Relevant bibliographies by topics / Endothelial membrane

Academic literature on the topic 'Endothelial membrane'

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Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Endothelial membrane"

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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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Szczesny-Malysiak, Ewa, Marta Stojak, Roberto Campagna, Marek Grosicki, Marek Jamrozik, Patrycja Kaczara, and Stefan Chlopicki. "Bardoxolone Methyl Displays Detrimental Effects on Endothelial Bioenergetics, Suppresses Endothelial ET-1 Release, and Increases Endothelial Permeability in Human Microvascular Endothelium." Oxidative Medicine and Cellular Longevity 2020 (October 14, 2020): 1–16. http://dx.doi.org/10.1155/2020/4678252.

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Nrf2 is a master regulator of antioxidant cellular defence, and agents activating the Nrf2 pathway have been tested in various diseases. However, unexpected side effects of cardiovascular nature reported for bardoxolone methyl in patients with type 2 diabetes mellitus and stage 4 chronic kidney disease (the BEACON trial) still have not been fully explained. Here, we aimed to characterize the effects of bardoxolone methyl compared with other Nrf2 activators—dimethyl fumarate and L-sulforaphane—on human microvascular endothelium. Endothelial toxicity, bioenergetics, mitochondrial membrane potential, endothelin-1 (ET-1) release, endothelial permeability, Nrf2 expression, and ROS production were assessed in human microvascular endothelial cells (HMEC-1) incubated for 3 and 24 hours with 100 nM–5 μM of either bardoxolone methyl, dimethyl fumarate, or L-sulforaphane. Three-hour incubation with bardoxolone methyl (100 nM–5 μM), although not toxic to endothelial cells, significantly affected endothelial bioenergetics by decreasing mitochondrial membrane potential ( concentrations ≥ 3 μ M ), decreasing spare respiratory capacity ( concentrations ≥ 1 μ M ), and increasing proton leak ( concentrations ≥ 500 nM ), while dimethyl fumarate and L-sulforaphane did not exert such actions. Bardoxolone methyl at concentrations ≥ 3 μ M also decreased cellular viability and induced necrosis and apoptosis in the endothelium upon 24-hour incubation. In turn, endothelin-1 decreased permeability in endothelial cells in picomolar range, while bardoxolone methyl decreased ET-1 release and increased endothelial permeability even after short-term (3 hours) incubation. In conclusion, despite that all three Nrf2 activators exerted some beneficial effects on the endothelium, as evidenced by a decrease in ROS production, bardoxolone methyl, the most potent Nrf2 activator among the tested compounds, displayed a distinct endothelial profile of activity comprising detrimental effects on mitochondria and cellular viability and suppression of endothelial ET-1 release possibly interfering with ET-1–dependent local regulation of endothelial permeability.
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Hallmann, Rupert, Nathalie Horn, Manuel Selg, Olaf Wendler, Friederike Pausch, and Lydia M. Sorokin. "Expression and Function of Laminins in the Embryonic and Mature Vasculature." Physiological Reviews 85, no. 3 (July 2005): 979–1000. http://dx.doi.org/10.1152/physrev.00014.2004.

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Endothelial cells of the blood and lymphatic vasculature are polarized cells with luminal surfaces specialized to interact with inflammatory cells upon the appropriate stimulation; they contain specialized transcellular transport systems, and their basal surfaces are attached to an extracellular basement membrane. In adult tissues the basement membrane forms a continuous sleeve around the endothelial tubes, and the interaction of endothelial cells with basement membrane components plays an important role in the maintenance of vessel wall integrity. During development, the basement membrane of endothelium provides distinct spatial and molecular information that influences endothelial cell proliferation, migration, and differentiation/maturation. Microvascular endothelium matures into phenotypically distinct types: continuous, fenestrated, and discontinuous, which also differ in their permeability properties. Development of these morphological and physiological differences is thought to be controlled by both soluble factors in the organ or tissue environment and by cell-cell and cell-matrix interactions. Basement membranes of endothelium, like those of other tissues, are composed of laminins, type IV collagens, heparan sulfate proteoglycans, and nidogens. However, isoforms of all four classes of molecules exist, which combine to form structurally and functionally distinct basement membranes. The endothelial cell basement membranes have been shown to be unique with respect to their laminin isoform composition. Laminins are a family of glycoprotein heterotrimers composed of an α, β, and γ chain. To date, 5α, 4β, and 3γ laminin chains have been identified that can combine to form 15 different isoforms. The laminin α-chains are considered to be the functionally important portion of the heterotrimers, as they exhibit tissue-specific distribution patterns and contain the major cell interaction sites. Vascular endothelium expresses only two laminin isoforms, and their expression varies depending on the developmental stage, vessel type, and the activation state of the endothelium. Laminin 8 (composed of laminin α4, β1, and γ1 chains) is expressed by all endothelial cells regardless of their stage of development, and its expression is strongly upregulated by cytokines and growth factors that play a role in inflammatory events. Laminin 10 (composed of laminin α5, β1, and γ1 chains) is detectable primarily in endothelial cell basement membranes of capillaries and venules commencing 3–4 wk after birth. In contrast to laminin 8, endothelial cell expression of laminin 10 is upregulated only by strong proinflammatory signals and, in addition, angiostatic agents such as progesterone. Other extracellular matrix molecules, such as BM40 (also known as SPARC/osteonectin), thrombospondins 1 and 2, fibronectin, nidogens 1 and 2, and collagen types VIII, XV, and XVIII, are also differentially expressed by endothelium, varying with the endothelium type and/or pathophysiological state. The data argue for a dynamic endothelial cell extracellular matrix that presents different molecular information depending on the type of endothelium and/or physiological situation. This review outlines the unique structural and functional features of vascular basement membranes, with focus on the endothelium and the laminin family of glycoproteins.
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Lovatt, Matthew, Khadijah Adnan, Gary Peh, and Jodhbir Mehta. "Regulation of Oxidative Stress in Corneal Endothelial Cells by Prdx6." Antioxidants 7, no. 12 (December 4, 2018): 180. http://dx.doi.org/10.3390/antiox7120180.

