Journal articles: '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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Tretyakov, A. V., and H. W. Farber. "Endothelial cell phospholipid distribution and phospholipase activity during acute and chronic hypoxia." American Journal of Physiology-Cell Physiology 265, no. 3 (September 1, 1993): C770—C780. http://dx.doi.org/10.1152/ajpcell.1993.265.3.c770.

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We have previously reported alterations in cyclooxygenase metabolism in cultured aortic and pulmonary arterial endothelial cells exposed to acute and chronic hypoxia. These alterations depended on the duration and degree of the hypoxic exposure, on the vascular bed from which the endothelial cells were derived, and possibly on the availability of arachidonic acid secondary to modifications in metabolic substrate, membrane phospholipids, and/or membrane phospholipase activity. To investigate this last point further, we have compared plasma membrane phospholipid distribution and phospholipase activity in cultured aortic and pulmonary arterial endothelial cells exposed to both acute and chronic hypoxia, using two different precursors (acetic acid and arachidonic acid) and three different membrane preparations (cell homogenates, partially purified plasma membranes, and highly purified plasma membranes). We found that exposure to acute and chronic hypoxia has profound and complicated effects on endothelial cell phospholipid composition and phospholipase activity and that these effects depend on the origin of the endothelial cells and the duration of hypoxia. Furthermore, we found that the alterations in endothelial cell phospholipid distribution in response to hypoxia depend on the purity of the plasma membrane preparation and the metabolic precursor used to study phospholipid metabolism. Finally, these studies suggested that alterations in phospholipids during hypoxia occurred to a greater extent in compartments of endothelial cells other than the plasma membranes and that the well-recognized tolerance of endothelial cells to hypoxia may be due, in part, to preservation of the integrity of their plasma membranes during exposure to acute and chronic hypoxia.

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Predescu, Sanda A., Dan N. Predescu, and Asrar B. Malik. "Molecular determinants of endothelial transcytosis and their role in endothelial permeability." American Journal of Physiology-Lung Cellular and Molecular Physiology 293, no. 4 (October 2007): L823—L842. http://dx.doi.org/10.1152/ajplung.00436.2006.

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Caveolae transcytosis with its diverse mechanisms–fluid phase, adsorptive, and receptor-mediated–plays an important role in the continuous exchange of molecules across the endothelium. We will discuss key features of endothelial transcytosis and caveolae that have been studied recently and have increased our understanding of caveolae function in transcytosis at the molecular level. During transcytosis, caveolae “pinch off” from the plasma membrane to form discrete vesicular carriers that shuttle to the opposite front of endothelial cells, fuse with the plasma membrane, and discharge their cargo into the perivascular space. Endothelial transcytosis exhibits distinct properties, the most important being rapid and efficient coupling of endocytosis to exocytosis on opposite plasma membrane. We address herein the membrane fusion-fission reactions that underlie transcytosis. Caveolae move across the endothelial cells with their cargo predominantly in the fluid phase through an active process that bypasses the lysosomes. Endothelial transcytosis is a constitutive process of vesicular transport. Recent studies show that transcytosis can be upregulated in response to pathological stimuli. Transcytosis via caveolae is an important route for the regulation of endothelial barrier function and may participate in different vascular diseases.

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Baydoun, Lamis, Lisanne Ham, Vincent Borderie, Isabel Dapena, Jingzhen Hou, Laurence E. Frank, Silke Oellerich, and Gerrit R. J. Melles. "Endothelial Survival After Descemet Membrane Endothelial Keratoplasty." JAMA Ophthalmology 133, no. 11 (November 1, 2015): 1277. http://dx.doi.org/10.1001/jamaophthalmol.2015.3064.

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Lin, Mike T., John P. Adelman, and James Maylie. "Modulation of endothelial SK3 channel activity by Ca2+-dependent caveolar trafficking." American Journal of Physiology-Cell Physiology 303, no. 3 (August 1, 2012): C318—C327. http://dx.doi.org/10.1152/ajpcell.00058.2012.

