Relevant bibliographies by topics / Endothelial cells

Academic literature on the topic 'Endothelial cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 31 July 2024

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Journal articles on the topic "Endothelial cells"

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Cardell, LO, R. Uddman, and L. Edvinsson. "Endothelins: A Role in Cerebrovascular Disease?" Cephalalgia 14, no. 4 (August 1994): 259–65. http://dx.doi.org/10.1046/j.1468-2982.1994.1404259.x.

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Vasoactive factors produced and released by the endothelium exert a powerful influence on vascular tone in the cerebral circulation. Impaired endothelium-dependent responses, such as decreased production of endothelium-derived relaxing factors, and/or release of endothelium-derived contractile factors may give rise to different pathophysiological conditions. Among the endothelium-derived contractile factors the endothelins have recently received particular attention. Endothelin-1 is the major isoform in the endothelin family, which also includes endothelin-2 and endothelin-3. Endothelin-1 is synthesized within the endothelium of cerebral vessels, whereas both endothelin-1 and endothelin-3 in addition have been identified in neurons and glia. Recent electrophysiological work has suggested a neuromodulatory role for these peptides, but at present the general interest is mainly focused on their vasoactive role. Physiological stimuli such as hypoxia, anoxia, and hemodynamic shear stress will stimulate the endothelial endothelin production. In the brain, at least two types of specific subreceptors have been cloned; ETA receptors, exclusively associated with blood vessels and ETB receptors also found on glial, epithelial, and ependymal cells. The endothelins seem so far to be the most potent vasoconstrictors yet identified. The circulating plasma levels of immunoreactive endothelin are low. Since more than 80% of the total amount released from endothelial cells seems to be secreted towards the underlying smooth muscle, endothelins have been ascribed a local vasoregulatory role. Endothelins are believed to be involved in several of our most common cerebrovascular diseases and the present review comments on their possible pathophysiological role in subarachnoid haemorrhage, cerebral ischemia, and migraine.
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Mebazaa, A., E. Mayoux, K. Maeda, L. D. Martin, E. G. Lakatta, J. L. Robotham, and A. M. Shah. "Paracrine effects of endocardial endothelial cells on myocyte contraction mediated via endothelin." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 5 (November 1, 1993): H1841—H1846. http://dx.doi.org/10.1152/ajpheart.1993.265.5.h1841.

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Endocardial endothelium is reported to modulate myocardial contraction by releasing diffusible factors, but the nature of the agent(s) responsible is unknown. In the present study we investigated the potential role of endothelin in these effects. Cultured sheep endocardial endothelial cells were found to express endothelin-1 mRNA and to release endothelin-1 into superfusing solution. This superfusate induced positive inotropic effects in isolated rat cardiac myocytes, associated with an increase in the cytosolic Ca2+ transient. Similar positive inotropic effects were induced by vascular endothelial cell superfusate as well as by synthesized endothelin-1, administered at concentrations similar to those present in the superfusate. Incubation of endocardial endothelial cell superfusate with endothelin-1-specific antiserum reduced the free endothelin-1 concentration to undetectable levels and abolished both the positive inotropic effect and the rise in cytosolic Ca2+. These findings indicate that endocardial endothelial cells may modulate myocardial contraction in part through the release of endothelin-1 and suggest that endocardial as well as vascular endothelium could exert potent paracrine effects on myocardium.
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Rosolowsky, L. J., and W. B. Campbell. "Endothelial cells stimulate aldosterone release from bovine adrenal zona glomerulosa cells." American Journal of Physiology-Endocrinology and Metabolism 266, no. 1 (January 1, 1994): E107—E117. http://dx.doi.org/10.1152/ajpendo.1994.266.1.e107.

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Intra-adrenal factors promote basal as well as adrenocorticotropic hormone (ACTH)-, angiotensin-, and flow-induced steroid secretion. Because endothelial cells respond to changes in flow and are in a close anatomical relationship to steroidogenic cells, we examined the effect of endothelial cells on the secretion of aldosterone from zona glomerulosa (ZG) cells. Endothelial cells and endothelial cell-conditioned medium (EC-CM) stimulated the release of aldosterone from ZG cells. The stimulatory effect was related to the concentration of endothelial cells or EC-CM. The maximal stimulatory effect was 60-70% of the maximal effect of ACTH. Endothelial cells alone did not produce aldosterone. Human fibroblasts were ineffective in promoting aldosterone release. Endothelial cells and EC-CM failed to stimulate cortisol release from zona fasciculata cells. Treatment of the EC-CM with trypsin and pronase abolished the activity, indicating that a protein mediated the effect. However, the EC-CM activity could be distinguished from angiotensin, endothelin-1, and bradykinin. The factor stimulated the formation of pregnenolone but not the conversion of corticosterone to aldosterone. This endothelium-derived steroidogenic factor appeared to be a novel stimulus to aldosterone secretion. This study represents the first demonstration that endothelial cells alter endocrine function in vitro.
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Westerweel, Peter E., and Marianne C. Verhaar. "Protective Actions of PPAR-γActivation in Renal Endothelium." PPAR Research 2008 (2008): 1–9. http://dx.doi.org/10.1155/2008/635680.

