Journal articles: 'Capillary endothelial cells'

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Vigne, P., R. Marsault, J. P. Breittmayer, and C. Frelin. "Endothelin stimulates phosphatidylinositol hydrolysis and DNA synthesis in brain capillary endothelial cells." Biochemical Journal 266, no. 2 (March 1, 1990): 415–20. http://dx.doi.org/10.1042/bj2660415.

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Endothelin-1 (ET-1) is a novel vasoconstricting and cardiotonic peptide that is synthesized by the vascular endothelium. Bovine aortic endothelial cells which secrete ET in vitro lack membrane receptor sites for the peptide. Endothelial cells from rat brain microvessels that do not secrete ET in vitro express large amounts of high-affinity receptors for 125I-labelled ET-1 (Kd 0.8 nM). The ET receptor is recognized by sarafotoxin S6b and the different ET peptides with the following order of potency: ET-1 (Kd 0.5 nM) approximately equal to ET-2 (Kd 0.7 nM) greater than sarafotoxin S6b (Kd 27 nM) greater than ET-3 (Kd 450 nM). This structure-activity relationship is different from those found in vascular smooth muscle cells, renal cells and cardiac cells. ET-1 stimulates DNA synthesis in brain capillary endothelial cells. It is more potent than basic fibroblast growth factor. The action of ET on endothelial cells from microvessels involves phosphatidylinositol hydrolysis and intracellular Ca2+ mobilization. These observations suggest that brain endothelial cells might be an important target for ET.

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Dehouck, Bénédicte, Marie-Pierre Dehouck, Jean-Charles Fruchart, and Roméo Cecchelli. "Upregulation of the Low Density Lipoprotein Receptor at the Blood-Brain Barrier: Intercommunications between Brain Capillary Endothelial Cells and Astrocytes." Review & Expositor 84, no. 1 (February 1987): 465–73. http://dx.doi.org/10.1177/003463738708400125.

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In contrast to the endothelial cells in large vessels where LDL receptors are downregulated, brain capillary endothelial cells in vivo express an LDL receptor. Using a cell culture model of the blood-brain barrier consisting of a coculture of brain capillary endothelial cells and astrocytes, we observed that the capacity of endothelial cells to bind LDL is enhanced threefold when cocultured with astrocytes. We next investigated the ability of astrocytes to modulate endothelial cell LDL receptor expression. We have shown that the lipid requirement of astrocytes increases the expression of endothelial cell LDL receptors. Experiments with dialysis membranes of different pore size showed that this effect is mediated by a soluble factor(s) with relative molecular mass somewhere between 3,500 and 14,000. Substituting astrocytes with smooth muscle cells or brain endothelium with endothelium from the aorta or the adrenal cortex did not enhance the luminal LDL receptor expression on endothelial cells, demonstrating the specificity of the interactions. This factor(s) is exclusively secreted by astrocytes cocultured with brain capillary endothelial cells, but it also upregulates the LDL receptor on other cell types. This study confirms the notion that the final fine tuning of cell differentiation is under local control.

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Dehouck, B., M. P. Dehouck, J. C. Fruchart, and R. Cecchelli. "Upregulation of the low density lipoprotein receptor at the blood-brain barrier: intercommunications between brain capillary endothelial cells and astrocytes." Journal of Cell Biology 126, no. 2 (July 15, 1994): 465–73. http://dx.doi.org/10.1083/jcb.126.2.465.

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In contrast to the endothelial cells in large vessels where LDL receptors are downregulated, brain capillary endothelial cells in vivo express an LDL receptor. Using a cell culture model of the blood-brain barrier consisting of a coculture of brain capillary endothelial cells and astrocytes, we observed that the capacity of endothelial cells to bind LDL is enhanced threefold when cocultured with astrocytes. We next investigated the ability of astrocytes to modulate endothelial cell LDL receptor expression. We have shown that the lipid requirement of astrocytes increases the expression of endothelial cell LDL receptors. Experiments with dialysis membranes of different pore size showed that this effect is mediated by a soluble factor(s) with relative molecular mass somewhere between 3,500 and 14,000. Substituting astrocytes with smooth muscle cells or brain endothelium with endothelium from the aorta or the adrenal cortex did not enhance the luminal LDL receptor expression on endothelial cells, demonstrating the specificity of the interactions. This factor(s) is exclusively secreted by astrocytes cocultured with brain capillary endothelial cells, but it also upregulates the LDL receptor on other cell types. This study confirms the notion that the final fine tuning of cell differentiation is under local control.

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Ganz, Peter R., Denis Dupuis, Anil K. Dudani, and Sofia Hashemi. "Characterization of plasminogen binding to human capillary and arterial endothelial cells." Biochemistry and Cell Biology 69, no. 7 (July 1, 1991): 442–48. http://dx.doi.org/10.1139/o91-067.

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Phenotypic diversity of endothelial cells that line the various vascular spaces has been well established. However, it is not known if biochemical differences also exist, particularly in the numbers of receptors for plasma proteins. Equilibrium binding techniques were used to assess potential differences in the binding of 125I-labelled plasminogen to cultured human umbilical arterial endothelial cells and capillary endothelium, as compared with umbilical venous cells. The kinetic behaviour of plasminogen binding to all three types of cells was similar, with optimal binding occurring between 20 and 30 min of incubation. Binding of plasminogen to arterial, capillary, and venous cells was concentration dependent and reversible upon addition to excess unlabelled plasminogen. Scatchard analyses showed that artery, capillary, and venous endothelial cells all possess low affinity sites for plasminogen with Kd values of 0.30 ± 0.07, 0.40 ± 0.06, and 0.40 ± 0.08 μM, respectively. Vein cells also possess an additional higher affinity binding site with a Kd of 0.07 ± 0.01 μM, exhibiting a 6-fold greater affinity for plasminogen than the lower affinity sites on capillary and arterial endothelial cells. Assuming a stoichiometry of 1:1 for binding, the data indicate that arterial and capillary endothelial cells contain approximately 4.2 (± 0.9) × 106 and 4.1 (± 0.6) × 106 plasminogen receptors per cell. Venous cells contain both low and high density binding sites with 6.2 (± 0.8) × 106 and 12.4 (± 2.4) × 106 sites per endothelial cell. The presence of a higher affinity site on vein cells, but not on artery or capillary cells, may signal functional differences relating to fibrinolytic activity on the surface of these cells. Ligand blotting experiments, in which labelled plasminogen was adsorbed to polypeptides recovered from endothelial cell lysates, identified polypeptides of 46, 45, and 37 kDa, which may constitute the plasminogen-binding sites–receptors on endothelial cells.Key words: plasminogen, endothelial cells, receptors, fibrinolysis.

