-Dependent Vasodilation." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3424.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Diekman, Mattheus Jozef Maria. "Thyroid hormones, lipids and endothelium." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2000. http://dare.uva.nl/document/84351.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Souadkia, Nahed. "Hookworms and the vascular endothelium." Thesis, University of Nottingham, 2010. http://eprints.nottingham.ac.uk/11412/.

Full text

Abstract:

Background. Necator americanus is one of the major causes of human hookworm infection, affecting over 800 million people worldwide. Hookworm infections cause gastro-intestinal bleeding, anaemia and iron deficiency, and are associated with high rates of morbidity, especially in children. Although chemotherapy has proven effective, high rates of reinfection are reported in socioeconomically developing countries, possibly due to the short-term efficacy of anthelmintic drugs in addition to individual predisposition to these infections, raising interests in developing suitable alternatives to chemotherapy which are capable of providing complete, long-term protection against hookworms. Understanding of the molecular mechanisms used by Necator americanus larvae to penetrate the human skin and the vasculature would therefore aid the development of effective vaccines against this important pathogen. Methods. First, Necator americanus larval exsheathing fluid (EF) and excretory/secretory products (ES) were profiled using gel electrophoresis and enzyme assays. Protease inhibitors against the main protease classes were used to determine which proteases are present in larval products. Second, the interaction of larval EF and ES products with human skin and extracellular matrix (ECM) macromolecules including collagens I, III, IV and V, fibronectin and laminin was investigated using western blots and protein separation by gel electrophoresis. Third, the impact of Necator americanus larval EF and ES on the endothelial barrier was examined using human umbilical vein endothelial cells (HUVEC). Permeability, an essential endothelial barrier function, was assessed during treatment with larval products, using transendothelial electrical resistance (TEER), and post-treatment using albumin-tracer flux. Finally, at the cellular level, responses to treatment with larval products were assessed by investigating molecular changes at cell-cell vascular endothelial (VE)-cadherin junctions and actin filaments, and by determining levels of secreted inflammatory cytokines, IL-6 and IL-8, and vascular endothelial growth factor (VEGF) in the culture medium. Results. It would appear that a repertoire of larval proteases, including serine, cysteine, aspartyl and metalloprotinases, caused partial degradation of skin macromolecules, collagens I, III, IV and laminin while fibronectin was fully degraded. Proteolysis of skin- and ECM macromolecules was related to the characteristic presence of proteolytic enzymes in larval products. The presence of transglutaminase activity was confirmed in both EF and ES products. Larval proteases caused a dose related increase in endothelial permeability, characterised by a decrease in monolayer resistance (TEER) with increased permeation of albumin tracer, which was minimal in the presence of a cocktail of protease inhibitors. These barrier changes were associated with disruption of junctional VE-cadherin and F-actin, the formation of intercellular gaps and an increase in endothelial secretion of IL-6 and IL-8. Conclusions. Necator americanus larvae produce a repertoire of proteolytic enzymes which could play an important role in negotiating the skin and breaching the endothelium to gain access to the host’s blood circulation.

APA, Harvard, Vancouver, ISO, and other styles

18

D'Cruz, David Pascal. "Autoimmunity, endothelium and vascular disease." Thesis, King's College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298705.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

McGrath, James L. (James Lionel). "Measuring actin dynamics in endothelium." Thesis, Massachusetts Institute of Technology, 1994. http://hdl.handle.net/1721.1/38015.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

Simeone, Stefania. "Gene expression in the vasculature of mice overexpressing human endothelin-1 in the endothelium." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86854.

Full text

Abstract:

Endothelin-1 (ET-1), an endothelium-derived vasoconstrictor peptide, plays a role in the pathophysiology of cardiovascular disease. Transgenic mice that overexpress human preproET-1 selectively in the endothelium exhibit endothelial dysfunction and hypertrophic remodeling of resistance-size arteries in the absence of blood pressure elevation. In order to understand the mechanisms whereby ET-1 directly induces vascular damage, we determined the changes in gene expression in mesenteric arteries of these mice using genome-wide expression profiling. This study revealed a set of genes potentially regulated by ET-1, which might be implicated in ET-1 induced-vascular damage. Our findings suggest that increased endothelium-restricted ET-1 expression results in early changes in gene expression, which increase lipid biosynthesis and decrease bone morphogenetic protein (BMP)-4 expression, and may contribute, at least in part, to ET-1-induced vascular damage. These results have the potential of defining ET-1 gene targets, which may facilitate the discovery of new therapeutic approaches against detrimental effects of ET-1.
Keywords: endothelin-1, gene expression, lipid biosynthesis, BMP4
L'endothéline-1 (ET-1), un puissant peptide vasoconstricteur produit par l'endothélium, joue un rôle dans la pathophysiologie des maladies cardiovasculaire. Des souris transgéniques surexprimant la prépro-ET-1 humaine dans l'endothélium présentent une dysfonction endothéliale et un remodelage hypertrophique des artères de résistance en l'absence d'hypertension. Pour comprendre les mécanismes expliquant les modifications vasculaires de ces animaux, nous avons étudié les changements transcriptomiques dans les artères mésentériques. Cette étude a révélé une série de gènes régulés par l'ET-1 qui pourrait être impliquée dans les dommages vasculaires induits par l'ET-1. Ces résultats suggèrent qu'une augmentation d'expression d'ET-1 augmente la biosynthèse de lipides et diminue l'expression de la « bone morphogenic protein » (BMP)-4, ce qui pourrait contribuer, du moins en partie, aux développements des dommages vasculaires induits par l'ET-1. Ces résultats ont le potentiel de définir des cibles de l'ET-1 qui pourraient faciliter la découverte de nouvelles approches thérapeutiques contre les effets nuisibles de l'ET-1.
Mots clés: endothéline -1, changements transcriptomiques, biosynthèse de lipides, BMP4

APA, Harvard, Vancouver, ISO, and other styles

21

Florian, Maria 1953. "The role of estrogen in the maintenance of healthy endothelium /." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111873.

Full text

Abstract:

The place of estrogen in women's health remains controversial. Premenopausal women have a lower prevalence of cardiovascular disease (CVD) than men and in observational studies hormone replacement therapy (HRT) decreases CVD in postmenopausal women. However, prospective randomized trials of secondary and primary prevention have failed to substantiate an overall protective effect from HRT and have even shown some harm. To explain this paradox it is necessary to better understand the effects of estrogen on the vascular wall. Estrogen rapidly mediates the activation of eNOS and increases the production of nitric oxide (NO), an important factor for endothelial health. In ovariectomized rats estrogen reduces production of superoxide (O2-) by NAD(P)H oxidase. The decreased function is associated with a decrease in the p47phox component of NAD(P)H oxidase and its interaction with the multicomponent enzyme. In these rats estrogen did not alter eNOS expression and bioavailability of NO, which is in contrast to its acute effects. This highlights the difference between chronic and acute studies. The decrease in O2-production suggests the intracellular signaling.
Estrogen has antiapoptotic effects. Oxidized low-density lipoprotein (oxLDL) and the inflammatory cytokine TNFalpha increased apoptosis which is associated with atherosclerosis. In human umbilical vein endothelial cells (HUVEC), estrogen decreased the extent of TNFalpha and oxLDL induced apoptosis as indicated by the expression of cleaved caspase-3 and FACS assay. Estrogen also preserves the antiapoptotic mitochondrial Bcl-2 and Bcl-xL proteins.
Estrogen has angiogenic properties that can help a healthy endothelium respond to injury. However, estrogen increases the angiogenesis caused by TNFalpha and this could lead to revascularization in the plaques of women with advanced disease.
Overall the balance between the positive and negative aspects of the effects of estrogen on the vascular wall could explain the paradoxical response in older women.

APA, Harvard, Vancouver, ISO, and other styles

22

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

Full text

Abstract:

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 resistance to detachment by flow electric cellsubstrate impedance sensing (ECIS). The results of standard and ECIS methods showed both dose and time dependent responses in cell adhesion and spreading. In addition, OPN promoted haptotactic migration of EPCs in Boyden chamber assays. LEPCs seeded onto 10μM OPN substrates and exposed to laminar flow had grater survival and higher resistance to detachment than OPN/static and flow only conditions. CD44 and !1 integrins were only responsible for approximately 50% of LEPCs adhesion to OPN compared to the unblocked condition. Western blots showed that Rho GTPases were activated in L-EPCs seeded on OPN. However, this activation could not be completely blocked by either CD44 or !1 integrin antagonists. These data confirm the direct effects of OPN on EPCs adhesion, and suggest that OPN works by mediating cell adhesion during vascular injury.