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Small- and intermediate-conductance Ca2+-activated K+ channels (SK3/Kcnn3 and IK1/Kcnn4) are expressed in vascular endothelium. Their activities play important roles in regulating vascular tone through their modulation of intracellular concentration ([Ca2+]i) required for the production of endothelium-derived vasoactive agents. Activation of endothelial IK1 or SK3 channels hyperpolarizes endothelial cell membrane potential, increases Ca2+ influx, and leads to the release of vasoactive factors, thereby impacting blood pressure. To examine the distinct roles of IK1 and SK3 channels, we used electrophysiological recordings to investigate IK1 and SK3 channel trafficking in acutely dissociated endothelial cells from mouse aorta. The results show that SK3 channels undergo Ca2+-dependent cycling between the plasma membrane and intracellular organelles; disrupting Ca2+-dependent endothelial caveolae cycling abolishes SK3 channel trafficking. Moreover, transmitter-induced changes in SK3 channel activity and surface expression modulate endothelial membrane potential. In contrast, IK1 channels do not undergo rapid trafficking and their activity remains unchanged when either exo- or endocytosis is block. Thus modulation of SK3 surface expression may play an important role in regulating endothelial membrane potential in a Ca2+-dependent manner.

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Hwang, Anita M., and Jimmy K. Lee. "Descemet-stripping Automated Endothelial Keratoplasty—A Review." US Ophthalmic Review 04, no. 01 (2011): 80. http://dx.doi.org/10.17925/usor.2011.04.01.80.

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Descemet-stripping automated endothelial keratoplasty (DSAEK) has become the procedure of choice to treat corneal endothelial dysfunction. The technique involves replacing the diseased host endothelium with a graft consisting of a thin layer of posterior stroma, Descemet membrane, and endothelium. In comparison to penetrating keratoplasty (PK), DSAEK confers quicker visual and structural recovery with absence of corneal surface incisions or sutures, and limits astigmatism. DSAEK has been proved to successfully achieve favorable visual acuity and graft clarity in bullous keratopathy, posterior polymorphous dystrophy, and failed PK grafts. This article discusses various DSAEK surgical techniques, short- and longterm post-surgical results, complications, and comparisons with other types of keratoplasty. With the advent of Descemet membrane endothelial keratoplasty (DMEK), in which only Descemet membrane is transplanted, visual rehabilitation may be attained sooner.

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Hwang, Anita M., and Jimmy K. Lee. "Descemet’s Stripping Automated Endothelial Keratoplasty – A Review." European Ophthalmic Review 03, no. 02 (2009): 71. http://dx.doi.org/10.17925/eor.2009.03.02.71.

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Descemet’s stripping automated endothelial keratoplasty (DSAEK) has become the procedure of choice to treat corneal endothelial dysfunction. The technique involves replacing the diseased host endothelium with a graft consisting of a thin layer of posterior stroma, Descemet’s membrane and endothelium. In comparison with penetrating keratoplasty (PK), DSAEK confers quicker visual and structural recovery with absence of corneal surface incisions or sutures, and also limits astigmatism. DSAEK has been proved to successfully achieve favourable visual acuity and graft clarity in bullous keratopathy, posterior polymorphous dystrophy and failed PK grafts. This literature review discusses various DSAEK surgical techniques, short- and long-term post-surgical results, complications and comparisons with other types of keratoplasty. With the advent of Descemet’s membrane endothelial keratoplasty (DMEK), in which only Descemet’s membrane is transplanted, visual rehabilitation may be attained sooner.

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Bkaily, Ghassan, Levon Avedanian, Johny Al-Khoury, Chantale Provost, Moni Nader, Pedro D'Orléans-Juste, and Danielle Jacques. "Nuclear membrane receptors for ET-1 in cardiovascular function." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 300, no. 2 (February 2011): R251—R263. http://dx.doi.org/10.1152/ajpregu.00736.2009.

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Plasma membrane endothelin type A (ETA) receptors are internalized and recycled to the plasma membrane, whereas endothelin type B (ETB) receptors undergo degradation and subsequent nuclear translocation. Recent studies show that G protein-coupled receptors (GPCRs) and ion transporters are also present and functional at the nuclear membranes of many cell types. Similarly to other GPCRs, ETA and ETB are present at both the plasma and nuclear membranes of several cardiovascular cell types, including human cardiac, vascular smooth muscle, endocardial endothelial, and vascular endothelial cells. The distribution and density of ETARs in the cytosol (including the cell membrane) and the nucleus (including the nuclear membranes) differ between these cell types. However, the localization and density of ET-1 and ETB receptors are similar in these cell types. The extracellular ET-1-induced increase in cytosolic ([Ca]c) and nuclear ([Ca]n) free Ca2+ is associated with an increase of cytosolic and nuclear reactive oxygen species. The extracellular ET-1-induced increase of [Ca]c and [Ca]n as well as intracellular ET-1-induced increase of [Ca]n are cell-type dependent. The type of ET-1 receptor mediating the extracellular ET-1-induced increase of [Ca]c and [Ca]n depends on the cell type. However, the cytosolic ET-1-induced increase of [Ca]n does not depend on cell type. In conclusion, nuclear membranes' ET-1 receptors may play an important role in overall ET-1 action. These nuclear membrane ET-1 receptors could be targets for a new generation of antagonists.