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Renal endothelial damage is pivotal in the initiation and progression of renal disease. Damaged renal endothelium may be regenerated through proliferation of local endothelium and circulation-derived endothelial progenitor cells. Activation of the PPAR-γ-receptors present on endothelial cells affects their cellular behavior. Proliferation, apoptosis, migration, and angiogenesis by endothelial cells are modulated, but may involve both stimulation and inhibition depending on the specific circumstances. PPAR-γ-receptor activation stimulates the production of nitric oxide, C-type natriuretic peptide, and superoxide dismutase, while endothelin-1 production is inhibited. Together, they augment endothelial function, resulting in blood pressure lowering and direct renoprotective effects. The presentation of adhesion molecules and release of cytokines recruiting inflammatory cells are inhibited by PPAR-γ-agonism. Finally, PPAR-γ-receptors are also found on endothelial progenitor cells and PPAR-γ-agonists stimulate progenitor-mediated endothelial repair. Together, the stimulatory effects of PPAR-γ-agonism on endothelium make an important contribution to the beneficial actions of PPAR-γ-agonists on renal disease.
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Saenz de Tejada, I., M. P. Carson, A. de las Morenas, I. Goldstein, and A. M. Traish. "Endothelin: localization, synthesis, activity, and receptor types in human penile corpus cavernosum." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 4 (October 1, 1991): H1078—H1085. http://dx.doi.org/10.1152/ajpheart.1991.261.4.h1078.

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The localization, synthesis, and activity of endothelin and the receptor types mediating its effects in penile corpus cavernosum were investigated in whole tissue and in cultured cells derived from this tissue. With immunocytochemistry, utilizing an antiendothelin 1 (ET-1) monoclonal antibody, endothelin-like immunoreactivity was localized intensely in the endothelium and to a lesser degree in the trabecular smooth muscle. Human corpus cavernosum endothelial cells in culture expressed preproendothelin 1 mRNA, as determined by Northern blot analysis. Significant amounts of endothelin-like immunoreactivity were measured by radioimmunoassay in the supernatants of corpus cavernosum endothelial cells in culture. Endothelins are potent constrictors and caused long-lasting contractions of corporeal strips in organ chambers. Equilibrium binding analysis of endothelins to their receptor sites revealed high-affinity, specific, and saturable binding of labeled endothelins to corporeal membranes. Competition binding experiments demonstrated receptors with high affinity for ET-1 and -2 and low affinity for ET-3 and another, less abundant, set of receptors with high affinity for ET-1, -2, and -3. Affinity labeling of endothelins to corporeal membranes, followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis, revealed that ET-1 and -2 cross-linked specifically to three different molecular mass components (75, 52, and 34 kDa). ET-3 bound only to the 34-kDa component. It is concluded that human corpus cavernosum endothelium has the ability to synthesize and release endothelin, that endothelins contract corporeal smooth muscle, and that at least two distinct endothelin receptors may exist and are differentiated by their affinity for ET-3.
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Dehouck, Marie-Pierre, Paul Vigne, Gérard Torpier, Jean Philippe Breittmayer, Roméo Cecchelli, and Christian Frelin. "Endothelin-1 as a Mediator of Endothelial Cell–Pericyte Interactions in Bovine Brain Capillaries." Journal of Cerebral Blood Flow & Metabolism 17, no. 4 (April 1997): 464–69. http://dx.doi.org/10.1097/00004647-199704000-00012.

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Endothelial cells and pericytes are closely associated in brain capillaries. Together with astrocytic foot processes, they form the blood–brain barrier. Capillaries were isolated from bovine brain cortex. Pure populations of endothelial cells and pericytes were isolated and cultured in vitro. Polarized monolayers of endothelial cells preferentially secreted immunoreactive endothelin-1 (Et-1) at their abluminal (brain-facing) membrane. They did not express receptors for Et-1. Pericytes expressed BQ-123-sensitive ETA receptors for endothelins as evidenced by 125I-Et-1 binding experiments. These receptors were coupled to phospholipase C as demonstrated by intracellular calcium measurements using indo-1-loaded cells. Addition of Et-1 to pericytes induced marked changes in the cell morphology that were associated with a reorganization of F-actin and intermediate filaments. It is concluded that Et-1 is a paracrine mediator at the bovine blood–brain barrier and that capillary pericytes are target cells for endothelium-derived Et-1.
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CPK, Cheung. "T Cells, Endothelial Cell, Metabolism; A Therapeutic Target in Chronic Inflammation." Open Access Journal of Microbiology & Biotechnology 5, no. 2 (2020): 1–6. http://dx.doi.org/10.23880/oajmb-16000163.