APA, Harvard, Vancouver, ISO, and other styles

23

Wang, Xin. "Endothelial cell activation and injury in umbilical placental vascular disease." Thesis, The University of Sydney, 2003. https://hdl.handle.net/2123/27854.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Nakao, Kazuhiro. "ENDOTHELIUM-DERIVED C-TYPE NATRIURETIC PEPTIDE CONTRIBUTES TO BLOOD PRESSURE REGULATION BY MAINTAINING ENDOTHELIAL INTEGRITY." 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225500.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

SCRIMIERI, ROBERTA. "ENDOTHELIUM IN PETRI DISH (2D) OR ON-A-CHIP (3D): STUDIES ON ENDOTHELIAL FUNCTION / DYSFUNCTION." Doctoral thesis, Università degli Studi di Milano, 2022. http://hdl.handle.net/2434/887953.

Full text

Abstract:

Endothelial cells (ECs) form the inner layer of all the blood vessels and, due to this strategic localization, they constantly face oscillating blood glucose concentrations in relation to the pre- and post- prandial cycles. They do not represent a passive barrier between blood and tissues, but they play a wide variety of pivotal roles to control vascular homeostasis. Uncontrolled hyperglycaemia elicits ECs to become dysfunctional, leading to the onset of endothelial dysfunction, defined as a shift of properties of the endothelium toward a proinflammatory and prothrombotic phenotype characterised by altered release of Nitric Oxide (NO) and overproduction of pro-inflammatory cytokines and Reactive Oxygen Species (ROS). Endothelial dysfunction is classically described in patients affected by diabetes and has a role in the pathogenesis of many cardiovascular complications associated with this pathology. In particular, diabetes is a group of life-long chronic metabolic disorders characterized by high levels of glucose in the blood and by a predisposition to premature atherosclerosis, the main reason for high morbidity and impaired life expectancy in patients. To investigate the effects of high glucose on ECs, Human Umbilical Vein Endothelial Cells (HUVEC) were cultured in the presence of either high glucose-containing medium or of blood sera collected from diabetic patients. Cells were seeded both in 2D cell culture systems on flat dishes, a method which has yielded major advances in our knowledge about endothelial pathophysiology, and in 3D microfluidic chips, which show a higher degree of structural complexity allowing perfusion, thus generating shear stress fundamental for endothelial homeostasis. In 2- and 3- D, the cells were cultured until they reach confluence to reproduce the physiological inner layer of a blood vessel as closely as possible. High glucose rapidly alters the cellular redox balance resulting in a higher production of ROS associated with a lower content of the antioxidant glutathione (GSH). ROS induce iNOS, which overproduces NO leading to endothelial hyperpermeability. In parallel, mitochondrial dysfunction occurs as a result of the imbalance in mitochondrial dynamics in favour of mitochondrial fission. This evidence is connected to the higher storage of triglycerides caused by both enhanced lipogenesis and reduced β-oxidation. The next step was to individuate a countermeasure that might prevent the detrimental effects of high glucose on HUVEC. Numerous observational studies demonstrated that the circulating levels of Vitamin D3 (VitD) are low in patients affected by diabetes. In these experimental models, VitD is capable of blocking the increase of ROS production, thus preventing all the harmful effects caused by high glucose on HUVEC. In summary, the results reveal that it is fundamental to keep glycaemia within the physiological range in diabetic patients, preventing hyperglycaemic peaks, and that VitD could represents a serviceable tool to control the redox equilibrium, thus re-establishing NO levels and permeability and mitochondrial fitness, to limit or at least delay the insurgence of endothelial dysfunction caused by high fasting glucose concentrations.

APA, Harvard, Vancouver, ISO, and other styles

26

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.