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Bing, R. J., A. Termin, A. Conforto, R. Dudek, and M. J. Hoffmann. "Membrane function and vascular reactivity." Bioscience Reports 13, no. 2 (April 1, 1993): 61–67. http://dx.doi.org/10.1007/bf01145958.

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This communication examines the possibility that nitric oxide (NO) production by endothelial cells results from changes in cell membrane fluidity. Lysophosphatidylcholine (LPC) alters fluidity of the endothelial cell membranes causing vascular relaxation. Through membrane alterations LPC influences function of a number of membrane receptors and modulates enzyme activity. As a result of detergent action, lysophosphatidylcholine (LPC) causes activation of guanylate cyclase, stimulates syalytransferase and regulates protein kinase C activity. It has already been demonstrated that ionic detergents, such as Triton X-100 also cause vascular relaxation, possibly induced by NO production from endothelial cells. It is postulated that production of nitric oxide results from changes in membrane viscosity; this may represent a mechanism for its regulation in biological systems.

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Ang, Marcus, Mark R. Wilkins, Jodhbir S. Mehta, and Donald Tan. "Descemet membrane endothelial keratoplasty." British Journal of Ophthalmology 100, no. 1 (May 19, 2015): 15–21. http://dx.doi.org/10.1136/bjophthalmol-2015-306837.

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Birbal, Rénuka S., Jack Parker, Martin Dirisamer, Ana Janićijević, Lamis Baydoun, Isabel Dapena, and Gerrit R. J. Melles. "Descemet Membrane Endothelial Transfer." Cornea 37, no. 2 (February 2018): 141–44. http://dx.doi.org/10.1097/ico.0000000000001395.

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Moshirfar, Majid, Allison Jarstad, and Yousuf M. Khalifa. "Descemet Membrane Endothelial Keratoplasty." Cornea 32, no. 4 (April 2013): e52-e53. http://dx.doi.org/10.1097/ico.0b013e31827c2163.

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Droutsas, Konstantinos, Eleftherios Giallouros, Gerrit R. J. Melles, Klio Chatzistefanou, and Walter Sekundo. "Descemet Membrane Endothelial Keratoplasty." Cornea 32, no. 8 (August 2013): 1075–79. http://dx.doi.org/10.1097/ico.0b013e31828f0e3c.

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Lam, Fook Chang, Marieke Bruinsma, and Gerrit R. J. Melles. "Descemet membrane endothelial transfer." Current Opinion in Ophthalmology 25, no. 4 (July 2014): 353–57. http://dx.doi.org/10.1097/icu.0000000000000061.

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Bayyoud, Tarek, Helmut Wilhelm, Faik Gelisken, Peter Martus, Karl Ulrich Bartz-Schmidt, and Sebastian Thaler. "Descemet Membrane Endothelial Keratoplasty." Cornea 39, no. 7 (July 2020): 841–45. http://dx.doi.org/10.1097/ico.0000000000002320.

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Price, Marianne O., and Francis W. Price. "Descemet Membrane Endothelial Keratoplasty." International Ophthalmology Clinics 50, no. 3 (2010): 137–47. http://dx.doi.org/10.1097/iio.0b013e3181e21a6f.

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Chaurasia, Sunita, Francis W. Price, Lauren Gunderson, and Marianne O. Price. "Descemet's Membrane Endothelial Keratoplasty." Ophthalmology 121, no. 2 (February 2014): 454–58. http://dx.doi.org/10.1016/j.ophtha.2013.09.032.

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Price, Marianne O., Amanda Scanameo, Matthew T. Feng, and Francis W. Price. "Descemet's Membrane Endothelial Keratoplasty." Ophthalmology 123, no. 6 (June 2016): 1232–36. http://dx.doi.org/10.1016/j.ophtha.2016.02.001.

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Price, Marianne O., Arthur W. Giebel, Kelly M. Fairchild, and Francis W. Price. "Descemet's Membrane Endothelial Keratoplasty." Ophthalmology 116, no. 12 (December 2009): 2361–68. http://dx.doi.org/10.1016/j.ophtha.2009.07.010.

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Guerra, Frederico P., Arundhati Anshu, Marianne O. Price, Arthur W. Giebel, and Francis W. Price. "Descemet's Membrane Endothelial Keratoplasty." Ophthalmology 118, no. 12 (December 2011): 2368–73. http://dx.doi.org/10.1016/j.ophtha.2011.06.002.