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The role of metabolic reprogramming in the coordination of the immune response has gained increasing consideration in recent years. Indeed, it has become clear that changes in the metabolic status of immune cells can alter their functional properties. During inflammation, stimulated immune cells need to generate sufficient energy and biomolecules to support growth, proliferation and effector functions, including migration, cytotoxicity and production of cytokines. Thus, immune cells switch from oxidative phosphorylation to aerobic glycolysis, increasing their glucose uptake. A similar metabolic reprogramming has been described in endothelial cells which have the ability to interact with and modulate the function of immune cells and vice versa. Nonetheless, this complicated interplay between local environment, endothelial and immune cells metabolism, and immune functions remains incompletely understood. We analyze the metabolic reprogramming of endothelial and T cells during inflammation and we highlight some key components of this metabolic switch that can lead to the development of new therapeutics in chronic inflammatory disease.
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Zhang, Zhong, Kristie Payne, and Thomas L. Pallone. "Syncytial communication in descending vasa recta includes myoendothelial coupling." American Journal of Physiology-Renal Physiology 307, no. 1 (July 1, 2014): F41—F52. http://dx.doi.org/10.1152/ajprenal.00178.2014.

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Using dual cell patch-clamp recording, we examined pericyte, endothelial, and myoendothelial cell-to-cell communication in descending vasa recta. Graded current injections into pericytes or endothelia yielded input resistances of 220 ± 21 and 128 ± 20 MΩ, respectively ( P < 0.05). Injection of positive or negative current into an endothelial cell depolarized and hyperpolarized adjacent endothelial cells, respectively. Similarly, current injection into a pericyte depolarized and hyperpolarized adjacent pericytes. During myoendothelial studies, current injection into a pericyte or an endothelial cell yielded small, variable, but significant change of membrane potential in heterologous cells. Membrane potentials of paired pericytes or paired endothelia were highly correlated and identical. Paired measurements of resting potentials in heterologous cells were also correlated, but with slight hyperpolarization of the endothelium relative to the pericyte, −55.2 ± 1.8 vs. −52.9 ± 2.2 mV ( P < 0.05). During dual recordings, angiotensin II or bradykinin stimulated temporally identical variations of pericyte and endothelial membrane potential. Similarly, voltage clamp depolarization of pericytes or endothelial cells induced parallel changes of membrane potential in the heterologous cell type. We conclude that the descending vasa recta endothelial syncytium is of lower resistance than the pericyte syncytium and that high-resistance myoendothelial coupling also exists. The myoendothelial communication between pericytes and endothelium maintains near identity of membrane potentials at rest and during agonist stimulation. Finally, endothelia membrane potential lies slightly below pericyte membrane potential, suggesting a tonic role for the former to hyperpolarize the latter and provide a brake on vasoconstriction.
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Jaffredo, T., R. Gautier, A. Eichmann, and F. Dieterlen-Lievre. "Intraaortic hemopoietic cells are derived from endothelial cells during ontogeny." Development 125, no. 22 (November 15, 1998): 4575–83. http://dx.doi.org/10.1242/dev.125.22.4575.

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We have investigated the developmental relationship of the hemopoietic and endothelial lineages in the floor of the chicken aorta, a site of hemopoietic progenitor emergence in the embryo proper. We show that, prior to the onset of hemopoiesis, the aortic endothelium uniformly expresses the endothelium-specific membrane receptor VEGF-R2. The onset of hemopoiesis can be determined by detecting the common leukocyte antigen CD45. VEGF-R2 and CD45 are expressed in complementary fashion, namely the hemopoietic cluster-bearing floor of the aorta is CD45(+)/VEGF-R2(−), while the rest of the aortic endothelium is CD45(−)/VEGF-R2(+). To determine if the hemopoietic clusters are derived from endothelial cells, we tagged the E2 endothelial tree from the inside with low-density lipoproteins (LDL) coupled to DiI. 24 hours later, hemopoietic clusters were labelled by LDL. Since no CD45(+) cells were inserted among endothelial cells at the time of vascular labelling, hemopoietic clusters must be concluded to derive from precursors with an endothelial phenotype.
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Hendrickx, Jan, Kris Doggen, Ellen O. Weinberg, Pascale Van Tongelen, Paul Fransen, and Gilles W. De Keulenaer. "Molecular diversity of cardiac endothelial cells in vitro and in vivo." Physiological Genomics 19, no. 2 (October 4, 2004): 198–206. http://dx.doi.org/10.1152/physiolgenomics.00143.2004.

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In addition to a number of common features, cardiovascular endothelium displays structural, functional, and genetic differences according to its position in the cardiovascular tree. In the heart, endocardial and cardiac microvascular endothelia (CMVE) interact directly with surrounding cardiomyocytes, whereas the endothelium within blood vessels interacts with smooth muscle cells. In this study, we investigated whether cardiac endothelial cells were distinct from aortic endothelial (AE) cells at the transcriptional level. Using Affymetrix microarray technology and subsequent real-time PCR analyses for validation, we identified sets of genes with marked preferential expression in cultured endocardial endothelium (EE) compared with cultured AE and vice versa. Among the genes preferentially expressed in EE, some were also expressed in cultured CMVE. Immunohistochemical staining of cardiac and aortic tissue revealed that the endothelial genetic diversity observed in culture reflects, in part, a physiological diversity existing in vivo. The identification of a set of genes preferentially expressed in EE provides new insights in the functional adaptations of this endothelial subtype to its intracavitary localization and to its role in the control of ventricular performance.
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Dissertations / Theses on the topic "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/.