Full text

Abstract:

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 are potent elastases and collagenases leading to protease degradation and remodeling of the extracellular matrix structural components. Conversely, atheroprotective unidirectional laminar shear stress (LS) (15 dynes/cm2) decreased elastase and gelatinase activities of endothelial cells through a shear stress mediated reduction in cathepsins K, L, and S activity. Their endogenous inhibitor, cystatin C, was found to be inversely regulated by shear stress; LS increased its secretion by endothelial cells while OS decreased it. Binding of free cystatin C in the conditioned media to carboxymethylated papain coated agarose beads led to an increase in cathepsin activity since the available cathepsin was not inhibited. To verify these findings in human samples, immunohistochemical analysis of cystatin C and cathepsin K was performed on human coronary arteries. Cathepsin K stained strongly in the endothelial layer of vessels with degraded internal elastic lamina while cystatin C staining intensity was strongest overlying minimally diseased vessels. Additional roles for cathepsins K, L, and S were found in endothelial cell alignment in response to unidirectional laminar shear stress, endothelial cell migration, and programmed cell death. We conclude that there is an inverse regulation of cathepsins and cystatin C in endothelial cells by LS and OS and identify the cathepsin family of proteases as potential targets for therapeutic intervention of cardiovascular disease development at sites of disturbed flow.

APA, Harvard, Vancouver, ISO, and other styles

27

Mancini, Maria L. "Novel Roles for Endoglin in Vascular Development and Maintenance of Vascular Integrity." Fogler Library, University of Maine, 2007. http://www.library.umaine.edu/theses/pdf/ManciniML2007.pdf.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

Brown, Marena Dessette. "Sickle cell-endothelial interactions : modulation of cell adhesion molecule expression." Diss., Georgia Institute of Technology, 1995. http://hdl.handle.net/1853/11306.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Magid, Richard. "Engineering molecular reporters to investigate the effects of shear stress upon endothelial cells." Thesis, Georgia Institute of Technology, 2000. http://hdl.handle.net/1853/13754.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Lindberg, Lars. "Endothelial function during ischemia-reperfusion and effects of inhalation of nitric oxide." Lund : Dept. of Anesthesiology and Intensive Care, University of Lund, 1996. http://catalog.hathitrust.org/api/volumes/oclc/38164585.html.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Ajne, Gunilla. "Endothelin and the regulation of peripheral and uteroplacental vascular tone during pregnancy /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-144-X/.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Ni, Chih-Wen. "Discovery of mechanosensitive microrna and messenger RNA in mouse arterial endothelium and in cultured endothelial cells." Diss., Georgia Institute of Technology, 2010. http://hdl.handle.net/1853/34674.

Full text

Abstract:

Atherosclerosis is a major contributor to cardiovascular disease and accounts for an estimated one third of deaths overall. In order to address the hemodynamic components of disease pathogenesis, researchers have focused on mechanotransduction of flow-dependent shear stress in the vascular endothelium as a source of novel pathological mechanisms. Understanding how unidirectional, laminar blood flow protects vessels from atherogenesis, while disturbed, oscillatory blood flow promotes it, stands to provide enormous insight into disease pathogenesis and may provide powerful, specific new therapies for cardiovascular disease intervention. The overall objective of this dissertation was to determine which microRNAs (miRNAs) and mRNAs are regulated by different flow conditions in vascular endothelial cells in vitro and in mouse carotid artery endothelium in vivo, and to identify which miRNAs mediate flow-dependent vascular inflammation. The overall hypothesis of this project was that oscillatory shear (OS) and laminar shear (LS) stress differentially alter the expression of mechanosensitive miRNAs each capable of regulating complex networks of gene expression, which in turn leads to inflammation in endothelial cells. This hypothesis was tested using both in vitro and in vivo approaches, high throughput microarray analyses, and functional validation of specific targets by PCR. The findings from the partial carotid ligation model show that acute exposure to disturbed flow results in accelerated endothelial dysfunction and atherosclerosis in vivo. High-throughput microarrays reveal distinct expression profiles of both miRNAs and mRNAs in mouse endothelium exposed to disturbed flow suggesting the regulatory mechanisms by which miRNAs regulate mRNAs resulting in EC inflammation, the earliest stage of atherosclerosis. This in vivo study provides new insight into the mechanisms of flow induced atherosclerosis. In particular, the upregulation of miR-663 due to OS in HUVEC causes monocyte adhesion, but not endothelial apoptosis, in an ICAM-1 dependent manner. miR-663 regulates a group of genes including transcriptional factors and inflammatory genes which may also mediate OS-induced EC inflammation. Collectively, revealing the profiles of miRNAs and mRNAs regulated by hemodynamic flow provides a better understanding in vascular diseases and provide potential target for developing effective preventative therapeutic approaches in cardiovascular diseases.