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Cursiefen, Claus. "Descemet Membrane Endothelial Keratoplasty." JAMA Ophthalmology 131, no. 1 (January 1, 2013): 88. http://dx.doi.org/10.1001/jamaophthalmol.2013.609.

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Shanbhag, Swapna S., Abhishek Hoshing, and Sayan Basu. "Descemet Membrane Endothelial Keratoplasty." JAMA Ophthalmology 133, no. 6 (June 1, 2015): 724. http://dx.doi.org/10.1001/jamaophthalmol.2015.0475.

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Matsuzaki, Ikuo, Shampa Chatterjee, Kris DeBolt, Yefim Manevich, Qunwei Zhang, and Aron B. Fisher. "Membrane depolarization and NADPH oxidase activation in aortic endothelium during ischemia reflect altered mechanotransduction." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 1 (January 2005): H336—H343. http://dx.doi.org/10.1152/ajpheart.00025.2004.

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We previously showed that “ischemia” (abrupt cessation of flow) leads to rapid membrane depolarization and increased generation of reactive oxygen species (ROS) in lung microvascular endothelial cells. This response is not associated with anoxia but, rather, reflects loss of normal shear stress. This study evaluated whether a similar response occurs in aortic endothelium. Plasma membrane potential and production of ROS were determined by fluorescence microscopy and cytochrome c reduction in flow-adapted rat or mouse aorta or monolayer cultures of rat aortic endothelial cells. Within 30 s after flow cessation, endothelial cells that had been flow adapted showed plasma membrane depolarization that was inhibited by pretreatment with cromakalim, an ATP-sensitive K+ (KATP) channel agonist. Flow cessation also led to ROS generation, which was inhibited by cromakalim and the flavoprotein inhibitor diphenyleneiodonium. Aortic endothelium from mice with “knockout” of the KATP channel (KIR6.2) showed a markedly attenuated change in membrane potential and ROS generation with flow cessation. In aortic endothelium from mice with knockout of NADPH oxidase (gp91phox), membrane depolarization was similar to that in wild-type mice but ROS generation was absent. Thus rat and mouse aortic endothelial cells respond to abrupt flow cessation by KATP channel-mediated membrane depolarization followed by NADPH oxidase-mediated ROS generation, possibly representing a cell-signaling response to altered mechanotransduction.

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Kim, Gee-Hyun, Min Ji Ha, Dong Jin Chang, Woong Joo Whang, Yong-Soo Byun, Hyung Bin Hwang, Kyung Sun Na, et al. "Repeat Descemet Membrane Endothelial Keratoplasty after Descemet Membrane Endothelial Keratoplasty Graft Failure." Journal of the Korean Ophthalmological Society 62, no. 5 (May 15, 2021): 702–8. http://dx.doi.org/10.3341/jkos.2021.62.5.702.

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Yoeruek, Efdal, and Karl-Ulrich Bartz-Schmidt. "Secondary Descemet Membrane Endothelial Keratoplasty After Failed Primary Descemet Membrane Endothelial Keratoplasty." Cornea 32, no. 11 (November 2013): 1414–17. http://dx.doi.org/10.1097/ico.0b013e31828321c1.

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Baydoun, Lamis, Korine van Dijk, Isabel Dapena, Fayyaz U. Musa, Vasilis S. Liarakos, Lisanne Ham, and Gerrit R. J. Melles. "Repeat Descemet Membrane Endothelial Keratoplasty after Complicated Primary Descemet Membrane Endothelial Keratoplasty." Ophthalmology 122, no. 1 (January 2015): 8–16. http://dx.doi.org/10.1016/j.ophtha.2014.07.024.

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Okochi, Norihiko, and Hideshi Hattori. "Transfer Printing of Micropatterned Endothelial Cells." MEMBRANE 32, no. 5 (2007): 281–86. http://dx.doi.org/10.5360/membrane.32.281.

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Yum, Hae Ri, Man Soo Kim, and Eun Chul Kim. "Retrocorneal Membrane After Descemet Membrane Endothelial Keratoplasty." Cornea 32, no. 9 (September 2013): 1288–90. http://dx.doi.org/10.1097/ico.0b013e318296e0f7.

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Marchenko, S. M., and S. O. Sage. "Smooth muscle cells affect endothelial membrane potential in rat aorta." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 2 (August 1, 1994): H804—H811. http://dx.doi.org/10.1152/ajpheart.1994.267.2.h804.