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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 artery disease (CAD) and peripheral artery disease (PAD). Induced pluripotent stem cells (iPSCs) can be derived from plentiful sources of adult somatic cells, such as dermal fibroblasts (3, 4). Human iPSCs have been differentiated to endothelial cells (iPSC-ECs) and, more recently, induced endothelial cells (iECs) have been generated by direct differentiation of fibroblasts, which bypasses the pluripotent intermediate (5-11). IPSC-ECs and iECs have potential advantages over other cell types in that they can be generated in large quantities, they are not of embryonic origin and they have minimal immunogenicity. Endothelial cells have been produced via many different reprogramming and differentiation protocols, but little work has been done to determine which of these methods generates populations of cells with the greatest therapeutic potential. The studies presented in this thesis show that both iPSC-ECs and iECs have endothelial functionality in vitro and can enhance ischaemia mediated angiogenesis in a murine model of PAD. Our findings suggest that iPSC-ECs may be the more robust cell type as they demonstrate superior survival and engraftment potential in vivo. We have also generated novel data showing that iPSC-ECs enhance wound perfusion, increase wound collagen content and accelerate wound closure, which suggests they are a promising candidate therapy for chronic wounds and diabetic ulcers. Overall, the work presented in this thesis provides evidence to support the development of clinical-grade iPSC-ECs and iECs for therapeutic angiogenesis in cardiovascular disease settings.
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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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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 vene. Il termine angiogenesi si riferisce invece alla formazione di nuovi vasi sanguigni a partire da vasi preesistenti. Il processo è attivato da fattori pro-angiogenici che promuovono la migrazione e proliferazione delle cellule endoteliali e l'anastomosi dei vasi neoformati. In seguito, i nuovi vasi subiranno rimodellamenti secondari, come la regressione di particolari capillari, per formare un network vascolare maturo e funzionale. I fattori di crescita endoteliali vascolari (VEGFs) svolgono un ruolo cruciale, sia durante il processo di vasculogenesi e angiogenesi, che nel mantenimento della funzionalità vascolare. La trasduzione del segnale attivata dai VEGFs è complessa. La risposta intracellulare è attivata dal legame dei VEGFs con specifici recettori di membrana (VEGFRs). L'intensità e la durata del segnale sono invece modulate dal legame dei VEGFs con co-recettori e dall'interazione del complesso VEGF/recettore con chinasi, fosfatasi e altre proteine coinvolte nel trasporto del complesso all'interno della cellula. L'angiogenesi e l’integrità dei vasi sono processi fisiologici strettamente controllati. Infatti, un'angiogenesi non controllata e la perdita d’integrità di membrana con l’aumento di permeabilità portano a disfunzione vascolare e conseguenze patologiche. Negli ultimi anni, la disfunzione vascolare e l'alterazione del signalling del VEGF nel tessuto vascolare sono state associate all'insorgenza di numerose malattie neurodegenerative, incluso l'Alzheimer (Review I). Recenti studi suggeriscono un importante ruolo della β-amyloid precursor protein (APP), proteina chiave nello sviluppo della malattia di Alzheimer, nel mantenimento dell'omeostasi cellulare nel cervello, tuttavia la funzione di questa proteina a livello vascolare e la sua interazione con il signalling del VEGF sono tuttora ignote (Review II). In questo lavoro di tesi ho esaminato il ruolo di APP nella regolazione e modulazione del signalling VEGFA/VEGFR2 e nel mantenimento della funzionalità vascolare (Paper I). Ho inoltre studiato il ruolo del signalling di VEGF nel differenziamento di arterie e vene durante lo sviluppo vascolare embrionale utilizzando il modello in vivo di zebrafish (Paper II). Il mio lavoro di ricerca ha contribuito ad ampliare la conoscenza sulla complessa modulazione del signalling di VEGF nel tessuto vascolare, sia durante lo sviluppo embrionale, che durante l'omeostasi vascolare.
The 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.
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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.
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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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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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 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.
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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.
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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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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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 endothelial cells was very weak and could be overcome by as little as 5 femtomol hydrogen peroxide per cell. The effects were directly related to the amount of H2O2 available to each cell, rather than the concentration. Exposure to relatively low amounts of H2O2 (<0.5 picomol/cell) led to reduced endothelial cell function including prostacyclin production and mitochondrial dehydrogenase activity, and inhibited cell migration and proliferation. The cells showed gradual, partial recovery from these damaging effects. At low amounts (0.1 to 0.5 picomol/cell) H2O2 induced endothelial cell apoptosis within 48 hours of the exposure. After this time, some of the surviving cells showed evidence of senescence and could remain in culture for up to 30 days. Senescence was accompanied by an increase in cytoplasmic volume and accumulation of lipofusion. Investigation of -galactosidase activity suggested that the increased enzyme expression was linked to cell cycle rather than senescence. In conclusion, endothelial cells are very sensitive to oxidative damage but the nature of the damage is related to the degree of oxidative stress. The effects of oxidative stress may play an important role in atherosclerotic and cardiovascular diseases.
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Books on the topic "Endothelial cells"

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1941-, Ryan Una S., ed. Endothelial cells. Boca Raton, Fla: CRC Press, 1988.