APA, Harvard, Vancouver, ISO, and other styles

34

Johansson, Kristina. "Mental Stress and Endothelium-Dependent Vasodilation." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis, 2002. http://publications.uu.se/theses/91-554-5305-8/.

Full text

APA, Harvard, Vancouver, ISO, and other styles

35

Lundman, Pia. "Effects of triglycerides on the endothelium /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4881-X/.

Full text

APA, Harvard, Vancouver, ISO, and other styles

36

Gamble, Jennifer Ruth. "Regulation of leukocyte adhesion to endothelium /." Title page, contents and abstract only, 1994. http://web4.library.adelaide.edu.au/theses/09PH/09phg1898.pdf.

Full text

APA, Harvard, Vancouver, ISO, and other styles

37

Tang, Hoi-ching Eva. "Endothelium-dependent contractions in rodent aortae." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/HKUTO/record/B39558447.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Branniff, Emma. "Regulation of ROBO4 expression in endothelium." Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.443579.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

Tang, Hoi-ching Eva, and 鄧凱澄. "Endothelium-dependent contractions in rodent aortae." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39558447.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Gardner-Medwin, Janet. "The endothelium in primary Raynaud's phenomenon." Thesis, University of Nottingham, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360542.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Satcher, Robert L. "A mechanical model of vascular endothelium." Thesis, Massachusetts Institute of Technology, 1993. http://hdl.handle.net/1721.1/12555.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Schuller, Bradley W. "Selective irradiation of the vascular endothelium." Thesis, Massachusetts Institute of Technology, 2007. http://hdl.handle.net/1721.1/44787.

Full text

Abstract:

Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Nuclear Science and Engineering, 2007.
"September 2007."
Includes bibliographical references.
We developed a unique methodology to selectively irradiate the vascular endothelium in vivo to better understand the role of vascular damage in causing normal tissue radiation side-effects.The relationship between vascular endothelial cell apoptosis and intestinal crypt stem cell death was evaluated using uniform whole-body and selective vascular irradiation techniques. Mice received whole-body epithermal neutron beam irradiation. Additional dose was selectively targeted to endothelial cells from the short-ranged (5-9 [mu]m) particles released from neutron capture reactions in 10B confined to the blood by incorporation into 70-90 nm-diameter liposomes. Mice also received uniform photon doses above and below the threshold for death from the gastrointestinal (GI) syndrome. When plotted versus neutron beam dose, the crypt microcolony assay showed the same dose response for both the neutron beam-only and neutron beam plus boronated liposome groups. The added dose selectively delivered to the microvasculature did not cause any additional crypt loss. Jejunal cross-sections were prepared 4 hrs after irradiation and stained with TUNEL to observe and score apoptotic cells in the villus lamina propria. To uniquely identify the type of cell undergoing apoptosis in the lamina propria, intestinal specimens from various mice in the TUNEL studies were sectioned and stained with Meca-32 to identify endothelial cells and caspase-3 to identify apoptotic cells and visualized using dual-fluorescence microscopy. The TUNEL data showed a low level (~2 apoptotic cells per villus) of apoptosis in the lamina propria for both the uniform (photon or neutron) and selective vascular irradiation conditions that was independent of the administered dose.
(cont.) The dual-fluorescence studies indicated that most apoptotic bodies in the lamina propria were not endothelial cells but, rather, apoptotic leukocytes. These data demonstrate that there is no causal relationship between vascular endothelial cell apoptosis and crypt stem cell death in the mouse small intestine.
by Bradley W. Schuller.
Ph.D.

APA, Harvard, Vancouver, ISO, and other styles

43

HYNES, MICHAEL RAY. "ENDOTHELIUM-DEPENDENT RELAXATION OF BLOOD VESSELS." Diss., The University of Arizona, 1987. http://hdl.handle.net/10150/184134.