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Felice, Francesca, Ester Belardinelli, Alessandro Frullini, Tatiana Santoni, Egidio Imbalzano, and Rossella Di Stefano. "Effect of aminaphtone on in vitro vascular permeability and capillary-like maintenance." Phlebology: The Journal of Venous Disease 33, no. 9 (October 23, 2017): 592–99. http://dx.doi.org/10.1177/0268355517737662.

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Objectives Aminaphtone, a naphtohydrochinone used in the treatment of capillary disorders, may affect oedema in chronic venous insufficiency. Aim of study is to investigate the effect of aminaphtone on vascular endothelial permeability in vitro and its effects on three-dimensional capillary-like structures formed by human umbilical vein endothelial cells. Method Human umbilical vein endothelial cells were treated with 50 ng/ml VEGF for 2 h and aminaphtone for 6 h. Permeability assay, VE-cadherin expression and Matrigel assay were performed. Results VEGF-induced permeability was significantly decreased by aminaphtone in a range concentration of 1–20 µg/ml. Aminaphtone restored VE-cadherin expression. Finally, 6 h pre-treatment with aminaphtone significantly preserved capillary-like structures formed by human umbilical vein endothelial cells on Matrigel up to 48 h compared to untreated cells. Conclusions Aminaphtone significantly protects endothelium permeability and stabilises endothelial cells organised in capillary-like structures, modulating VE-cadherin expression. These data might explain the clinical benefit of aminaphtone on chronic venous insufficiency.

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Montesano, R., and L. Orci. "Intracellular diaphragmed fenestrae in cultured capillary endothelial cells." Journal of Cell Science 89, no. 3 (March 1, 1988): 441–47. http://dx.doi.org/10.1242/jcs.89.3.441.

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The endothelium of visceral capillaries is characterized by the occurrence of numerous fenestrae, which are usually bridged by a thin, single-layered diaphragm. Both in vivo and in vitro, diaphragmed fenestrae perforate the endothelial cell cytoplasm in the most attenuated regions of the cell. We report here that in capillary endothelial cells grown under experimental conditions promoting the development of intracellular lumina (for example, suspension within a three-dimensional collagen matrix), diaphragmed fenestrae can form in a unique, previously undescribed intracellular location - that is, within thin cytoplasmic septa separating contiguous luminal compartments.

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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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Sage, E. Helene. "Secretion of SPARC by endothelial cells transformed by polyoma middle T oncogene inhibits the growth of normal endothelial cells in vitro." Biochemistry and Cell Biology 70, no. 7 (July 1, 1992): 579–92. http://dx.doi.org/10.1139/o92-089.

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Endothelioma cells expressing the polyoma virus middle T oncogene induced hemangiomas in mice by the recruitment of nonproliferating endothelial cells from host blood vessels (Williams et al. 1989). I now report that SPARC, a Ca2+-binding glycoprotein that perturbs cell–matrix interactions and inhibits the endothelial cell cycle, is produced by endothelioma cells and is in part responsible for the alterations in the morphology and growth that occur when nontransformed bovine aortic endothelial cells are cocultured with endothelioma cells. Normal endothelial cells cocultured with two different middle T-positive endothelial cell lines, termed End cells, exhibited changes in shape that were accompanied by the formation of cell clusters. Media conditioned by End cells repressed proliferation of normal endothelial cells, but enhanced that of an established line of murine capillary endothelium. Radiolabeling studies revealed no apparent differences in the profile of proteins secreted by aortic or capillary cells cultured in End cell conditioned media. Characterization of proteins produced by End cells led to the identification of type IV collagen, laminin, entactin, and SPARC as major secreted products. Although SPARC did not affect the morphology of End or capillary cells, it was associated with overt changes in the shape of aortic endothelial cells. Moreover, SPARC and a synthetic peptide from SPARC domain II inhibited the incorporation of [3H]thymidine by aortic cells, but had minimal to no effect on the capillary endothelial cell line. The inhibition of growth exhibited by aortic endothelial cells cultured in End cell conditioned media could be partially reversed by antibodies specific for SPARC and SPARC peptides. These studies indicate a potential role for SPARC in the generation of hemangiomas by End cells in vivo, a process that requires normal (host) endothelial cells to disengage from the extracellular matrix, withdraw from the cell cycle, migrate, and reassociate into the disorganized cellular networks that comprise cavernous and capillary hemangiomas.Key words: endothelial cells, hemangioma, cell proliferation, SPARC.

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Anderson, Christopher R., Ana M. Ponce, and Richard J. Price. "Absence of OX-43 antigen expression in invasive capillary sprouts: identification of a capillary sprout-specific endothelial phenotype." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 1 (January 2004): H346—H353. http://dx.doi.org/10.1152/ajpheart.00772.2003.

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Endothelial cells exhibit a number of unique phenotypes, some of which are angiogenesis dependent. To identify a capillary sprout-specific endothelial phenotype, we labeled angiogenic rat mesentery tissue using a microvessel and capillary sprout marker (laminin), selected endothelial cell markers (CD31, tie-2, and BS-I lectin), and the OX-43 monoclonal antibody, which recognizes a 90-kDa membrane glycoprotein of unknown function. In tissues that were stimulated through wound healing and compound 48/80 application, double-immunolabeling experiments with an anti-laminin antibody revealed that the OX-43 antigen was expressed strongly in all microvessels. However, the OX-43 antigen was completely absent from a large percentage (>85%) of the capillary sprouts that were invading the avascular tissue space. In contrast, sprouts that were introverting back into the previously vascularized tissue retained high levels of OX-43 antigen expression. Double-labeling experiments with endothelial markers indicated that the OX-43 antigen was expressed by microvessel endothelium but was absent from virtually all invasive capillary sprout endothelial cells. We conclude that the absence of OX-43 antigen expression marks a novel, capillary sprout-specific, endothelial cell phenotype. Endothelial cells of this phenotype are particularly abundant in capillary sprouts that invade avascular tissue during angiogenesis.