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The inner layer of the cornea, the corneal endothelium, is post-mitotic and unable to regenerate if damaged. The corneal endothelium is one of the most transplanted tissues in the body. Fuchs’ endothelial corneal dystrophy (FECD) is the leading indication for corneal endothelial transplantation. FECD is thought to be an age-dependent disorder, with a major component related to oxidative stress. Prdx6 is an antioxidant with particular affinity for repairing peroxidised cell membranes. To address the role of Prdx6 in corneal endothelial cells, we used a combination of biochemical and functional studies. Our data reveal that Prdx6 is expressed at unusually high levels at the plasma membrane of corneal endothelial cells. RNAi-mediated knockdown of Prdx6 revealed a role for Prdx6 in lipid peroxidation. Furthermore, following induction of oxidative stress with menadione, Prdx6-deficient cells had defective mitochondrial membrane potential and were more sensitive to cell death. These data reveal that Prdx6 is compartmentalised in corneal endothelial cells and has multiple functions to preserve cellular integrity.
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Kim, Joanna, and John A. Cooper. "Septins regulate junctional integrity of endothelial monolayers." Molecular Biology of the Cell 29, no. 14 (July 15, 2018): 1693–703. http://dx.doi.org/10.1091/mbc.e18-02-0136.

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Junctional integrity of endothelial monolayers is crucial to control movement of molecules and cells across the endothelium. Examining the structure and dynamics of cell junctions in endothelial monolayers, we discovered a role for septins. Contacts between adjacent endothelial cells were dynamic, with protrusions extending above or below neighboring cells. Vascular endothelial cadherin (VE-cadherin) was present at cell junctions, with a membrane-associated layer of F-actin. Septins localized at cell-junction membranes, in patterns distinct from VE-cadherin and F-actin. Septins assumed curved and scallop-shaped patterns at junctions, especially in regions of positive membrane curvature associated with actin-rich membrane protrusions. Depletion of septins led to disrupted morphology of VE-cadherin junctions and increased expression of VE-cadherin. In videos, septin-depleted cells displayed remodeling at cell junctions; regions with VE-cadherin were broader, and areas with membrane ruffling were wider. Septin depletion and junction disruption led to functional loss of junctional integrity, revealed by decreased transendothelial electric resistance and increased transmigration of immune cells. We conclude that septins, as cytoskeletal elements associated with the plasma membrane, are important for cell junctions and junctional integrity of endothelial monolayers, functioning at regions of positive curvature in support of actin-rich protrusions to promote cadherin-based cell junctions.
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Minshall, Richard D., William C. Sessa, Radu V. Stan, Richard G. W. Anderson, and Asrar B. Malik. "Caveolin regulation of endothelial function." American Journal of Physiology-Lung Cellular and Molecular Physiology 285, no. 6 (December 2003): L1179—L1183. http://dx.doi.org/10.1152/ajplung.00242.2003.

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Caveolae are the sites in the cell membrane responsible for concentrating an array of signaling molecules critical for cell function. Recent studies have begun to identify the functions of caveolin-1, the 22-kDa caveolar protein that oligomerizes and inserts into the cytoplasmic face of the plasma membrane. Caveolin-1 appears to regulate caveolar internalization by stabilizing caveolae at the plasma membrane rather than controlling the shape of the membrane invagination. Because caveolin-1 is a scaffolding protein, it has also been hypothesized to function as a “master regulator” of signaling molecules in caveolae. Deletion of the caveolin-1 gene in mice resulted in cardiac hypertrophy and lung fibrosis, indicating its importance in cardiac and lung development. In the endothelium, caveolin-1 regulates nitric oxide signaling by binding to and inhibiting endothelial nitric oxide synthase (eNOS). Increased cytosolic Ca2+or activation of the kinase Akt leads to eNOS activation and its dissociation from caveolin-1. Caveolae have also been proposed as the vesicle carriers responsible for transcellular transport (transcytosis) in endothelial cells. Transcytosis, the primary means of albumin transport across continuous endothelia, occurs by fission of caveolae from the membrane. This event is regulated by tyrosine phosphorylation of caveolin-1 and dynamin. As Ca2+influx channels and pumps are localized in caveolae, caveolin-1 is also an important determinant of Ca2+signaling in endothelial cells. Many of these findings were presented in San Diego, CA, at the 2003 Experimental Biology symposium “Caveolin Regulation of Endothelial Function” and are reviewed in this summary.
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Lucotte, Bertrand M., Chloe Powell, Jay R. Knutson, Christian A. Combs, Daniela Malide, Zu-Xi Yu, Mark Knepper, et al. "Direct visualization of the arterial wall water permeability barrier using CARS microscopy." Proceedings of the National Academy of Sciences 114, no. 18 (April 3, 2017): 4805–10. http://dx.doi.org/10.1073/pnas.1620008114.