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The effects of vasoconstrictors on membrane potential of endothelium of intact rat aorta were investigated using the patch-clamp technique. Norepinephrine, endothelin (ET)-1, 5-hydroxytryptamine (5-HT), vasopressin, and angiotensin II evoked depolarization and oscillations in membrane potential. The alpha 1-adrenoreceptor agonist phenylephrine (PE), but not the alpha 2-agonist clonidine or the beta-agonist isoproterenol, evoked oscillations. The antagonist of 5-HT2-receptors, ketanserin, inhibited 5-HT-evoked oscillations. ET-3, unlike ET-1, did not evoke oscillations. The antagonists of voltage-operated Ca2+ channels, nifedipine and verapamil, inhibited vasoconstrictor-evoked oscillations, and the Ca2+ channel agonist BAY K 8644 enhanced oscillations. Acetylcholine and sodium nitroprusside inhibited PE-evoked oscillations. The inhibitors of NO synthase, N omega-nitro-L-arginine and NG-methyl-L-arginine, as well as methylene blue, enhanced oscillations. The intima of rat aorta with endothelium was removed from underlying smooth muscle. In this preparation, acetylcholine evoked a response similar to that in the intact vessel, but PE and ET-1 were without effect. These data suggest that vasoconstrictors acting on receptors on aortic smooth muscle evoke a response that is transferred to the endothelium and evokes depolarization and oscillations in endothelial membrane potential.

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Horvat, R., A. Hovorka, G. Dekan, H. Poczewski, and D. Kerjaschki. "Endothelial cell membranes contain podocalyxin--the major sialoprotein of visceral glomerular epithelial cells." Journal of Cell Biology 102, no. 2 (February 1, 1986): 484–91. http://dx.doi.org/10.1083/jcb.102.2.484.

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Podocalyxin is the major sialoprotein in the glycocalyx of glomerular podocytes. Here we report on its extraglomerular localization, using a monospecific antibody which was obtained by affinity purification of IgG on nitrocellulose transfers of glomerular podocalyxin. By indirect immunofluorescence, podocalyxin was found in the blood vessels of several organs (lung, heart, kidney, small intestine, brain, pancreas, aorta, the periportal blood vessels in liver, and the central arteries of follicles of the spleen, but not in the endothelia that line the sinusoids of the latter organs). By immunoelectron microscopy--using immunogold conjugates in diffusion ("pre-embedding") and surface ("postembedding") procedures--podocalyxin was localized on the luminal membrane domain of endothelial cells, in a patchy distribution. The presence of podocalyxin was confirmed in SDS extracts of lung tissue by immunoblotting. We conclude that (a) podocalyxin is a widespread component of endothelial plasma membranes, (b) it is restricted to the luminal membrane domain, and (c) it is distributed unevenly on the endothelial cell surface.

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Paffett, Michael L., Jay S. Naik, Melissa A. Riddle, Steven D. Menicucci, Antonio J. Gonzales, Thomas C. Resta, and Benjimen R. Walker. "Altered membrane lipid domains limit pulmonary endothelial calcium entry following chronic hypoxia." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 4 (October 2011): H1331—H1340. http://dx.doi.org/10.1152/ajpheart.00980.2010.

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Agonist-induced Ca2+ entry into the pulmonary endothelium depends on activation of both store-operated Ca2+ (SOC) entry and receptor-operated Ca2+ (ROC) entry. We previously reported that pulmonary endothelial cell SOC entry and ROC entry are reduced in chronic hypoxia (CH)-induced pulmonary hypertension. We hypothesized that diminished endothelial Ca2+ entry following CH is due to derangement of caveolin-1 (cav-1) containing cholesterol-enriched membrane domains important in agonist-induced Ca2+ entry. To test this hypothesis, we measured Ca2+ influx by fura-2 fluorescence following application of ATP (20 μM) in freshly isolated endothelial cells pretreated with the caveolar-disrupting agent methyl-β-cyclodextrin (mβCD; 10 mM). Cholesterol depletion with mβCD attenuated agonist-induced Ca2+ entry in control endothelial cells to the level of that from CH rats. Interestingly, endothelial membrane cholesterol was lower in cells isolated from CH rats compared with controls although the density of caveolae did not differ between groups. Cholesterol repletion with a cholesterol:mβCD mixture or the introduction of the cav-1 scaffolding peptide (AP-cav; 10 μM) rescued ATP-induced Ca2+ entry in endothelia from CH arteries. Agonist-induced Ca2+ entry assessed by Mn2+ quenching of fura-2 fluorescence was also significantly elevated by luminal AP-cav in pressurized intrapulmonary arteries from CH rats to levels of controls. Similarly, patch-clamp experiments revealed diminished inward current in response to ATP in cells from CH rats compared with controls that was restored by AP-cav. These data suggest that CH-induced pulmonary hypertension leads to reduced membrane cholesterol that limits the activity of ion channels necessary for agonist-activated Ca2+ entry.