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Ladoux, Annie, and Christian Frelin. "Endothelins inhibit adenylate cyclase in brain capillary endothelial cells." Biochemical and Biophysical Research Communications 180, no. 1 (October 1991): 169–73. http://dx.doi.org/10.1016/s0006-291x(05)81271-9.

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Vigne, Paul, and Christian Frelin. "Endothelins activate phospholipase A2 in brain capillary endothelial cells." Brain Research 651, no. 1-2 (July 1994): 342–44. http://dx.doi.org/10.1016/0006-8993(94)90716-1.

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Dalrymple, Nadine A., and Erich R. Mackow. "Roles for Endothelial Cells in Dengue Virus Infection." Advances in Virology 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/840654.

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Dengue viruses cause two severe diseases that alter vascular fluid barrier functions, dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). The endothelium is the primary fluid barrier of the vasculature and ultimately the effects of dengue virus infection that cause capillary leakage impact endothelial cell (EC) barrier functions. The ability of dengue virus to infect the endothelium provides a direct means for dengue to alter capillary permeability, permit virus replication, and induce responses that recruit immune cells to the endothelium. Recent studies focused on dengue virus infection of primary ECs have demonstrated that ECs are efficiently infected, rapidly produce viral progeny, and elicit immune enhancing cytokine responses that may contribute to pathogenesis. Furthermore, infected ECs have also been implicated in enhancing viremia and immunopathogenesis within murine dengue disease models. Thus dengue-infected ECs have the potential to directly contribute to immune enhancement, capillary permeability, viremia, and immune targeting of the endothelium. These effects implicate responses of the infected endothelium in dengue pathogenesis and rationalize therapeutic targeting of the endothelium and EC responses as a means of reducing the severity of dengue virus disease.

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Russell, Robert J., Shen-Ling Xia, Richard B. Dickinson, and Tanmay P. Lele. "Sarcomere Mechanics in Capillary Endothelial Cells." Biophysical Journal 97, no. 6 (September 2009): 1578–85. http://dx.doi.org/10.1016/j.bpj.2009.07.017.

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Guymer, Robyn H., Alan C. Bird, and Gregory S. Hageman. "Cytoarchitecture of Choroidal Capillary Endothelial Cells." Investigative Opthalmology & Visual Science 45, no. 6 (June 1, 2004): 1660. http://dx.doi.org/10.1167/iovs.03-0913.

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Kroll, K., I. S. Chan, and J. B. Bassingthwaighte. "Enzyme Holdup in Capillary Endothelial Cells." IFAC Proceedings Volumes 27, no. 1 (March 1994): 231–32. http://dx.doi.org/10.1016/s1474-6670(17)46216-1.

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de Groot, C. J., V. A. Chao, J. M. Roberts, and R. N. Taylor. "Human endothelial cell morphology and autacoid expression." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 4 (April 1, 1995): H1613—H1620. http://dx.doi.org/10.1152/ajpheart.1995.268.4.h1613.

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Human umbilical vein endothelial (HUVE) cells plated on plastic or gelatin-coated dishes grow as a “cobblestone” monolayer. By contrast, endothelial cells cultured on a complex matrix (e.g., Matrigel) form three-dimensional, capillary-like structures. In the current study, we verified the capillary phenotype of the latter structures and asked whether the morphological changes induced by extracellular matrix also affect human endothelial gene expression and function in vitro. Concentrations of cellular fibronectin, prostacyclin, and endothelin-1 were measured in the conditioned media by enzyme-linked immunosorbent and radioimmunoassays. Steady-state concentrations of HUVE mRNA were estimated by reverse transcription-polymerase chain reaction and quantified by Northern analyses to assess fibronectin and endothelin-1 gene expression. We found that the subjacent extracellular matrix affects the morphology, proliferation, and differentiation of HUVE cells in vitro. Cells cultured on gelatin were more mitotically active, expressed significantly less cellular fibronectin, made similar amounts of prostacyclin, and secreted significantly more endothelin-1 compared with the same cells grown on a Matrigel substrate.

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Kim, Jeong A., Nam D. Tran, Shur-Jen Wang, and Mark Fisher. "Pericytes Regulate Fibrinolytic Function of Brain Capillary Endothelial Cells." Stroke 32, suppl_1 (January 2001): 359. http://dx.doi.org/10.1161/str.32.suppl_1.359-a.

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P110 Our prior work has shown that astrocytes inhibit fibrinolysis of brain capillary endothelial cells (eg, Stroke 1999:30;1671–1677). The complex cellular microenvironment at the blood-brain barrier includes pericytes, which are adjacent to and share basement membrane with brain capillary endothelial cells. We analyzed the hemostatic regulatory role of pericytes in a blood-brain barrier model consisting of human brain pericytes cultured on transwell membrane inserts with human brain capillary endothelial cells. We measured fibrinolysis proteins and function in media conditioned by 48 hour co-culture of human brain capillary endothelial cells and human brain pericytes, as well as brain capillary endothelial mono-cultures. Compared to endothelial mono-cultures, pericyte-endothelial co-cultures exhibited levels of tissue plasminogen activator (tPA) protein reduced by 50±15% (p<.05). Co-culture preparations showed 32±13% (p<.05) increase in levels of plasminogen activator inhibitor-1 (PAI-1) protein, the primary inhibitor of tPA. tPA activity of co-culture preparations was 54±17% (p<.05) of endothelial mono-culture preparations. These data demonstrate that human brain pericytes have an important hemostatic regulatory role for endothelial-dependent fibrinolysis in vitro. These findings provide further support for brain-specific hemostasis, with pericytes as well as astrocytes playing key regulatory roles.

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Coutinho, G. C., O. Durieu-Trautmann, A. D. Strosberg, and P. O. Couraud. "Catecholamines stimulate the IFN-gamma-induced class II MHC expression on bovine brain capillary endothelial cells." Journal of Immunology 147, no. 8 (October 15, 1991): 2525–29. http://dx.doi.org/10.4049/jimmunol.147.8.2525.