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The artery wall is equipped with a water permeation barrier that allows blood to flow at high pressure without significant water leak. The precise location of this barrier is unknown despite its importance in vascular function and its contribution to many vascular complications when it is compromised. Herein we map the water permeability in intact arteries, using coherent anti-Stokes Raman scattering (CARS) microscopy and isotopic perfusion experiments. Generation of the CARS signal is optimized for water imaging with broadband excitation. We identify the water permeation barrier as the endothelial basolateral membrane and show that the apical membrane is highly permeable. This is confirmed by the distribution of the AQP1 water channel within endothelial membranes. These results indicate that arterial pressure equilibrates within the endothelium and is transmitted to the supporting basement membrane and internal elastic lamina macromolecules with minimal deformation of the sensitive endothelial cell. Disruption of this pressure transmission could contribute to endothelial cell dysfunction in various pathologies.
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Cao, Chunhua, Whaseon Lee-Kwon, Kristie Payne, Aurélie Edwards, and Thomas L. Pallone. "Descending vasa recta endothelia express inward rectifier potassium channels." American Journal of Physiology-Renal Physiology 293, no. 4 (October 2007): F1248—F1255. http://dx.doi.org/10.1152/ajprenal.00278.2007.

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Descending vasa recta (DVR) are capillary-sized microvessels that supply blood flow to the renal medulla. They are composed of contractile pericytes and endothelial cells. In this study, we used the whole cell patch-clamp method to determine whether inward rectifier potassium channels (KIR) exist in the endothelia, affect membrane potential, and modulate intracellular Ca2+ concentration ([Ca2+]cyt). The endothelium was accessed for electrophysiology by removing abluminal pericytes from collagenase-digested vessels. KIR currents were recorded using symmetrical 140 mM K+ solutions that served to maximize currents and eliminate cell-to-cell coupling by closing gap junctions. Large, inwardly rectifying currents were observed at membrane potentials below the equilibrium potential for K+. Ba2+ potently inhibited those currents in a voltage-dependent manner, with affinity k = 0.18, 0.33, 0.60, and 1.20 μM at −160, −120, −80, and −40 mV, respectively. Cs+ also blocked those currents with k = 20, 48, 253, and 1,856 μM at −160, −120, −80, and −40 mV, respectively. In the presence of 1 mM ouabain, increasing extracellular K+ concentration from 5 to 10 mM hyperpolarized endothelial membrane potential by 15 mV and raised endothelial [Ca2+]cyt. Both the K+-induced membrane hyperpolarization and the [Ca2+]cyt elevation were reversed by Ba2+. Immunochemical staining verified that both pericytes and endothelial cells of DVR express KIR2.1, KIR2.2, and KIR2.3 subunits. We conclude that strong, inwardly rectifying KIR2.x isoforms are expressed in DVR and mediate K+-induced hyperpolarization of the endothelium.
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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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Diecke, Friedrich P. J., Quan Wen, Jose M. Sanchez, Kunyan Kuang, and Jorge Fischbarg. "Immunocytochemical localization of Na+-HCO3− cotransporters and carbonic anhydrase dependence of fluid transport in corneal endothelial cells." American Journal of Physiology-Cell Physiology 286, no. 6 (June 2004): C1434—C1442. http://dx.doi.org/10.1152/ajpcell.00539.2003.

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In corneal endothelium, there is evidence for basolateral entry of HCO3− into corneal endothelial cells via Na+-HCO3− cotransporter (NBC) proteins and for net HCO3− flux from the basolateral to the apical side. However, how HCO3− exits the cells through the apical membrane is unclear. We determined that cultured corneal endothelial cells transport HCO3− similarly to fresh tissue. In addition, Cl− channel inhibitors decreased fluid transport by at most 16%, and inhibition of membrane-bound carbonic anhydrase IV by benzolamide or dextran-bound sulfonamide decreased fluid transport by at most 29%. Therefore, more than half of the fluid transport cannot be accounted for by anion transport through apical Cl− channels, CO2 diffusion across the apical membrane, or a combination of these two mechanisms. However, immunocytochemistry using optical sectioning by confocal microscopy and cryosections revealed the presence of NBC transporters in both the basolateral and apical cell membranes of cultured bovine corneal endothelial cells and freshly isolated rabbit endothelia. This newly detected presence of an apical NBC transporter is consistent with its being the missing mechanism sought. We discuss discrepancies with other reports and provide a model that accounts for the experimental observations by assuming different stoichiometries of the NBC transport proteins at the basolateral and apical sides of the cells. Such functional differences might arise either from the expression of different isoforms or from regulatory factors affecting the stoichiometry of a single isoform.
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Dissertations / Theses on the topic "Endothelial membrane"

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Burton, Victoria Jane. "Neutrophil migration through endothelial cells and their basement membrane." Thesis, University of Birmingham, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.532273.

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Secor, Jordan Douglas. "Phytochemical Antioxidants Induce Membrane Lipid Signaling in Vascular Endothelial Cells." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1338391553.

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Kline, Michelle A. "Membrane cholesterol regulates vascular endothelial cell viability, function, and lipid signaling." Connect to resource, 2008. http://hdl.handle.net/1811/32175.

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Alhumaid, Haidar S. "Nanoanalytical Studies of Bacterial Adhesion to the Membrane of Endothelial Cells." Ohio University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1470946411.

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Levy, Somin Gabriel. "The iridocorneal-endothelial syndrome : a study of cell and basement membrane pathology." Thesis, University College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.309311.

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Charles-Orszag, Arthur. "Cellular and molecular mechanisms of human endothelial cell plasma membrane remodeling by Neisseria meningitidis." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCB045/document.