Full text

Abstract:

Dilation of blood vessels in response to a large number of agents has been shown to be dependent on an intact vascular endothelium. The present studies examine some aspects of endothelium-dependent vasodilation in blood vessels of the rabbit and rat. Using the rabbit ear artery and the subtype-selective muscarinic antagonist pirenzepine, muscarinic receptors of the endothelium and smooth muscle cells were shown to be of the low affinity M₂ subtype. Inhibition of [³H](-)quinuclidinyl benzilate was used to determine affinity for the smooth muscle receptors while antagonism of methacholine induced vasodilation yielded the endothelial cell receptor affinity. The effect of increasing age (1-27 months) on endothelium-dependent relaxation was studied in aortic rings, perfused tail artery and perfused mesenteric bed of the Fisher 344 rat. Both aortic ring segments and perfused caudal arteries showed an age-related increase in sensitivity of endothelium-mediated relaxation to the cholinergic agonist methacholine. This increased sensitivity occurs between the ages of 6 and 12 months, with no further significant increase up to 27 months of age, suggesting this is a consequence of growth and development rather than old age. No difference with age in cholinergic relaxation was observed in the perfused mesenteric bed indicating either no change of sensitivity in smaller resistance vessels or an effect which is hidden in this more complex perfused system. In contrast to findings with cholinergic stimution, responses of the perfused caudal artery to the calcium ionophore A23187 were not altered with age. This suggests that the alteration with age in response to methacholine involves the muscarinic receptor or receptor coupling mechanism rather than the generation of, or response to, endothelium-derived relaxing factor (EDRF). The influence of endothelium on contractile responses was examined using the perfused caudal artery. Endothelium removal significantly increased contraction to the α-adrenergic agonists methoxamine and BH-T 920 as well as to transmural nerve stimulation. Inhibition of contraction to agents which must first cross the smooth muscle layer before reaching the endothelium suggests that a continuous or basal level of EDRF release is responsible for decreased contraction rather than an receptor stimulated release of EDRF.

APA, Harvard, Vancouver, ISO, and other styles

44

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.

Full text

Abstract:

Thesis (Ph.D.)--Indiana University, 2009.
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).

APA, Harvard, Vancouver, ISO, and other styles

45

Subramanian, Indhu. "Characterisation of the endothelial contribution to oncogenesis – a genetic approach." Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/16865.

Full text

Abstract:

Angiogenesis is the development of new blood vessels from existing vessels. Anti-angiogenic agents target the endothelial cells (ECs; the cells that line blood vessels) and have shown efficacy in solid tumours. However, current therapies are limited by their side effects. The goal of this project was to define new molecular targets for anti-angiogenic therapy using a mutational approach. Sleeping Beauty (SB) is a random insertional mutagenesis system for genetically modifying cellular behaviour. Endothelial-specific SB activation was achieved using angiopoietin receptor (Tie-2) promoter/enhancer sequences to drive Cre-recombinase expression. All SBxTie2-Cre (n=147) and no WT (n=89) mice became moribund within 1 year and were sacrificed. At necropsy, SBxTie2-Cre mice showed peripheral leukocytosis and elevated T- cell and/or myeloid cells in spleen and bone marrow by flow cytometry and immunohistochemistry. The leukaemic phenotype in SBxTie2-Cre mice was confirmed in vitro using colony forming unit assays which identified the endothelium, and not haematopoietic stem cells (HSCs), as the source of leukaemia. Further, when segregated into vascular endothelium (CD45-/CD31+/CD144+/CD73+) and haemogenic endothelium (HECs; CD45-/CD31+/CD144+/CD73-), the HECs gave rise to the leukaemic populations. This proves HECs initiated leukaemia in SBxTie2-Cre mice and is the first report of functional contributions of HECs to haematopoiesis and/or leukemogenesis in adult organisms. Targeted deep sequencing of DNA from spleens and thymus of SBxTie2-Cre mice identified genes know to be molecular drivers of leukaemia in humans (e.g. Notch1, Ets1, Erg), suggesting that human leukaemia may also have origins in “badly behaved” endothelial populations. This validates the SB model as a therapeutic platform for drug development for leukaemia and provides further, previously unrecognised genes that contribute to leukaemia offering new therapeutic targets to treat this disease.