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Raub, T. J., G. A. Sawada, and S. L. Kuentzel. "Expression of a widely distributed, novel sulfated membrane glycoprotein by bovine endothelia and certain transporting epithelia." Journal of Histochemistry & Cytochemistry 42, no. 9 (September 1994): 1237–50. http://dx.doi.org/10.1177/42.9.8064131.

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We generated monoclonal antibodies (MAbs) against cultured bovine brain microvessel endothelial cells (BMEC) for use as probes to study membrane protein traffic and polarity. One MAb recognized a heterogeneous family of acidic sulfoglycoproteins called gp4A4 with molecular weights of 50-65 KD and 85 KD. Gp4A4 is a long-lived integral membrane protein which resides mostly at the plasma membrane, and a portion appears to be in equilibrium with an intracellular pool via endocytosis. Gp4A4 is expressed by many endothelial cells, except for fenestrated capillaries in choroid plexus, and specific epithelial cells in bile duct, kidney, and choroid plexus. A comparison of indirect immunoperoxidase and immunofluorescence detection using semi-thin cryosections gave contrasting results on the apparent distribution of gp4A4 on the apical and basolateral membranes of cerebral endothelia and choroid plexus epithelia. Immunogold labeling of ultra-thin cryosections showed that gp4A4 was expressed by the apical and basolateral membrane domains of BMEC and choroid plexus epithelia. This was consistent with the results using indirect immunofluorescence microscopy. On an average, gp4A4 expression by cerebral endothelia was not asymmetric and was considerably variable between capillaries. These results emphasize the need to compare several different techniques in assessing polarized expression of cell surface antigens in vivo.

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Marcos-Ramiro, Beatriz, Diego García-Weber, Susana Barroso, Jorge Feito, María C. Ortega, Eva Cernuda-Morollón, Natalia Reglero-Real, et al. "RhoB controls endothelial barrier recovery by inhibiting Rac1 trafficking to the cell border." Journal of Cell Biology 213, no. 3 (May 2, 2016): 385–402. http://dx.doi.org/10.1083/jcb.201504038.

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Endothelial barrier dysfunction underlies chronic inflammatory diseases. In searching for new proteins essential to the human endothelial inflammatory response, we have found that the endosomal GTPase RhoB is up-regulated in response to inflammatory cytokines and expressed in the endothelium of some chronically inflamed tissues. We show that although RhoB and the related RhoA and RhoC play additive and redundant roles in various aspects of endothelial barrier function, RhoB specifically inhibits barrier restoration after acute cell contraction by preventing plasma membrane extension. During barrier restoration, RhoB trafficking is induced between vesicles containing RhoB nanoclusters and plasma membrane protrusions. The Rho GTPase Rac1 controls membrane spreading and stabilizes endothelial barriers. We show that RhoB colocalizes with Rac1 in endosomes and inhibits Rac1 activity and trafficking to the cell border during barrier recovery. Inhibition of endosomal trafficking impairs barrier reformation, whereas induction of Rac1 translocation to the plasma membrane accelerates it. Therefore, RhoB-specific regulation of Rac1 trafficking controls endothelial barrier integrity during inflammation.

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Cheng, Jade P. X., Carolina Mendoza-Topaz, Gillian Howard, Jessica Chadwick, Elena Shvets, Andrew S. Cowburn, Benjamin J. Dunmore, Alexi Crosby, Nicholas W. Morrell, and Benjamin J. Nichols. "Caveolae protect endothelial cells from membrane rupture during increased cardiac output." Journal of Cell Biology 211, no. 1 (October 12, 2015): 53–61. http://dx.doi.org/10.1083/jcb.201504042.

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Caveolae are strikingly abundant in endothelial cells, yet the physiological functions of caveolae in endothelium and other tissues remain incompletely understood. Previous studies suggest a mechanoprotective role, but whether this is relevant under the mechanical forces experienced by endothelial cells in vivo is unclear. In this study we have sought to determine whether endothelial caveolae disassemble under increased hemodynamic forces, and whether caveolae help prevent acute rupture of the plasma membrane under these conditions. Experiments in cultured cells established biochemical assays for disassembly of caveolar protein complexes, and assays for acute loss of plasma membrane integrity. In vivo, we demonstrate that caveolae in endothelial cells of the lung and cardiac muscle disassemble in response to acute increases in cardiac output. Electron microscopy and two-photon imaging reveal that the plasma membrane of microvascular endothelial cells in caveolin 1−/− mice is much more susceptible to acute rupture when cardiac output is increased. These data imply that mechanoprotection through disassembly of caveolae is important for endothelial function in vivo.