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Neisseria meningitidis est une bactérie diderme qui colonise le nasopharynx humain de façon commensale. Occasionnellement, elle franchit la barrière nasopharyngée et accède à la circulation sanguine où elle peut provoquer un choc septique et/ou une méningite Le pouvoir pathogène de N. meningitidis est lié à sa capacité à interagir avec les cellules endothéliales humaines. Après avoir adhéré aux cellules grâce à des organelles filamenteux, les pili de type IV, les bactéries induisent une déformation de la membrane plasmique de la cellule hôte sous la forme de protrusions riches en actine ressemblant à des filopodes. Ces protrusions permettent aux bactéries de résister aux forces de cisaillements générées par le flux sanguin et de proliférer à la surface des cellules. Contrairement à de nombreuses autres bactéries pathogènes, cette déformation de la membrane plasmique ne nécessite pas de polymérisation d’actine. Cependant, les mécanismes cellulaires et moléculaires de cette déformation sont inconnus. Dans cette étude, nous montrons que lorsque des bactéries individuelles adhèrent à la cellule hôte, la membrane plasmique se déforme en adhérant le long des fibres de pili de type IV de façon similaire au mouillage d’un liquide sur un solide. Les pili de type IV agissent donc comme un échafaudage extracellulaire qui guide les protrusions de membrane plasmique indépendamment du cytosquelette d’actine. Nous montrons également que la capacité de la membrane plasmique à se déformer le long de structures adhésives nanométriques est une propriété intrinsèque des cellules endothéliales. Ces travaux décrivent le mécanisme d’une étape importante de la pathophysiologie de N. meningitidis et mettent en évidence des propriétés nouvelles de la membrane plasmique des cellules humaines qui pourraient être impliquées dans d’autres processus fondamentaux de biologie cellulaire
Neisseria meningitidis is a diderm bacterium that is naturally found in the human nasopharynx as a commensal. Occasionally, it can cross the mucosa and reach the underlying blood vessels where it enters the circulation. Once in the bloodstream, it can cause severe septic shock and/or meningitis. The ability of N. meningitidis to cause disease is tightly linked to its ability to interact with human endothelial cells. In particular, upon bacterial adhesion via filamentous organelles called type IV pili, bacteria remodel the host cell plasma membrane in the form of actin-rich, filopodia-like protrusions. These protrusions allow bacteria to resist blood flow-generated shear stress and proliferate on top of the host cells. Unlike many other bacterial pathogens, plasma membrane remodeling induced by N. meningitidis does not require actin polymerization. Yet, the cellular and molecular mechanisms of this process are unknown. Here, we show that upon adhesion of individual bacteria, the host cell plasma membrane deforms by adhering along type IV pili fibers in a wetting-like fashion. Therefore, type IV pili act as an extracellular scaffold that guide plasma membrane protrusions in an F-actin-independent manner. We further show that the ability of the plasma membrane to deform along nanoscale adhesive structures is an intrinsic property of endothelial cells. Therefore, this study uncovers the mechanism of a key step of N. meningitidis pathophysiology and reveals novel properties of human cell plasma membrane that could be at play in other fundamental cellular processes
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Saavedra, García Paula. "FABP4: interactions with endothelial cell plasma membrane and effects on vascular smooth muscle cells." Doctoral thesis, Universitat Rovira i Virgili, 2016. http://hdl.handle.net/10803/348560.