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S, Ryan Una, ed. Endothelial cells. Boca Raton, Fla: CRC Press, 1988.

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Balistreri, Carmela Rita. Endothelial Progenitor Cells. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55107-4.

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Ryan, una s. endothelial cells: Vol. 1. Boca Raton, FL: CRC Press, 1995.

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J, Bicknell R., ed. Endothelial cellculture. Cambridge: Cambridge University Press, 1996.

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Fitchett, Caroline Jane. Lysophosphatidate signalling in endothelial cells. Wolverhampton: University of Wolverhampton, 2002.

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C, Aird William, ed. Endothelial cells in health and disease. Boca Raton: Taylor & Francis, 2005.

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Love, Graham P. Endothelin-I as a mediator of injury in vascular endothelial cells. Dublin: University College Dublin, 1997.

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Ricard, Cervera, Khamashta Munther A. A, and Hughes Graham R. V, eds. Antibodies to endothelial cells and vascular damage. Boca Raton, Fla: CRC Press, 1994.

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Dauphinee, Shauna M., and Aly Karsan. Endothelial dysfunction and inflammation. Basel: Birkhäuser, 2010.

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Book chapters on the topic "Endothelial cells"

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Stevens, T., G. H. Brough, T. M. Moore, P. Babal, and W. J. Thompson. "Endothelial cells." In Methods in Pulmonary Research, 403–26. Basel: Birkhäuser Basel, 1998. http://dx.doi.org/10.1007/978-3-0348-8855-4_16.

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Atkins, G. Brandon, Gabriela Orasanu, and Mukesh K. Jain. "Endothelial Cells." In Atherosclerosis, 105–16. Hoboken, NJ: John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118828533.ch9.

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Sturtzel, Caterina. "Endothelial Cells." In Advances in Experimental Medicine and Biology, 71–91. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57613-8_4.

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Gooch, Keith J., and Christopher J. Tennant. "Endothelial Cells." In Mechanical Forces: Their Effects on Cells and Tissues, 15–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-662-03420-0_2.

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Carreras, Enric, M. Diaz-Ricart, S. Jodele, O. Penack, and S. Vasu. "Early Complications of Endothelial Origin." In The EBMT Handbook, 373–83. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-44080-9_42.

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AbstractDuring HCT, the vascular endothelium is affected by conditioning, IS agents, inflammatory molecules released by injured cells and tissues, endotoxins translocated across injured mucosal barriers, the complex process of engraftment, and in allo-HCT immune alloreactivity. This endothelial damage can affect the entire vascular endothelium or that of specific organs and be the triggering event for several of the early complications grouped under denomination vascular endothelial syndromes of HCT.
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Kuwana, Masataka. "Endothelial Progenitor Cells." In Systemic Sclerosis, 39–56. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-55708-1_3.

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Kmieć, Zbigniew. "Sinusoidal Endothelial Cells." In Cooperation of Liver Cells in Health and Disease, 13–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-56553-3_3.

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Proske, Uwe, David L. Morgan, Tamara Hew-Butler, Kevin G. Keenan, Roger M. Enoka, Sebastian Sixt, Josef Niebauer, et al. "Endothelial Progenitor Cells." In Encyclopedia of Exercise Medicine in Health and Disease, 282. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2334.

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Stolz, Donna Beer. "Sinusoidal Endothelial Cells." In Molecular Pathology Library, 97–107. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-7107-4_7.

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Fischer, Johannes C. "Endothelial Progenitor Cells." In Cellular Diagnostics, 305–16. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000209168.

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Conference papers on the topic "Endothelial cells"

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Carter, A. J., W. G. Eisert, and T. H. Mμller. "DIFFERENTIAL STIMULATION OF INOSITOL TRISPHOSPHATE ACCUMULATION IN CULTURED HUMAN ENDOTHELIAL CELLS BY THROMBIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644736.

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Vascular endothelial cells possess specific receptors for thrombin, and thrombin can interact with these receptors to activate the endothelial cells. However, the signal transduction mechanisms which mediate the cellular responses are not yet characterised. The aim of this study therefore, was to determine whether thrombin influenced the inositol phosphate transduction pathway in cultured human endothelial cells. Endothelial cells were isolated from both large and small vessels; these were human umbilical vein and the microvasculature of human omentum respectively. The endothelial cells stained positively with antibodies against Factor VIII antigen and another endothelial cell specific antigen (BMA 120). Pure human thrombin (0.1 - 10 units/ml) induced a dose-dependent formation of inositol phosphate, inositol biphosphate and inositol trisphosphate (IP3) in endothelial cells from large vessels prelabelled with tritiated inositol. The formation of IP3 was significantly increased after 15 sec., maximal after 1 min. and had returned almost to baseline levels after 4 min. This time course is consistent with its role as a second messenger. When the enzymic activity of thrombin was removed with phenylalanyl-prolyl-arginine chloromethyl ketone or d i i sopr opyIfluorophosphate, thrombin lost its ability to stimulate the accumulation of IP3. Thrombin at all concentrations tested was unable to stimulate the formation of IP3 in small vessel endothelial cells. However, IP3 formation could be stimulated by bradykinin (0.1-10 μM) in cells from both small and large vessels. The results demonstrate that active thrombin can induce the formation of IP3 in large vessel endothelium. But that there are differences in the way small vessel endothelium responds to thrombin.
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de Agostini, A., J. Marcum, and R. Rosenberg. "THE BINDING OF ANTITHROMBIN TO CAPILLARY ENDOTHELIAL CELLS GROWN IN VITRO." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643343.