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Ndisang, Joseph Fomusi. "Glomerular Endothelium and its Impact on Glomerular Filtration Barrier in Diabetes: Are the Gaps Still Illusive?" Current Medicinal Chemistry 25, no. 13 (May 7, 2018): 1525–29. http://dx.doi.org/10.2174/0929867324666170705124647.

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Background: Glomerular capillaries are lined with highly specialized fenestrated endothelium which are primarily responsible to regulate high flux filtration of fluid and small solutes. During filtration, plasma passes through the fenestrated endothelium and basement membrane before it reaches the slit diaphragm, a specialized type of intercellular junction that connects neighbouring podocytes. Methods: A PubMed search was done for recent articles on components of the glomerular filtration barrier such as glomerular endothelial cells, podocytes and glomerular basement membrane, and the effect of diabetes on these structures. Results and Conclusion: Generally, the onset of kidney dysfunction in many diabetic patients is characterized by albuminuria/proteinuria, a pathophysiological event triggered by several factors including; (i) endothelial activation and shading of glycocalyx, (ii) loss of endothelial cell function, (ii) re-uptake of albumin by podocyte through a scavenger receptors and (iv) rearrangement of podocyte cytoskeleton. Howeover, as podocyte effacement does not always lead to proteinuria, the dynamic interplay between all constituents of the glomerular filtration barrier including podocytes, endothelial cells and the basement membrane may be fundamental for the effective filtration in healthy individuals. Thus, a putative cross-talk amongst podocytes, endothelial cells and the basement membrane in the homeostasis of glomerular function is envisaged. Although, the exact nature of this cross-talk remains to be clearly elucidated, it is possible that the interaction between: (i) glomerular endothelial cells and podocytes, (ii) glomerular endothelial cells and glomerular basement membrane, (iii) podocytes and glomerular basement membrane, and (iv) the simultaneous interaction amongst the three components collectively underpin effective filtration in healthy individuals. A comprehensive understanding of these different interactions still remains elusive. The elucidation of these multifaceted interactions will set the stage for greater understanding of the pathophysiology of kidney dysfunction.

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Schmid-Scho¨nbein, Geert W., Tadashi Kosawada, Richard Skalak, and Shu Chien. "Membrane Model of Endothelial Cells and Leukocytes. A Proposal for the Origin of a Cortical Stress." Journal of Biomechanical Engineering 117, no. 2 (May 1, 1995): 171–78. http://dx.doi.org/10.1115/1.2795999.

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Previous models of the erythrocyte membrane have been based on the assumption that the resting curvature of the membrane is either flat or has a small curvature relative to the overall cell dimension. In contrast, several recent experimental observations, both in leukocytes and in endothelial cells, suggest that local regions of the membrane may have high membrane curvature in the resting state. The resting curvature may be of the order of plasmalemmal vesicles in endothelial cells or surface membrane folds on leukocytes. A tension is required to unfold the membrane with strain energy which depends largely on mean curvature. It is proposed that the tendency of endothelial or leukocyte membranes to wrinkle in the unstressed state may provide a restoring force, i.e. a cortical tension.

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Meroni, PL, N. Del Papa, E. Raschi, P. Panzeri, MO Borghi, A. Tincani, G. Balestrieri, et al. "β2-Glycoprotein I as a ‘Cofactor’ for anti-phospholipid reactivity with endothelial cells." Lupus 7, no. 2_suppl (February 1998): 44–47. http://dx.doi.org/10.1177/096120339800700211.

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β2-glycoprotein I (β2GPI) is a cofactor for anti-phospholipid (aPL) binding to cardiolipin (CL)-coated plates. β2GPI is also able to bind to endothelial cell (EC) membranes as supported by in-vivo as well as by in-vitro studies. The PL-binding site in the fifth domain of the molecule is involved in the adhesion to endothelium. Actually, specific mutations in this molecular portion abolish endothelium binding and a synthetic peptide spanning the sequence Glu274 –Cys288 of the CL-binding site displays comparable adhesion to EC monolayers. Heparan sulphate appears to be one of the anionic EC membrane structures with which cationic β2GPI interacts, as supported by studies with heparitinase-treated EC. β2GPI binding to EC might be related to its activity as endothelial growth factor or as a lipid-carrying glycoprotein. Adhesion of β2GPI to endothelial membranes offers suitable epitopes for circulating aPL that, once bound, can induce cell activation

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Qi, Xiaolin, Ting Liu, Man Du, and Hua Gao. "Endothelial Plaques as Sign of Hyphae Infiltration of Descemet’s Membrane in Fungal Keratitis." Journal of Ophthalmology 2020 (May 26, 2020): 1–6. http://dx.doi.org/10.1155/2020/6083854.