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Fatty acid-binding protein 4 (FABP4) és una adipoquina secretada pel teixit adipós implicada en la regulació del metabolisme energètic i la inflamació. S'han detectat nivells elevats de FABP4 circulant en persones amb factors de risc cardiovascular i aterosclerosi, encara que no hi ha moltes dades sobre FABP4 i l'aterosclerosi en humans. Alguns estudis han demostrat que FABP4 té un efecte directe sobre els teixits perifèrics, concretament promovent la disfunció endotelial. La disfunció endotelial juga un paper clau en el desenvolupament de lesions ateroscleròtiques, així com la migració i proliferació de cèl·lules de múscul llis vascular. No obstant això, el mecanisme d'acció i funcions de FABP4 circulant són poc conegudes. La hipòtesi d'aquest treball és que FABP4 interacciona amb teixits perifèrics contribuint a la disfunció endotelial i remodelació vascular a partir de la interacció amb proteïnes de membrana plasmàtica, que actuarien com a elements d'ancoratge i/o receptors mitjançant rutes de senyalització intracel·lular, i/o internalització. Els nostres resultats indiquen que FABP4 exògena interactua específicament amb citoqueratina 1 (CK1) en les membranes cel·lulars endotelials i la seva inhibició farmacològica per BMS309403 disminueix lleugerament la formació d'aquests complexos. A més, FABP4 exògena travessa la membrana plasmàtica per entrar al citoplasma i nucli de cèl·lules endotelials (HUVECs). També hem demostrat que FABP4 exògena forma un complex amb CK1 en les cèl·lules del múscul llis vascular (HCASMCs) i que té un efecte directe induint la migració i proliferació de les HCASMCs a través de l'activació de la via de senyalització MAPK per la fosforilació de ERK1/2 i activació dels factors de transcripció nuclears c-myc i c-jun. Aquests resultats suggereixen que FABP4 circulant podria tenir un paper en el remodelat vascular i progressió de l'aterosclerosi. Aquestes dades contribueixen al nostre coneixement actual sobre el mecanisme d'acció de FABP4 circulant.
Fatty acid-binding protein 4 (FABP4) es una adipoquina secretada por el tejido adiposo implicada en la regulación del metabolismo energético y la inflamación. Se han detectado niveles elevados de FABP4 circulante en personas con factores de riesgo cardiovascular y aterosclerosis, aunque no hay muchos datos sobre FABP4 y aterosclerosis en humanos. Algunos estudios han demostrado que FABP4 tiene un efecto directo sobre los tejidos periféricos, concretamente promoviendo la disfunción endotelial. La disfunción endotelial juega un papel crucial en el desarrollo de lesiones ateroscleróticas, así como la migración y proliferación de células de músculo liso vascular. Sin embargo, el mecanismo de acción y las funciones de FABP4 circulante son desconocidos. La hipótesis de este trabajo es que FABP4 interacciona con tejidos periféricos contribuyendo a la disfunción endotelial y remodelación vascular a partir de la interacción con proteínas de membrana plasmática, que actuarían como elementos de anclaje y/o receptores mediando rutas de señalización intracelular, y/o internalización. Nuestros resultados indican que FABP4 exógena interactúa específicamente con citoqueratina 1 (CK1) en las membranas celulares endoteliales y su inhibición farmacológica por BMS309403 disminuye ligeramente la formación de estos complejos. Además, FABP4 exógena atraviesa la membrana plasmática para entrar en el citoplasma y núcleo de células endoteliales (HUVECs). También hemos demostrado que FABP4 exógena también forma un complejo con CK1 en las células del músculo liso vascular (HCASMCs) y que tiene un efecto directo sobre la migración y proliferación de HCASMCs a través de la activación de la vía de señalización MAPK por la fosforilación de ERK1/2 y activación los factores de transcripción nucleares c-myc y c-jun. Estos resultados sugieren que FABP4 circulante podría tener un papel en el remodelado vascular y en la progresión de la aterosclerosis. Estos datos contribuyen a nuestro conocimiento actual sobre el mecanismo de acción de FABP4 circulante.
Fatty acid-binding protein 4 (FABP4) is an adipose tissue-secreted adipokine that is involved in the regulation of energetic metabolism and inflammation. Increased levels of circulating FABP4 have been detected in individuals with cardiovascular risk factors and atherosclerosis, although there is not much data on FABP4 in human atherosclerosis. Some studies have demonstrated that FABP4 has a direct effect on peripheral tissues, specifically promoting endothelial dysfunction. Endothelial dysfunction plays crucial roles in the development of atherosclerotic lesions as well as migration and proliferation of vascular smooth muscle cells. However, the mechanism of action and functions of circulating FABP4 are unknown. The hypothesis of this study is that circulating FABP4 has a direct effect on peripheral tissues. In particular at vessel wall level, FABP4 contributes to endothelial dysfunction and artery wall remodelling through interaction with endothelial plasma membrane proteins that act as anchoring elements and/or receptors mediating intracellular signalling, and/or FABP4 internalization. FABP4 acts on smooth muscle cells influencing cell migration and proliferation as well. Our results indicate that exogenous FABP4 interacts with specifically CK1 on endothelial cell membranes and the pharmacological FABP4 inhibition by BMS309403 decreases the formation of these complexes slightly. Furthermore, exogenous FABP4 crosses the plasma membrane to enter the cytoplasm and nucleus in HUVECs. In addition, we also demonstrated that exogenous FABP4 forms a complex with CK1 on vascular smooth muscle cells (HCASMCs) and has a direct effect of FABP4 on the migration and proliferation of HCASMCs through the activation of the ERK1/2 MAPK signalling pathway and activating the nuclear transcription factors c-myc and c-jun. Taking all these results together, it suggests that circulating FABP4 could have a role in vascular remodelling and atherosclerosis progression. These data contribute to our current knowledge regarding the mechanism of action of circulating FABP4.
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Brockmann, Tobias [Verfasser]. "Klinisch-experimentelle Ergebnisse nach „Descemet Membrane Endothelial Keratoplasty“ unter Verwendung von Trypanblau / Tobias Brockmann." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2019. http://d-nb.info/1191180875/34.

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Wardeh, Rima [Verfasser], and Walter [Akademischer Betreuer] Sekundo. "Long-Term Results after DMEK (Descemet’s Membrane Endothelial Keratoplasty) / Rima Wardeh ; Betreuer: Walter Sekundo." Marburg : Philipps-Universität Marburg, 2020. http://d-nb.info/1205879730/34.

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Sandberg, Christina Ann. "Vascular Endothelial Growth Factor in the Aqueous Humor of Dogs With and Without Intraocular Disease." Thesis, Virginia Tech, 2009. http://hdl.handle.net/10919/43367.

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Vascular endothelial growth factor A (VEGF) is a potent mediator of blood vessel formation throughout the body. Intraocular diseases characterized by inflammation, hypoxia or neoplasia induce new blood vessel formation within the eye. The end result of such blood vessel formation may be blinding sequellae such as glaucoma from outflow obstruction or hyphema from intraocular hemorrhage. Elevated VEGF concentrations in the aqueous humor and vitreous are documented in a number of human intraocular disease processes, including tumors, retinal detachment and uveitic glaucoma. Pharmacotherapy inhibiting VEGF expression demonstrates promise for control of some of these ophthalmic conditions. We quantified and compared VEGF concentrations in canine aqueous humor samples from 13 dogs with normal eyes and 226 eyes from 178 dogs with a variety of ophthalmic diseases by ELISA. Dogs with primary cataract, diabetic cataract, primary glaucoma, uveitic glaucoma, aphakic/pseudophakic glaucoma, retinal detachment, lens luxation and neoplasia were evaluated. Elevated VEGF concentrations were found in all disease conditions tested as compared to normal dogs excepting cataracts and diabetic cataracts. Elevated aqueous humor VEGF concentrations were found in dogs with pre-iridal fibrovascular membranes (PIFM) as compared to dogs without PIFM. These results are consistent with the hypothesis that VEGF has a role in the causation or progression of a variety of canine ocular disorders.
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Books on the topic "Endothelial membrane"

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Jacob, Soosan. Descemet’s Membrane Endothelial Keratoplasty. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-2034-9.

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Horst, Robenek, and Severs Nicholas J, eds. Cell interactions in atherosclerosis. Boca Raton: CRC, 1992.