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Abstract The brain has been considered for a long time as an immunologically privileged site because of the lack of a true lymphatic system and the existence of several barriers that isolate it from the periphery. In the last few years, it became evident that cells in the central nervous system (astrocytes, microglial cells, and brain capillary endothelial cells) can be induced to express class II MHC and present Ag to T lymphocytes. The brain capillary endothelial cells, which are strategically located at the interface between blood and brain, could be involved in the initiation of immune responses within the brain parenchyma. We have previously characterized bovine brain capillary endothelial cells in culture and shown that they maintain in vitro a fully differentiated phenotype associated with the blood-brain barrier endothelium. In order to assess the role of these cells in the development of immune responses in the brain, we initiated the present study on the regulation of their class II MHC surface expression. Our data indicate that this expression on bovine brain capillary endothelial cells is inducible by IFN-gamma and further stimulated by catecholamines through activation of beta-adrenergic receptors. However, this latter effect is not mimicked by forskolin, theophylline, or dibutyryl-cAMP, suggesting the involvement of a cAMP-independent mechanism.

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Marsden, P. A., D. M. Dorfman, T. Collins, B. M. Brenner, S. H. Orkin, and B. J. Ballermann. "Regulated expression of endothelin 1 in glomerular capillary endothelial cells." American Journal of Physiology-Renal Physiology 261, no. 1 (July 1, 1991): F117—F125. http://dx.doi.org/10.1152/ajprenal.1991.261.1.f117.

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Endothelin (ET)-1 is a powerful vasoconstrictor known to be produced and secreted by endothelial cells lining large vessels. Because ET-1 stimulates glomerular mesangial cell contraction, glomerular capillary endothelial cells (GEN), normally situated in close apposition to mesangial cells, were examined for potential ET expression and secretion. Cultured bovine GEN released ET in a time-dependent fashion. ET secretion was significantly stimulated by bradykinin, an agonist known to activate phospholipase C in these cells. Preproendothelin 1 (preproET-1) mRNA levels in GEN rose in a biphasic manner on stimulation with bradykinin. The early increments (at 30 min) were not dependent on new protein synthesis, whereas the late rise (6 h after addition of bradykinin) appeared to be protein synthesis dependent. Neither early or late bradykinin-stimulated preproET-1 mRNA expression in glomerular endothelial cells was due to inhibition of mRNA breakdown. Both phases of preproET-1 mRNA expression were observed with other glomerular endothelial cell calcium-mobilizing agonists, namely thrombin, and were mimicked by the calcium ionophore ionomycin. By contrast, the protein kinase C activator phorbol myristate acetate only enhanced preproET-1 mRNA expression at 30 min and suppressed expression thereafter. It is concluded that GEN have the potential to express and secrete ET-1 in a phospholipase C-regulated fashion. Furthermore, because glomerular mesangial cells respond to this peptide, the findings raise the possibility of paracrine regulation of mesangial cell tone by glomerular endothelial cell-derived ET-1.

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Noireaud, Jacques, and Ramaroson Andriantsitohaina. "Recent Insights in the Paracrine Modulation of Cardiomyocyte Contractility by Cardiac Endothelial Cells." BioMed Research International 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/923805.

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The cardiac endothelium is formed by a continuous monolayer of cells that line the cavity of the heart (endocardial endothelial cells (EECs)) and the luminal surface of the myocardial blood vessels (intramyocardial capillary endothelial cells (IMCEs)). EECs and IMCEs can exercise substantial control over the contractility of cardiomyocytes by releasing various factors such as nitric oxide (NO)viaa constitutive endothelial NO-synthase (eNOS), endothelin-1, prostaglandins, angiotensin II, peptide growth factors, and neuregulin-1. The purpose of the present paper is actually to shortly review recent new information concerning cardiomyocytes as effectors of endothelium paracrine signaling, focusing particularly on contractile function. The modes of action and the regulatory paracrine role of the main mediators delivered by cardiac endothelial cells upon cardiac contractility identified in cardiomyocytes are complex and not fully described. Thus, careful evaluation of new therapeutic approaches is required targeting important physiological signaling pathways, some of which have been until recently considered as deleterious, like reactive oxygen species. Future works in the field of cardiac endothelial cells and cardiac function will help to better understand the implication of these mediators in cardiac physiopathology.

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Acarregui, Michael J., Katherine M. England, Joshua T. Richman, and Jennifer L. Littig. "Characterization of CD34+cells isolated from human fetal lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 284, no. 2 (February 1, 2003): L395—L401. http://dx.doi.org/10.1152/ajplung.00202.2002.

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The large capillary mass of the newborn lung demands the presence of endothelial cell precursors in lung tissue before development of the pulmonary capillary bed. The objective of this investigation was to isolate and characterize putative endothelial cell precursors from developing human lung. CD34, a cell surface marker for hematopoietic progenitor cells, endothelial precursor cells, and small vessel endothelial cells, was employed as an immunological “handle” for the selection of the desired cells. When CD34+cells were isolated from midtrimester human fetal lung tissue, then maintained in culture, the isolated cells expressed immunoreactivity for the endothelial cell marker von Willebrand factor and the vascular endothelial growth factor receptors KDR and Flt-1. However, only 5% or fewer of the cells expressed PECAM, an important factor in cell-cell interactions and a marker for endothelial cells associated with vessels. The CD34+cells endocytosed acetylated low-density lipoprotein and formed capillary-like structures when incubated in a cushion of Matrigel. RT-PCR analysis of mRNA for endothelial cell-related proteins Flt-1, Tie-2, and endothelial nitric oxide synthase demonstrated expression of these mRNAs by the isolated cells for at least 16 cell passages. These observations demonstrate that capillary endothelial cell precursors can be isolated from developing human lung and maintained in cell culture. These cells represent a potentially important tool for investigating the regulation of mechanisms governing development of the air-blood barrier in the human lung.

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Kitchens, CS, and JF Pendergast. "Human thrombocytopenia is associated with structural abnormalities of the endothelium that are ameliorated by glucocorticosteroid administration." Blood 67, no. 1 (January 1, 1986): 203–6. http://dx.doi.org/10.1182/blood.v67.1.203.203.