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Cloned endothelial cells from rat epididymal fat pads synthesize anticoagulantly active heparan sulfate proteoglycans containing the disaccharide, GlcA→ AMN-3,6-O-SO3, which is a marker for the antithrombin-binding domain of heparin. To demonstrate that antithrombin (AT) binds to cell surface heparan sulfate, a binding assay employing 125I-AT and cell monolayers has been developed. Post-confluent endothelial cells (7 days) were incubated with radiolabeled AT for 1 h at 4° and washed with PBS. Bound radioactivity was quantitated after solubilizing whole cells. Under these conditions, ∼1% (2174±50 cpm/5x104 cells) of the 125I-AT bound to the endothelial cell monolayer, whereas none of the radiolabeled protein bound to CHO cells or bovine smooth muscle cells. Utilization of unlabeled AT (1 μM) in experiments conducted as described above resulted in a reduction (73%) of the binding of the labeled species to endothelial cells. To assess whether heparan sulfate was responsible for AT binding, cell monolayers were incubated for 1 h at 37° with purified Flavobacterium heparinase (0.2 units). Over 90% of 125I-AT binding to these cellular elements was suppressed with the bacterial enzyme. Internalization of radiolabeled AT by endothelial cells was examined by incubating the protease inhibitor and cells at 4° and 37 . An initial rapid binding was observed at both temperatures. At 4° AT binding plateaued within 15 min, whereas at 37° binding did not plateau until 60 min and was 30% greater than that observed at 4. These data suggest that surface-associated AT can be internalized by endothelial cells. In addition, AT binding was shown to increase with the length of endothelial cell postconfluence, indicating an accumulation of heparan sulfate by these cells during quiescence. In conclusion, our studies support the hypothesis that the vascular endothelium is coated with heparan sulfate-bound AT, which is responsible for the antithrombotic properties of these natural surfaces.
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Krishnan, Ramaswamy, Elizabeth Peruski Canovic, Andreea L. Iordan, Athanassios P. Pirentis, Kavitha Rajendran, Greeshma Manomohan, Michael L. Smith, James P. Butler, Jeffrey J. Fredberg, and Dimitrije Stamenović. "Cytoskeletal Fluidization and Resolidification are Required for Reorientation of Endothelial Cells." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80431.

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Vascular endothelial cells are subjected to routine mechanical stretch. In response, cellular microstructures rearrange locally as the cell body realigns globally [1–5]. These responses, which underlie the vital functions of the endothelium, are often explained in terms of upstream mechanosensing and downstream cell signaling [2–5].
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Weidert, Eric, Payal Khanna, Francisco Vital-Lopez, and Cheng Dong. "Model Simulations Reveal VCAM-1 Augment PAK Activation Rates to Amplify p38 MAPK and VE-Cadherin Phosphorylation." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80364.

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Metastasis is a complex process mediated by both adhesion molecules and chemokine secretion [1]. One important event during cancer metastasis is tumor cell extravasation through the endothelium [1]. In melanoma cancer, tumor cell extravasation is mediated by very late antigen (VLA)-4 molecule adhesion to vascular cell adhesion molecules (VCAM)-1 on endothelial cells [2]. High expression levels of VLA-4 integrin are associated with a marked increase in melanoma extravasation through endothelial layers [2]. The binding of VLA-4 to VCAM -1 induces the activation of downstream mitogen activated protein kinase (MAPK) signaling cascades, which regulate the vascular endothelial (VE)-cadherin junctions that hold together endothelial cells [2].
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Shatos, M., J. Doherty, D. Allen, and J. Hoak. "ALTERATIONS IN VASCULAR ENDOTHELIAL CELL FUNCTION BY OXYGEN-FREE RADICALS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643365.