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Knabb, Maureen, D. Neil Granger, Rafael Rubio, and Joey P. Granger. Endothelial Luminal Membrane-Glycocalyx: Functionalities in Health and Disease. Morgan & Claypool Life Science Publishers, 2017.

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Knabb, Maureen, D. Neil Granger, Rafael Rubio, and Joey P. Granger. Endothelial Luminal Membrane-Glycocalyx: Functionalities in Health and Disease. Morgan & Claypool Life Science Publishers, 2017.

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Knabb, Maureen, D. Neil Granger, Rafael Rubio, and Joey P. Granger. Endothelial Luminal Membrane-Glycocalyx: Functionalities in Health and Disease. Morgan & Claypool Life Science Publishers, 2017.

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1951-, Price Francis W., and Price Marianne O. 1952-, eds. DSEK: What you need to know about endothelial keratoplasty. Thorofare, NJ: SLACK Inc., 2009.

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Almeda, Dariela. Investigating the effect of liposomal membrane fluidity and antibody lateral mobility on endothelial cell targeting. 2014.

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Lennon, Rachel, and Neil Turner. The molecular basis of glomerular basement membrane disorders. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0320_update_001.

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The glomerular basement membrane (GBM) is a condensed network of extracellular matrix molecules which provides a scaffold and niche to support the function of the overlying glomerular cells. Within the glomerulus, the GBM separates the fenestrated endothelial cells, which line capillary walls from the epithelial cells or podocytes, which cover the outer aspect of the capillaries. In common with basement membranes throughout the body, the GBM contains core components including collagen IV, laminins, nidogens, and heparan sulphate proteoglycans. However, specific isoforms of these proteins are required to maintain the integrity of the glomerular filtration barrier.Across the spectrum of glomerular disease there is alteration in glomerular extracellular matrix (ECM) and a number of histological patterns are recognized. The GBM can be thickened, expanded, split, and irregular; the mesangial matrix may be expanded and glomerulosclerosis represents a widespread accumulation of ECM proteins associated with loss of glomerular function. Whilst histological patterns may follow a sequence or provide diagnostic clues, there remains limited understanding about the mechanisms of ECM regulation and how this tight control is lost in glomerular disease. Monogenic disorders of the GBM including Alport and Pierson syndromes have highlighted the importance of both collagen IV and laminin isoforms and these observations provide important insights into mechanisms of glomerular disease.
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Ware, Lorraine B. Pathophysiology of acute respiratory distress syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0108.

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The acute respiratory distress syndrome (ARDS) is a syndrome of acute respiratory failure characterized by the acute onset of non-cardiogenic pulmonary oedema due to increased lung endothelial and alveolar epithelial permeability. Common predisposing clinical conditions include sepsis, pneumonia, severe traumatic injury, and aspiration of gastric contents. Environmental factors, such as alcohol abuse and cigarette smoke exposure may increase the risk of developing ARDS in those at risk. Pathologically, ARDS is characterized by diffuse alveolar damage with neutrophilic alveolitis, haemorrhage, hyaline membrane formation, and pulmonary oedema. A variety of cellular and molecular mechanisms contribute to the pathophysiology of ARDS, including exuberant inflammation, neutrophil recruitment and activation, oxidant injury, endothelial activation and injury, lung epithelial injury and/or necrosis, and activation of coagulation in the airspace. Mechanical ventilation can exacerbate lung inflammation and injury, particularly if delivered with high tidal volumes and/or pressures. Resolution of ARDS is complex and requires coordinated activation of multiple resolution pathways that include alveolar epithelial repair, clearance of pulmonary oedema through active ion transport, apoptosis, and clearance of intra-alveolar neutrophils, resolution of inflammation and fibrinolysis of fibrin-rich hyaline membranes. In some patients, activation of profibrotic pathways leads to significant lung fibrosis with resultant prolonged respiratory failure and failure of resolution.
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Elger, Marlies, and Wilhelm Kriz. The renal glomerulus. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0043.

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The glomerulus performs its functions with three major cell types. Endothelial cells and visceral epithelial cells (podocytes) lie on the inside and outside of the glomerular basement membrane, and together these three structures form the glomerular filtration barrier. Mesangial cells sit in the axial region. Pathologies of all these regions and cell types can be identified. Parietal epithelial cells lining Bowman’s capsule participate in crescent formation, and at the tubular pole some of these cells seem to represent a stem cell population for tubular cells and podocytes. The extraglomerular mesangium and juxtaglomerular apparatus complete the description of the glomerular corpuscle. The structure of these elements, and how they relate to function, are illustrated in detail.
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Book chapters on the topic "Endothelial membrane"

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Satué, María, Fook Chang Lam, Isabel Dapena, Marieke Bruinsma, and Gerrit R. J. Melles. "Descemet Membrane Endothelial Transfer (DMET)." In Mastering Endothelial Keratoplasty, 239–51. New Delhi: Springer India, 2016. http://dx.doi.org/10.1007/978-81-322-2818-9_15.

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Kirkpatrick, C. James, Helma Rixen, Thomas Axer, Ursula Schmitz, Guenter Hollweg, Doris Klee, Rudi Wajda, Martin Kampe, Eike Fischer, and Christian Mittermayer. "Endothelial Cell-Basement Membrane Interactions." In Vascular Dynamics, 135–48. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-7856-3_11.

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Shah, Shaily Dinesh, Ashley Brissette, and Christopher S. Sales. "Descemet’s Membrane Endothelial Keratoplasty (DMEK)." In Operative Dictations in Ophthalmology, 69–76. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-53058-7_16.