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Abstract Capillary fragility is characteristic of severe thrombocytopenia. This mechanical weakness may not be solely accounted for by decreased ability of platelets to repair endothelial breaks. Platelets may have a role in maintaining endothelial hemostasis. This laboratory has demonstrated thinning of capillary endothelium in experimental thrombocytopenia. We now report similar findings in human thrombocytopenia. Capillary endothelium supplying either skin or skeletal muscle was found to have a mean thickness only half that of normal as well as frequent very thinned areas, including some fenestrations. All findings reverted toward normal after four days of prednisone administration at a time the degree of thrombocytopenia was equally severe. These findings are consistent with the hypothesis that platelets are necessary for normal structure and function of endothelial cells and that glucocorticosteroid administration may ameliorate the pathophysiology of thrombocytopenia.

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Kitchens, CS, and JF Pendergast. "Human thrombocytopenia is associated with structural abnormalities of the endothelium that are ameliorated by glucocorticosteroid administration." Blood 67, no. 1 (January 1, 1986): 203–6. http://dx.doi.org/10.1182/blood.v67.1.203.bloodjournal671203.

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Capillary fragility is characteristic of severe thrombocytopenia. This mechanical weakness may not be solely accounted for by decreased ability of platelets to repair endothelial breaks. Platelets may have a role in maintaining endothelial hemostasis. This laboratory has demonstrated thinning of capillary endothelium in experimental thrombocytopenia. We now report similar findings in human thrombocytopenia. Capillary endothelium supplying either skin or skeletal muscle was found to have a mean thickness only half that of normal as well as frequent very thinned areas, including some fenestrations. All findings reverted toward normal after four days of prednisone administration at a time the degree of thrombocytopenia was equally severe. These findings are consistent with the hypothesis that platelets are necessary for normal structure and function of endothelial cells and that glucocorticosteroid administration may ameliorate the pathophysiology of thrombocytopenia.

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Tewes, B. J., and H. J. Galla. "Lipid Polarity in Brain Capillary Endothelial Cells." Endothelium 8, no. 3 (2001): 207–20. http://dx.doi.org/10.3109/10623320109051566.

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Matsuyama, Tomomasa, and Takaji Iida. "Primary Culture of Tilapia Capillary Endothelial Cells." Fish Pathology 35, no. 3 (2000): 163–64. http://dx.doi.org/10.3147/jsfp.35.163.

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Tewes, B. J., and H. J. Galla. "Lipid Polarity in Brain Capillary Endothelial Cells." Endothelium 8, no. 3 (January 2001): 207–20. http://dx.doi.org/10.1080/10623320109051566.

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Ghinea, N., A. Fixman, D. Alexandru, D. Popov, M. Hasu, L. Ghitescu, M. Eskenasy, M. Simionescu, and N. Simionescu. "Identification of albumin-binding proteins in capillary endothelial cells." Journal of Cell Biology 107, no. 1 (July 1, 1988): 231–39. http://dx.doi.org/10.1083/jcb.107.1.231.

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Isolated fat tissue microvessels and lung, whose capillary endothelia express in situ specific binding sites for albumin, were homogenized and subjected to SDS-gel electrophoresis and electroblotting. The nitrocellulose strips were incubated with either albumin-gold (Alb-Au) and directly visualized, or with [125I]albumin (monomeric or polymeric) and autoradiographed. The extracts of both microvascular endothelium and the lung express albumin-binding proteins (ABPs) represented by two pairs of polypeptides with major components of molecular mass 31 and 18 kD. The ABP peptides have pIs 8.05 to 8.75. Rabbit aortic endothelium, used as control, does not express detectable amounts of ABPs. The ABPs subjected to electrophoresis bind specifically and with high affinity (Kd = approximately 60 X 10(-9)M) both monomeric and polymeric albumin: the binding is saturable at approximately 80 nM concentration and 50% inhibition is reached at 5.5 micrograms/ml albumin concentration. Sulfhydryl-reducing agents beta-mercaptoethanol and dithiothreitol do not markedly affect the ABPs electrophoretic mobility and binding properties. As indicated by cell surface iodination of isolated capillary endothelium followed by electroblotting, autoradiography, and incubation with Alb-Au, the bands specifically stained by this ligand are also labeled with radioiodine.

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Lombardi, T., R. Montesano, M. B. Furie, S. C. Silverstein, and L. Orci. "In vitro modulation of endothelial fenestrae: opposing effects of retinoic acid and transforming growth factor beta." Journal of Cell Science 91, no. 2 (October 1, 1988): 313–18. http://dx.doi.org/10.1242/jcs.91.2.313.

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Cultured endothelial cells isolated from fenestrated capillaries express many properties characteristic of their in vivo differentiated phenotype, including the formation of a limited number of fenestrae. In this study, we have investigated whether physiological factors that control cell differentiation might regulate the surface density of fenestrae in capillary endothelial cells. We have found that treatment of the cultures with retinoic acid (10 microM) induces a more than threefold increase in the surface density of endothelial fenestrae, whereas transforming growth factor beta (TGF beta) (2 ng ml-1) causes a sevenfold decrease in the surface density of these structures. These results show that the expression of endothelial fenestrae is susceptible to bidirectional modulation by physiological signals, and suggest that retinoids and TGF beta may participate in the regulation of fenestral density of capillary endothelium in vivo.

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Gavrilovskaya, Irina, Elena Gorbunova, Valery Matthys, Nadine Dalrymple, and Erich Mackow. "The Role of the Endothelium in HPS Pathogenesis and Potential Therapeutic Approaches." Advances in Virology 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/467059.