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The vascular endothelium is a target for oxidant-induced damage in many disease states including hyperoxia, inflammation, ischemia and reperfusion injury. However, little is known concerning oxidant injury to endothelial cells and its relationship to hemostasis. Our studies have focused on the ability of oxygen free radicals to injure and/or alter selected vascular endothelial cell functions pertinent to the regulation of hemostasis. Xanthine and xanthine oxidase, a well-characterized generating system for the production of the superoxide anion radical (O− 2) was used to sublethally injure human umbilical vein endothelial cells (HUVE) in vitro. We examined the effects of a 15 min exposure of HUVE cells to xanthine (50μM), and xanthine oxidase (2.5-100mU) (previously determined to be non-toxic using trypan blue dye exclusion) on platelet adherence, and prostacyclin release using established assays. The antioxidant enzymes superoxide dismutase (SOD) 200μg/ml and catalase 50μg/ml were added to endothelium incubation systems to evaluate any protective effects upon O− 2-induced alterations. All experiments were conducted in a serum-free HEPES-Tyrode's buffer, pH 7.4 incubation system. Our results show that exposure of HUVE cells to sublethal concentrations of oxygen free radical generating systems causes significant enhancement of platelet adherence (65%) to injured endothelium. A 12-fold increase in prostacyclin release resulted after a 15 min treatment with xanthine and xanthine oxidase. The addition of exogenous PGI2 (150nM) to platelet-endothelial systems did not completely prevent the enhanced platelet adherence suggesting that lack of prostacyclin was not completely responsible for the adherence of platelets to O− 2 injured cells. When SOD and catalase, scavengers of O− 2 and H2O− 2, were added to treated cells, platelet adherence decreased by 42-77% and prostacyclin release approached that of control cultures. These data implicate an active participation of activated metabolites of molecular oxygen in the alteration of vascular endothelial cell function.
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Reutelingsperger, C. P. M., W. Buurman, G. Horn-stra, and H. C. Horn-stra. "IMMUNOLOGICAL AND CHEMICAL DETECTION OF VAC IN CULTURED ENDOTHELIAL CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643913.

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Recently we reported the presence in human umbilical cord vessels of an anticoagulatory protein (VAC, Mr = 32,000) which inhibits phospholipid dependent procoagulant reactions through a high affinity binding, in the presence of calcium, to the phospholipid surface. The mechanism of anticoagulation differs fundamentally from those of the well-known physiological anticoagulants.Polyclonal antibodies, raised in rabbits against purified VAC, bind in cultured endothelial cell lysates to an antigen with Mr = 32,000, as was revealed with immunoblotting techniques. It is demonstrated with chemical techniques, that this antigen is identical to VAC.VAC appears to be an intracellular protein, attached to fine granular structures, which are located outside the nuclear area. Quiescent endothelial cells do neither secrete VAC in detectable amounts, nor contain detectable VAC on the extracellular side of their plasma membrane. In the presence of 1 mM calcium, endothelial VAC binds reversibly, as was indicated with EDTA, to the subcellular structures of the endothelial cell. Once VAC is bound to the subcellular structures, their apparent procoagulant activities are diminished, as was shown in a one-stage coagulation assay.Based on these findings, we propose that the presence of VAC in endothelial cells supplies the endothelium with an additional anticoagulatory mechanism, which can be activated after cell injury, when intracellular structures become exposed to plasma constituents. VAC then controls the formation of procoagulant complexes, localized to the subcellular structures.
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Szatmary, Alex C., Rohan J. Banton, and Charles D. Eggleton. "Deformation of White Blood Cells Firmly Adhered to Endothelium." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80894.

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Circulating white blood cells adhere to endothelium near an infection site; this occurs because infection causes ligands to be expressed on activated endothelium. Initially, a white blood cell rolls on the substrate, but eventually forms a firm adhesion, allowing it to crawl through the endothelial layer toward the infected tissue. A computational model of bond kinetics, cell deformability, and fluid dynamics was used to model the forces experienced by a cell during this process. The cell was modeled as a fluid-filled membrane; on its surface were hundreds of deformable microvilli—little fingers, ruffles in the white blood cell’s wrinkly membrane. These microvilli were deformable and their tips were decorated with PSGL-1 chemical receptors which bound to P-selectin ligands on the surface. Softer cells and cells subjected to higher fluid shear stress deformed more, and having more contact area, they formed more bonds and were able to resist more hydrodynamic load.
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Safwan-Zaiter, Hasan, Kay-Dietrich Wagner, and Nicole Wagner. "The Senescence Marker p16Ink4a—A Player of Liver Endothelial Cells Physiology." In Cells 2023. Basel Switzerland: MDPI, 2023. http://dx.doi.org/10.3390/blsf2023021013.

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Lim, Yi Chung, and David S. Long. "Aortic Hemodynamics and Endothelial Gene Expression: An Animal Specific Approach." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53312.

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Atherosclerosis is a major cause of morbidity and mortality in the developed world. This disease is identified by endothelial dysfunction, inflammation and the accumulation of lipids and cellular elements within the intima of medium and large-sized arteries. Within these arteries, the distribution of atherosclerotic lesions is non-uniform; the inner wall of curved sections and the outer walls of bifurcations are susceptible sites. Evidence suggests that the focal nature of the disease is mediated in part by local fluid mechanical stresses at the interface between flowing blood and the vessel wall. Strategically located at this interface is the monolayer of cells known as the endothelium. Although it was once considered to be an inert cell layer, the endothelium is a highly complex and metabolically dynamic cell layer. As a result, local fluid mechanical stresses at the wall of arteries may alter the phenotype of endothelial cells (ECs). With that in mind, the aim of this study is to better characterize the modulation of the endothelial cell phenotype in response to blood flow induced wall shear stress (WSS).
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Lewis, R. M., P. B. Jahrling, B. P. Griffin, and T. M. Cosgriff. "THE EFFECTS OF HEMORRHAGIC FEVER VIRUS INFECTION OF ENDOTHELIAL CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643352.