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Sáles, Christopher S., Zachary M. Mayko, Mark A. Terry, and Michael D. Straiko. "Descemet Membrane Endothelial Keratoplasty (DMEK) Surgery with a Standardized Technique." In Mastering Endothelial Keratoplasty, 143–71. New Delhi: Springer India, 2016. http://dx.doi.org/10.1007/978-81-322-2818-9_9.

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Plante, Gérard E., and Mouna Chakir. "Passive Endothelial Transport: Studies in Experimental Arterial Hypertension, Diabetes Mellitus and Chronic Renal Failure." In Membrane Physiopathology, 185–206. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2616-2_12.

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Jacob, Soosan. "Techniques for Graft Visualization and Identification of Graft Orientation: Endoilluminator-Assisted Descemet’s Membrane Endothelial Keratoplasty (E-DMEK) and Others." In Mastering Endothelial Keratoplasty, 217–26. New Delhi: Springer India, 2016. http://dx.doi.org/10.1007/978-81-322-2818-9_13.

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Bhagyalaksmi, A., and J. A. Frangos. "Membrane Phospholipid Metabolism in Sheared Endothelial Cells." In Biofluid Mechanics, 533. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-52338-0_67.

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Mourik, J. A., J. C. Giltay, O. C. Leeksma, and J. Zandbergen-Spaargaren. "Membrane glycoproteins of endothelial cells and platelets." In Molecular Biology of the Arterial Wall, 148–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-83118-8_47.

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Block, Edward R. "Factors Affecting the Fluidity of the Endothelial Cell Plasma Membrane." In Vascular Endothelium, 29–42. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-8532-5_3.

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Hagedorn, Martin, and Jörg Wilting. "Chick Chorioallantoic Membrane Assay: Growth Factor and Tumor-induced Angiogenesis and Lymphangiogenesis." In Methods in Endothelial Cell Biology, 247–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18725-4_23.

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Conference papers on the topic "Endothelial membrane"

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Shao, Jin-Yu, and Baoyu Liu. "Cellular Membrane Tether Retraction: Experiment and Model." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80760.

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During leukocyte rolling on the endothelium, membrane tethers can be extracted simultaneously from both leukocytes and endothelial cells because of the force imposed by the blood flow [1]. Tether extraction has been shown to stabilize leukocyte rolling by increasing the lifetime of the adhesive selectin-ligand bonds that mediate leukocyte rolling [2]. Over the past two decades, tether extraction has been studied extensively, both experimentally and theoretically. In contrast, much less is known about tether retraction.
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García-Onrubia, Luis, Nick Stanojcic, Jing Hua, and Maninder Bhogal. "OP-4 Descemet membrane endothelial keratoplasty patching (DMEP) – selective endothelial replacement in eyes with localised endothelial dysfunction." In 2022 Proceedings of the Bowman Club Meeting, 25th March. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/bmjophth-2022-bcm.4.

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Baudin, B., L. Drouet, J. L. Carrier, M. Bérard, and Q. Y. Wu. "DISTRIBUTION OF ENDOTHELIAL MARKERS ALONG THE VASCULAR TREE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643357.

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Few specific markers of the endothelial cells are available. Von Willebrand factor has been recognized as the most specific but we have shown that its intracellular content and extracellular release varies largely along the vascular tree of the pig. Synthesis is maximal in capillaries and in pulmonary artery endothelial cells. Synthesis is almost nil in the aorta. Intermediary values are encountered in the inferior vena cava. We studied the distribution of angiotensin converting enzyme (ACE) in endothelial cells along the vascular tree, as synthesis, storage, membrane expression and release of this enzyme is totally different from that of von Willebrand factor. Primary culture of endothelial cells from various origin of the vascular tree were studied. ACE was assessed by a functional radiometric assay using a specific substrate, cellular expression depends : 1 - on culture conditions (medium with serum, adult pig serum, foetal calf serum, medium without serum), 2 - on time in culture and 3 - on the degree of cellular confluency. ACE is easily measured both in cellular extract and in the medium. After cellular fractionation, ACE is concentrated in membrane fractions. Changes were found between the arterial and venous endothelial cells but no significant variation in the distribution between intracellular and released ACE were noted. Arterial endothelium (aortic and pulmonary artery) behaved similarly while in venous endothelium (inferior vena cava) both the cellular and the releasable ACE decreased. A specific antibody to the cellular form of the porcine ACE is being raised to complete these functional studies by antigenic dosages and immunolocalization.
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Tabouillot, Tristan, Hari S. Muddana, and Peter J. Butler. "Shear Stress Induces Time- and Domain-Dependent Changes in Lipid Dynamics of Endothelial Cell Membranes." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206882.

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Endothelial cells (ECs) form the inner lining of the blood vasculature and are exposed to shear stress (τ), the tangential component of hemodynamic forces. ECs transduce τ into biochemical signals possibly via EC-membrane perturbations. We have previously used confocal-FRAP on the DiI-stained plasma membranes of confluent cultured bovine aortic ECs (BAECs) to show that τ induces a rapid, spatially heterogeneous, and time-dependent increase in the lateral diffusion of the fluorescent lipoid probe in the BAEC membrane [1]. We now present evidence at the single molecule level that shear stress differentially perturbs membrane domains that are defined by their selective staining by lipoid dyes (DiI) of differing alkyl chain lengths. This study is the first to directly measure perturbation by shear stress of endothelial cell membrane microdomains.
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Belvitch, Patrick, Mary Brown, Sara Camp, Djanybek Adyshev, Jessica Siegler, Joe G. N. Garcia, and Steven Dudek. "Cortactin Regulates Pulmonary Endothelial Cytoskeletal Structure And Membrane Dynamics." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5512.