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American hantaviruses cause a highly lethal acute pulmonary edema termed hantavirus pulmonary syndrome (HPS). Hantaviruses nonlytically infect endothelial cells and cause dramatic changes in barrier functions of the endothelium without disrupting the endothelium. Instead hantaviruses cause changes in the function of infected endothelial cells that normally regulate fluid barrier functions of capillaries. The endothelium of arteries, veins, and lymphatic vessels is unique and central to the function of vast pulmonary capillary beds, which regulate pulmonary fluid accumulation. The endothelium maintains vascular barrier functions through a complex series of redundant receptors and signaling pathways that serve to both permit fluid and immune cell efflux into tissues and restrict tissue edema. Infection of the endothelium provides several mechanisms for hantaviruses to alter capillary permeability but also defines potential therapeutic targets for regulating acute pulmonary edema and HPS disease. Here we discuss interactions of HPS causing hantaviruses with the endothelium, potential endothelial cell-directed permeability mechanisms, and therapeutic targeting of the endothelium as a means of reducing the severity of HPS disease.

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Rorvik, M. C., D. P. Allison, J. A. Hotchkiss, H. P. Witschi, and S. J. Kennel. "Antibodies to mouse lung capillary endothelium." Journal of Histochemistry & Cytochemistry 36, no. 7 (July 1988): 741–49. http://dx.doi.org/10.1177/36.7.3290332.

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We are interested in developing monoclonal antibodies (MoAbs) that recognize specific cell types in the lung of BALB/c mice. Normal mouse lung homogenate was used to immunize F344 rats and hybridomas were produced by fusion of rat spleen cells with mouse myeloma SP 2/0. Two hybridomas were selected which produced MoAbs active in immunohistochemistry of lung cells. MoAb 273-34A and 411-201B both show extensive peroxidase staining of capillary endothelial cells within alveolar walls of lungs at the light microscopic level. To demonstrate cell specificity, immunoelectron microscopy with gold-labeled antibody was performed. Lightly fixed lungs were frozen and thin-sectioned before staining with MoAb and 5-nm gold particles coupled to secondary antibody. Quantitative analyses of these cryosections show that both antibodies, used at optimal concentrations, are specific for binding to capillary endothelial cells. More than 95% of the gold particles are associated with capillary endothelial cells on the thin side of the alveolar wall. When capillaries adjoined thick septa containing interstitial cells, about two thirds of the gold particles were associated with endothelial cells and about one quarter with interstitial cells. These MoAbs should be useful in studying the role of endothelial cells in toxic lung injury.

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Ziche, Marina, Lucia Morbidelli, Piero Dolara, and Alberto Giotti. "Endothelin promote growth and migration of capillary endothelial cells in vitro." Pharmacological Research 22 (September 1990): 506. http://dx.doi.org/10.1016/s1043-6618(09)80506-9.

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Rabiu, F. I. "Role of endothelial cell junctions in transendothelial cancer cell migration. A review." Dutse Journal of Pure and Applied Sciences 7, no. 4a (February 3, 2022): 121–43. http://dx.doi.org/10.4314/dujopas.v7i4a.14.

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During metastasis, tumour cells must become migratory and travel towards a capillary within the tumour. They then degrade the matrix surrounding the pericytes and endothelial cells, insert themselves between endothelial cells, transverse the capillary wall, to then enter the blood stream. This process depends on the motile behaviour of the tumour cells as well as the role of endothelial cell-cell junctions, both including adherens junctions and tight junctions. Circulating tumour cells must next, adhere to the walls of the capillary at the site of secondary tumour formation. Here, they again traverse the capillary wall to enter tissues distant from the primary tumour. This review aim to discuss the basic architecture of the endothelial junctional complex as well as the role played by these components towards the transendothelial migration of cancer cells from the primary site to the secondary site. Proper understanding of the role played by each of these components could invariably lead to the development of novel adjuvant cancer chemotherapy.

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Stevens, Reece P., Sunita S. Paudel, Santina C. Johnson, Troy Stevens, and Ji Young Lee. "Endothelial metabolism in pulmonary vascular homeostasis and acute respiratory distress syndrome." American Journal of Physiology-Lung Cellular and Molecular Physiology 321, no. 2 (August 1, 2021): L358—L376. http://dx.doi.org/10.1152/ajplung.00131.2021.

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Capillary endothelial cells possess a specialized metabolism necessary to adapt to the unique alveolar-capillary environment. Here, we highlight how endothelial metabolism preserves the integrity of the pulmonary circulation by controlling vascular permeability, defending against oxidative stress, facilitating rapid migration and angiogenesis in response to injury, and regulating the epigenetic landscape of endothelial cells. Recent reports on single-cell RNA-sequencing reveal subpopulations of pulmonary capillary endothelial cells with distinctive reparative capacities, which potentially offer new insight into their metabolic signature. Lastly, we discuss broad implications of pulmonary vascular metabolism on acute respiratory distress syndrome, touching on emerging findings of endotheliitis in coronavirus disease 2019 (COVID-19) lungs.

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Kaiser, Mathias, Malgorzata Burek, Stefan Britz, Frauke Lankamp, Steffi Ketelhut, Björn Kemper, Carola Förster, Christian Gorzelanny, and Francisco Goycoolea. "The Influence of Capsaicin on the Integrity of Microvascular Endothelial Cell Monolayers." International Journal of Molecular Sciences 20, no. 1 (December 30, 2018): 122. http://dx.doi.org/10.3390/ijms20010122.

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Microvascular endothelial cells are an essential part of many biological barriers, such as the blood–brain barrier (BBB) and the endothelium of the arteries and veins. A reversible opening strategy to increase the permeability of drugs across the BBB could lead to improved therapies due to enhanced drug bioavailability. Vanilloids, such as capsaicin, are known to reversibly open tight junctions of epithelial and endothelial cells. In this study, we used several in vitro assays with the murine endothelial capillary brain cells (line cEND) as a BBB model to characterize the interaction between capsaicin and endothelial tight junctions.

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Fujimoto, T., and S. J. Singer. "Immunocytochemical studies of endothelial cells in vivo. I. The presence of desmin only, or of desmin plus vimentin, or vimentin only, in the endothelial cells of different capillaries of the adult chicken." Journal of Cell Biology 103, no. 6 (December 1, 1986): 2775–86. http://dx.doi.org/10.1083/jcb.103.6.2775.