APA, Harvard, Vancouver, ISO, and other styles

46

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/.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

47

McNaull, Stewart A. "Analysis of sickle erythrocyte adherence to endothelium in confined flow channels." Diss., Georgia Institute of Technology, 1999. http://hdl.handle.net/1853/11019.

Full text

APA, Harvard, Vancouver, ISO, and other styles

48

Boyd, Nolan Lee. "The effect of shear stress on caveolae formation and function in endothelial cells." Diss., Available online, Georgia Institute of Technology, 2004:, 2003. http://etd.gatech.edu/theses/available/etd-04082004-180030/unrestricted/boyd%5Fnolan%5Fl%5F200312%5Fphd.pdf.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

Parker, Douglas George Anthony, and park0290@flinders edu au. "Lentivirus-mediated gene expression in corneal endothelium." Flinders University. Medicine, 2008. http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20081204.094431.

Full text

Abstract:

Modulation of corneal transplant rejection using gene therapy shows promise in experimental models but the most appropriate vector for gene transfer is yet to be determined. The overarching aim of the thesis was to evaluate the potential of a lentiviral vector for use in human corneal transplantation. Specific aims were: (i) to assess the ability of an HIV-1-based lentiviral vector to mediate expression of the enhanced yellow fluorescent protein (eYFP), and a model secreted protein interleukin-10 (IL10), in ovine and human corneal endothelium; and (ii) to examine the influence of lentivirus-mediated IL10 expression on the survival of ovine corneal allografts. Four lentiviral vectors expressing eYFP under the control of different promoters, were tested: the simian virus type-40 (SV40) early promoter, the phosphoglycerate kinase (PGK) promoter, the elongation factor-1alpha (EF) promoter, and the cytomegalovirus (CMV) promoter. Two lentiviral vectors expressing IL10 were tested: one containing the SV40 promoter and another containing a steroid-inducible promoter (GRE5). Lentivirus-mediated expression in transduced ovine and human corneal endothelium was assessed by fluorescence microscopy, real-time quantitative RT-PCR and ELISA, following alterations of transduction period duration (224 hr) and vector dose, as well as in the presence or absence of polybrene or dexamethasone (GRE5 vector). It was also compared to expression mediated by adenoviral vectors. Orthotopic transplantation of ex vivo transduced donor corneas was performed in outbred sheep. Allografts were reviewed daily for vascularisation and signs of immunological rejection. Lentivirus-mediated eYFP expression was delayed in ovine corneal endothelium compared to human. However, in both species the final transduction rate was greater than 80% and expression was stable for at least 14 d in vitro. Lentivirus-mediated expression in ovine and human corneal endothelium was higher with the viral promoters in comparison to the mammalian promoters. A 24 h transduction of ovine corneal endothelium with the lentiviral vector encoding IL10 resulted in expression levels which were increasing after 15 d of organ culture but logarithmically lower than those achieved by adenovirus. Shortening the lentiviral transduction period to 2 h led to a reduction in expression, but the addition of polybrene (40 micrograms / ml) to the transduction mixture restored expression to levels comparable to those attained after a 24 h transduction period. Lentivirus-mediated IL10 expression was higher and more rapid in human corneal endothelium compared to ovine corneas. Dexamethasone-responsive transgene expression was observed in both ovine and human corneal endothelium using the lentiviral vector containing the GRE5 promoter. Lentivirus-mediated expression in ovine corneal endothelium was stable for 28 d in vivo. A modest prolongation of ovine corneal allograft survival (median of 7 d) was achieved by transduction of donor corneas for 23 h with the lentivirus expressing IL10. Attempts to increase the expression of IL10 by the addition of polybrene (40 micrograms / ml) to the transduction mixture, resulted in a toxic effect on corneal allografts which abrogated the beneficial effect of IL10. The lentiviral vector shows potential for the stable expression of therapeutic transgenes in human corneal transplantation. However, the mechanisms underlying the species-specific differences in HIV-1-mediated transgene expression will need to be elucidated and overcome if the ovine preclinical model is to provide justification for a clinical trial.

APA, Harvard, Vancouver, ISO, and other styles

50

Sondén, Anders. "Shock wave effects on the vascular endothelium /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-183-7/.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!