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Background. To evaluate the relationship between corneal endothelial plaques and fungal hyphae infiltration in fungal keratitis. Methods. Retrospective cross-sectional study of 60 fungal keratitis patients who underwent keratoplasty between January 2013 and March 2017. The endothelial plaques were graded as follows: grade 1, 1–3 endothelial plaques; grade 2, 4–8 endothelial plaques; and grade 3, more than 8 endothelial plaques or dense, merging endothelial plaques. The fungal pathogen culture and histopathology of diseased Descemet’s membrane were evaluated. Results. According to endothelial plaque grading, 3 patients were grade 1, 29 patients were grade 2, and 28 patients were grade 3. The PK surgery was performed in 57 patients with endothelial plaques of grade 2 and grade 3 and DALK surgery in 3 patients of grade 1. The predominating fungal pathogens were Aspergillus species (63.2%). All 57 patients with grade 2 and grade 3 had fungal hyphae in Descemet’s membrane based on calcofluor white staining or PAS staining. In patients with grade 3, more hyphae and inflammatory cells were found in Descemet’s membrane. The immunohistochemical staining of endothelial plaques revealed that CD15 and CD68 were positive in most cells. During the follow-up, 2 out of 3 patients who underwent DALK had recurrent fungal keratitis. Conclusions. Endothelial plaques are considered as a sign of hyphae infiltrating Descemet’s membrane. PK should be performed once plaques are detected in endothelium during the surgery.

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Takahashi, M., K. Fukuda, K. Shimada, K. Barnes, A. J. Turner, M. Ikeda, H. Koike, Y. Yamamoto, and K. Tanzawa. "Localization of rat endothelin-converting enzyme to vascular endothelial cells and some secretory cells." Biochemical Journal 311, no. 2 (October 15, 1995): 657–65. http://dx.doi.org/10.1042/bj3110657.

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Endothelin is a potent vasoconstrictive peptide that is produced by vascular endothelial cells; it is formed from its precursor, big endothelin, by endothelin-converting enzyme (ECE). In this work, ECE was studied using specific monoclonal antibodies. In immunoblotting, ECE was estimated to be a 300 kDa protein on SDS/PAGE under non-reducing conditions, and 130 kDa under reducing conditions. Cross-linking experiments revealed that ECE is composed of two disulphide-linked subunits. Localization of ECE was studied at the cellular and subcellular levels in various rat tissues and cells. High-level expression of ECE was observed in membrane fractions of simian virus 40-transformed rat endothelial cells by immunoblotting, but the immunoreactive band was absent form aortic smooth muscle cells and cytosolic fractions of endothelial cells. In immunohistochemical analysis, ECE was found to be localized in the endothelial cells of the aorta, lung, kidney, liver and heart. Confocal immunofluorescent microscopy showed that most of the ECE in endothelial cells and cells transfected with ECE cDNA was clustered along the plasma membrane. Intact COS or CHO cells transfected with ECE cDNA rapidly and efficiently cleaved big endothelin-1 added to the culture medium. Thus endothelial cells express ECE on the plasma membrane and the active site of the enzyme faces outside the cells, i.e. it is an ectoenzyme. Other than endothelial cells, ECE was also present in some secretory cells. The enzyme was abundant in the adrenal gland, and localized in chromaffin cells. ECE was also highly condensed in pancreatic islet beta cells. It is concluded that ECE and endothelin may be involved in the regulated secretion of hormones.

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Mittal, V., R. Mittal, R. Jain, and V. S. Sangwan. "Incidental central tear in Descemet membrane endothelial complex during Descemet membrane endothelial keratoplasty." Case Reports 2014, jun27 1 (June 27, 2014): bcr2013202935. http://dx.doi.org/10.1136/bcr-2013-202935.

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Price, Marianne O., Marek Lisek, Meagan Kelley, Matthew T. Feng, and Francis W. Price. "Endothelium-in Versus Endothelium-out Insertion With Descemet Membrane Endothelial Keratoplasty." Cornea 37, no. 9 (September 2018): 1098–101. http://dx.doi.org/10.1097/ico.0000000000001650.

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Journal articles on the topic 'Endothelial membrane'

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