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It is currently believed that the intermediate filaments of endothelial cells contain vimentin subunits exclusively. This inference, however, is derived from studies of only a few types of endothelial cells. By double indirect immunofluorescence and immunoelectron microscopy, we have now examined the endothelial cells of the micro- and macrovasculature of a variety of tissues and organs of adult chicken in vivo for their content of desmin and vimentin. Endothelial cells of the peritubular capillary in the renal cortex, the hepatic sinusoid, and the splenic sinusoid were found to contain only desmin; those of the exocrine pancreas capillary contained both desmin and vimentin; and the endothelial cells of the macrovasculatures and of all the other microvasculatures examined, including the vasa recta of the renal medulla, contained only vimentin. Such heterogeneity suggests that different types of adult chicken endothelial cells may have different embryological origins. To the extent that desmin and vimentin intermediate filaments may be functionally distinct, these results also suggest that different capillary endothelial cells may have different functional properties.

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TAKAHASHI, TAKAMUNE, KEIKO TAKAHASHI, RAYMOND MERNAUGH, VLADIMIR DROZDOFF, CHRIS SIPE, HARALD SCHOECKLMANN, BARRY ROBERT, DALE R. ABRAHAMSON, and THOMAS O. DANIEL. "Endothelial Localization of Receptor Tyrosine Phosphatase, ECRTP/DEP-1, in Developing and Mature Renal Vasculature." Journal of the American Society of Nephrology 10, no. 10 (October 1999): 2135–45. http://dx.doi.org/10.1681/asn.v10102135.

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Abstract. Developmental assembly of the renal microvasculature requires spatially and temporally coordinated migration, assembly, differentiation, and maturation of endothelial cells in the context of adjacent epithelial and mesangial cells. In this study, endothelial expression and distribution of the receptor tyrosine phosphatase ECRTP/DEP-1 were evaluated during and after developmental assembly of the renal microvasculature. Monoclonal antibodies against ECRTP/DEP-1 ectodomain epitopes localize its expression to membrane surfaces of endothelial cells in glomerular, peritubular capillary, and arterial renal sites of mature human and murine kidney. During kidney development, ECRTP/DEP-1 immunostaining is evident on a subpopulation of metanephric mesenchymal cells and on putative progenitors of glomerular capillary endothelial cells early in their recruitment to developing glomeruli. ECRTP/DEP-1 is prominently displayed on luminal membrane surfaces with punctate accumulations at inter-endothelial contacts that overlap with vascular endothelial-cadherin staining. ECRTP/DEP-1 is recruited to inter-endothelial contacts in confluent cultured human renal and dermal microvascular endothelial cells, yet experimental dissociation of vascular endothelial-cadherin from endothelial junctional complexes fails to redistribute ECRTP/DEP-1. These findings indicate that ECRTP/DEP-1 is expressed in anticipation of glomerular capillary endothelial recruitment during development, and suggest that ECRTP/DEP-1 ectodomain interacts with endothelial surface ligands that are engaged by cell-cell contact.

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De Cesari, Chiara, Ivana Barravecchia, Olga V. Pyankova, Matteo Vezza, Marco M. Germani, Francesca Scebba, Jack J. W. A. van Loon, and Debora Angeloni. "Hypergravity Activates a Pro-Angiogenic Homeostatic Response by Human Capillary Endothelial Cells." International Journal of Molecular Sciences 21, no. 7 (March 28, 2020): 2354. http://dx.doi.org/10.3390/ijms21072354.

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Capillary endothelial cells are responsible for homeostatic responses to organismic and environmental stimulations. When malfunctioning, they may cause disease. Exposure to microgravity is known to have negative effects on astronauts’ physiology, the endothelium being a particularly sensitive organ. Microgravity-related dysfunctions are striking similar to the consequences of sedentary life, bed rest, and ageing on Earth. Among different countermeasures implemented to minimize the effects of microgravity, a promising one is artificial gravity. We examined the effects of hypergravity on human microvascular endothelial cells of dermal capillary origin (HMEC-1) treated at 4 g for 15 min, and at 20 g for 15 min, 3 and 6 h. We evaluated cell morphology, gene expression and 2D motility and function. We found a profound rearrangement of the cytoskeleton network, dose-dependent increase of Focal Adhesion kinase (FAK) phosphorylation and Yes-associated protein 1 (YAP1) expression, suggesting cell stiffening and increased proneness to motility. Transcriptome analysis showed expression changes of genes associated with cardiovascular homeostasis, nitric oxide production, angiogenesis, and inflammation. Hypergravity-treated cells also showed significantly improved motility and function (2D migration and tube formation). These results, expanding our knowledge about the homeostatic response of capillary endothelial cells, show that adaptation to hypergravity has opposite effect compared to microgravity on the same cell type.

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Grabb, Paul A., and Mark R. Gilbert. "Neoplastic and pharmacological influence on the permeability of an in vitro blood-brain barrier." Journal of Neurosurgery 82, no. 6 (June 1995): 1053–58. http://dx.doi.org/10.3171/jns.1995.82.6.1053.

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✓ The authors investigated the effects of glioma cells and pharmacological agents on the permeability of an in vitro blood-brain barrier (BBB) to determine the following: 1) whether malignant glia increase endothelial cell permeability; 2) how glucocorticoids affect endothelial cell permeability in the presence and absence of malignant glia; and 3) whether inhibiting phospholipase A2, the enzyme that releases arachidonic acid from membrane phospholipids, would reduce any malignant glioma—induced increase in endothelial cell permeability. Primary cultures of rat brain capillary endothelium were grown on porous membranes; below the membrane, C6, 9L rat glioma, T98G human glioblastoma, or no cells (control) were cocultured. Dexamethasone (0.1 µM), bromophenacyl bromide (1.0 µM), a phospholipase A2 inhibitor, or nothing was added to culture media 72 hours prior to assaying the rat brain capillary endothelium permeability. Permeability was measured as the flux of radiolabeled sucrose across the rat brain capillary endothelium monolayer and then calculated as an effective permeability coefficient (Pe). When neither dexamethasone nor bromophenacyl bromide was present, C6 cells reduced the Pe significantly (p < 0.05), whereas 9L and T98G cells increased Pe significantly (p < 0.05) relative to rat brain capillary endothelium only (control). Dexamethasone reduced Pe significantly for all cell preparations (p < 0.05). The 9L and T98G cell preparations coincubated with dexamethasone had the lowest Pe of all cell preparations. The Pe was not affected in any cell preparation by coincubation with bromophenacyl bromide (p > 0.45). These in vitro BBB experiments showed that: 1) malignant glia, such as 9L and T98G cells, increase Pe whereas C6 cells probably provide an astrocytic influence by reducing Pe; 2) dexamethasone provided significant BBB “tightening” effects both in the presence and absence of glioma cells; 3) the in vivo BBB is actively made more permeable by malignant glia and not simply because of a lack of astrocytic induction; 4) tumor or endothelial phospholipase A2 activity is probably not responsible for glioma-induced increased in BBB permeability; and 5) this model is useful for testing potential agents for BBB protection and for studying the pathophysiology of tumor-induced BBB disruption.