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Groeneveld-van Beek, Esther A., Kaemela Vasanthananthan, Jessica T. Lie, GerritRJ Melles, Jacqueline van der Wees, Silke Oellerich, and Viridiana Kocaba. "32 Corneal guttae after descemet membrane endothelial keratoplasty (DMEK)." In Abstracts of the European Eye Bank Association Virtual Meeting, 3–5 March 2022. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/bmjophth-2022-eeba.32.

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Fu, Lana, and Emma J. Hollick. "P-14 Descemet stripping endothelial keratoplasty versus Descemet membrane endothelial keratoplasty: 5-year graft survival and endothelial cell loss in patients with Fuchs’ endothelial dystrophy." In 2022 Proceedings of the Bowman Club Meeting, 25th March. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/bmjophth-2022-bcm.11.

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Kudo, Susumu, Ryoma Morigaki, Mariko Ikeda, Kotaro Oka, and Kazuo Tanishita. "Effect of Shear Stress on Mitochondrial Membrane Potential of Cultured Endothelial Cells." In ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0229.

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Abstract Endothelial cells line on the inner surface of the vascular is continuously exposed to shear stress by a blood flow in vivo. It is known that shear stress influences energy-dependent physical (Dewey et al., 1981, Levesque et al., 1985) and biochemical characteristics of endothelial cells (Arisaka et al., 1995). We, therefore, evaluated mitochondrial ATP synthesis activity by a confocal laser scanning microscope (CLSM) and a mitochondrial membrane potential probe, 5.5’, 6.6’-tetrachloro-1.1’,3,3’-tetrathylbenzimidazolocarbocyananine iodide (JC-1), when shear stress was loaded over cultured endothelial cells.
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Richardson, M., and R. M. K. W. Lee. "ENDOTHELIAL BASEMENT MEMBRANE PROTEOGLYCAN (PG) ALTERATIONS IN DEOXYCORTICOSTERONE (DOCA)-NaCl -INDUCED HYPERTENSIVE RAT MESENTERIC ARTERIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644893.

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Hypertension is associated with increased endothelial permeability. This has been previously associated with endothelial desquamation or alterations in junctional architecture.To determine if this increase in endothelial permeability was associated with changes in the basement membrane, especially the heperan sulphate (HS) PG, ruthenium red-stained sections of the superior mesenteric arteries of DOCA-NaCl treated rats were examined by transmission electron microscopy. After 3 weeks of treatment, some rats were hypertensive (DOCA-H), but some remained normotensive(DOCA-N). The intimal PG distribution was compared between DOCA-H, DOCA-N, and untreated normotensive controls. Compared to untreated controls, in DOCA-H arteries there was a reduction in basement membrane, including HS, and a small increase in other PGs. In DOCA-N arteries there was a much smaller change in PGdisribution. In the DOCA-H rats, there was evidence of increased endothelial permeability as shown by sub-endothelial oedema, and an increase in the wet/dryweight ratio of the kidneys.It is therefore possible that hypertension induces changes in endothelial cell metabolism which affect the production or maintenance of the basement membrane. Since the changes were not observed in the DOCA-Narteries they are not a result of the treatment. HS is generally accepted to be involved in the control of endothelial permeability, thus the observed loss of HS from hypertensive arteries may result in the increased endothelial permeability.Supported by The Heart and Stroke Foundation of Ontario.
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Schen, Aaron, Baoguo Chen, and Lisa X. Xu. "Preliminary Study of Vascular Endothelial Ca2+ Response to Elevated Temperature." In ASME 2001 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/imece2001/htd-24424.

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Abstract Local hyperthermia has been the subject of much research because of its great potential for therapeutic and clinic applications. It has been long recognized that a major factor, which affects tissue temperature elevation and heterogeneity during hyperthermia, is the augmentation of blood flow concomitant with the heating. The heat-induced change in local blood flow can be attributed to sympathetically mediated re-distribution of cardiac output and change in local flow resistance resulting from thermally stimulated regulation in diameters of arterioles. It has been found that the vascular endothelium significantly affects the dynamic response of the vessel diameter to thermal stimuli. Endothelial cells play key regulatory roles by producing several potent vasoactive agents and regulating coagulation states, i.e. endothelium derived relaxing factors (EDRFs). Most endothelial functions depend to various extents on changes in intracellular calcium concentration [Ca2+]i. A new approach to studying vascular thermo-regulation during hyperthermia has been developed in this research to quantitatively measure the dynamic response of vascular endothelial Ca2+ to temperature elevations using confocal fluorescence ratio imaging. The cell membrane permeable fluorescence dye Fura-2/AM esters were loaded into the vascular endothelial cells and ratio imaging of the fluorescent endothelial cell were taken under the excitation of 334 and 380nm wavelengths. The signal intensities were calibrated with the endothelial calcium ion concentration ([Ca2+]i) and temperatures ranged from 37°C to 44°C. This calibration will provide a means to quantitatively measure the vascular endothelial [Ca2+]i transients in in vivo tissue when subjected to temperature elevations from 38°C to 44°C, and thus to further understand the role of endothelium in thermally induced vascular regulation under hyperthermic conditions in the near future.
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Reports on the topic "Endothelial membrane"

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Yamamoto, Fumichiro. Phage Display Breast Carcinoma cDNA Libraries: Isolation of Clones Which Specifically Bind to Membrane Glycoproteins, Mucins, and Endothelial Cell Surface. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada398247.

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Yamamoto, Fumiichiro. Phage Display Breast Carcinoma cDNA Libraries: Isolation of Clones Which Specifically Bind to Membrane Glycoproteins, Mucins, and Endothelial Cell Surface. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada393178.

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