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Pichindé viral infection of strain 13 guinea pigs is a model for Lassa fever virus in humans. Infected animals show impaired platelet function and altered coagulation parameters. Human endothelial cells and the human endothe1ia1-1 ike cell line, EA926, were infected with Pichinde virus. Following infection, cultures were monitored by phase contract microscopy for cytopathic effect (CPE). Assays of supernatant were used to document viral growth and to measure those endothelial-produced components that might affect hemostasis. In addition, the cells were stimulated with phorbol ester (PMA), which stimulates the production of prostacyclin. Infection showed no noticeable effect on the endothelial cells or EA926 cells which were untreated with PMA. PHA-treated EA926 cells were subject to CPE. Factor VIII antigen was not significantly affected by viral infection, PMA treatment, or endotoxin exposure. The production of PGFl, measured as an estimate of prostacyclin synthesis, was dependent on the concentration of stimulating PMA. Infected cultures showed decreased responsiveness to PMA stimulation when infected by increasing concentrations of Pichindé. The most noticeable effect was noted when cultures were infected with a multiplicity of infection of 0.1 and 100 ng/ml PMA. Thromboxane B2 an estimate of thromboxane A2, showed no significant change. No detectable leukotriene C4 was produced and no significant change in leukotriene B4 was measured. The decreased prostacyclin production by the infected endothelial cells may indicate a role for the endothelium in the hemorrhagic syndrome that accompanies some viral diseases.
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Reports on the topic "Endothelial cells"

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Paul, Satashree. Flavivirus and its Threat. Science Repository, March 2021. http://dx.doi.org/10.31487/sr.blog.30.

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A number of studies found that the virus can activate the endothelial cells and affect the structure and function of the blood?brain barrier, promoting immune cell migration to benefit the virus nervous system target cells infected by flaviviruses.
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Quinn, Timothy P. Killing Prostate Cancer Cells and Endothelial Cells with a VEGF-Triggered Cell Death Receptor. Fort Belvoir, VA: Defense Technical Information Center, February 2003. http://dx.doi.org/10.21236/ada415526.

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Quinn, Timothy P. Killing Prostate Cancer Cells and Endothelial Cells With a VEGF-Triggered Cell Death Receptor. Fort Belvoir, VA: Defense Technical Information Center, February 2004. http://dx.doi.org/10.21236/ada423810.

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Quinn, Timothy P. Killing Prostate Cancer Cells and Endothelial Cells with a VEGF-Triggered Cell Death Receptor. Fort Belvoir, VA: Defense Technical Information Center, June 2005. http://dx.doi.org/10.21236/ada476353.

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Pumiglia, Kevin. Molecular Regulation of Endothelial Cells by NF-1. Fort Belvoir, VA: Defense Technical Information Center, July 2012. http://dx.doi.org/10.21236/ada567663.

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Pumiglia, Kevin. Molecular Regulation of Endothelial Cells by NF-1. Fort Belvoir, VA: Defense Technical Information Center, January 2013. http://dx.doi.org/10.21236/ada579995.

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Sosa Munguía, Paulina del Carmen, Verónica Ajelet Vargaz Guadarrama, Marcial Sánchez Tecuatl, Mario Garcia Carrasco, Francesco Moccia, and Roberto Berra-Romani. Diabetes mellitus alters intracellular calcium homeostasis in vascular endothelial cells: a systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0104.

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Review question / Objective: What are the effects of diabetes mellitus on the calcium homeostasis in vascular endothelial cells? -To describe the effects of diabetes on the mechanisms that regulate intracellular calcium; -To describe other molecules/mechanisms that alters intracellular Ca2+ homeostasis. Condition being studied: Diabetes mellitus is a pathology with a high incidence in the population, characterized by an increase in blood glucose. People with diabetes are 2-4 times more likely to suffer from a cardiovascular complication, such as total or partial loss of sight, myocardial infarction, kidney failure, among others. Cardiovascular complications have been reported to derive from dysfunction of endothelial cells, which have important functions in blood vessels. In order to understand the etiology of this poor function of endothelial cells, it is necessary to study the molecular mechanisms involved in these functions, to identify the effects of diabetes and thus, develop new research that will mitigate the effects of this pathology.
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Merkle, Carrie J. Studies on Breast Cancer Cell Interactions with Aged Endothelial Cells in Culture and Rat Models. Fort Belvoir, VA: Defense Technical Information Center, May 2006. http://dx.doi.org/10.21236/ada455981.

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Avraham, Hava. Studies of Vascular Endothelial Growth Factor (VEGF) Signaling in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada395916.

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Avraham, Hava. Studies of Vascular Endothelial Growth Factor (VEGF) Signaling in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada412712.

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