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Blanchette-Mackie, E. J., H. Masuno, N. K. Dwyer, T. Olivecrona, and R. O. Scow. "Lipoprotein lipase in myocytes and capillary endothelium of heart: immunocytochemical study." American Journal of Physiology-Endocrinology and Metabolism 256, no. 6 (June 1, 1989): E818—E828. http://dx.doi.org/10.1152/ajpendo.1989.256.6.e818.

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Lipoprotein lipase was immunolocalized by electron microscopy in hearts of young mice; 78% of lipoprotein lipase was in myocytes, 3-6% in extracellular space, and 18% in capillary endothelium. Lipoprotein lipase in myocytes was located primarily in sarcoplasmic reticulum, Golgi sacs, and transport vesicles and also in secretory vesicles at the cell periphery. Lipoprotein lipase in extracellular space was present near the orifice of secretory vesicles of myocytes and in narrow zones spanning the space between myocytes and capillary endothelium. The lowest concentration of lipase associated with endothelial cells was at the basal plasma membrane, whereas the highest concentration was at the surface of luminal projections. Lipoprotein lipase was associated with chylomicrons at the capillary surface but not with chylomicron remnants. Fasting mice for 48 h increased, in heart, lipoprotein lipase activity by 120% and immunolocalized lipase by 270%. The greatest increase (5-fold) occurred at the surface of intraluminal endothelial projections. The findings indicate that lipoprotein lipase in heart is synthesized by myocytes, transferred across extracellular space along cell surfaces and across endothelial cells via vesicles or intracellular channels, and concentrated at the surface of luminal projections of endothelium where the enzyme hydrolyzes triacylglycerol of chylomicrons and very low-density lipoproteins.

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Kawai, Nobutoshi, Richard M. McCarron, and Maria Spatz. "Endothelins stimulate sodium uptake into rat brain capillary endothelial cells through endothelin A-like receptors." Neuroscience Letters 190, no. 2 (May 1995): 85–88. http://dx.doi.org/10.1016/0304-3940(95)11507-s.

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Golat, Brian T., and Don F. Cameron. "Sertoli Cells Enhance Formation of Capillary-Like Structures in Vitro." Cell Transplantation 17, no. 10-11 (October 2008): 1135–44. http://dx.doi.org/10.3727/096368908787236512.

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Sertoli cells isolated from the testis (referred to as extratesticular Sertoli cells) have been shown to facilitate allo- and xenogeneic cell transplantations. It appears likely that the ability of these cells to enhance the success of cell engraftment is due, in part, to the retention of their intratesticular functions of trophic support and immunoprotection. Sertoli cells also are involved in the regulation of angiogenesis in the testis, which may also contribute to enhanced cell engraftment success facilitated by extratesticular Sertoli cells. Because the maintenance of the cell's intratesticular angiogenic function has not yet been evaluated for extratesticular Sertoli cells, this study examined the cell's ability to enhance angiogenesis in vitro. Sertoli cell conditioned media were derived from isolated rat Sertoli cell cultures and used in a rat aortic model of induced angiogenesis, in endothelial and smooth muscle cell monocultures, and in endothelial smooth muscle cocultures. An angiogenic rat cytokine array identified angiogenic factors in the control and conditioned media. Aorta sections incubated with Sertoli cell conditioned media showed a marked increase in the formation of capillary-like structures when compared to controls. Likewise, endothelial cells incubated in conditioned media organized into capillary-like structures not observed when incubated in control media. In coculture, smooth muscle cells were associated with endothelial cell-derived capillary-like structures only when incubated in conditioned media. Cytokine arrays indicated the presence and a qualitative increase of specific angiogenic growth factors in Sertoli cell conditioned media not observed in control media. Results indicate that extratesticular Sertoli cells retain their intratesticular angiogenic function in vitro.

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Fujimoto, T., and S. J. Singer. "Immunocytochemical studies of endothelial cells in vivo. II. Chicken aortic and capillary endothelial cells exhibit different cell surface distributions of the integrin complex." Journal of Histochemistry & Cytochemistry 36, no. 10 (October 1988): 1309–17. http://dx.doi.org/10.1177/36.10.2458407.

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Frozen sections of chicken tissues containing aortic and capillary endothelial cells were immunolabeled with two mouse monoclonal antibodies directed to different epitopes of the chicken integrin beta-chain. Integrin is an integral membrane protein complex that is believed to mediate a transmembrane linkage between the extracellular matrix and the actin cytoskeleton. In immunofluorescence experiments with semi-thin frozen sections, the aortic endothelial cells were labeled for integrin all around their surfaces, whereas capillary endothelial cells of heart and kidney were labeled only on their basal surfaces. At the immunofluorescence level of resolution, the distribution of integrin appeared to be correlated with that of F-actin in double-labeling experiments with NBD-phallacidin. These different distributions of integrin on the two types of endothelial cells were definitively confirmed by immunoelectron microscopic labeling with the monoclonal antibodies on ultra-thin frozen sections. These results therefore indicate that the luminal surfaces, as well as the underlying cytoskeleton of capillary endothelial cells, are significantly different in structure from those of aortic endothelial cells. These differences may reflect the vastly different hemodynamic stress to which the two types of endothelial cells are subjected, and in addition may mediate different adhesion properties of the luminal surfaces of the two cell types.

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Preisig-Müller, Regina, Michael Mederos y Schnitzler, Christian Derst, and Jürgen Daut. "Separation of cardiomyocytes and coronary endothelial cells for cell-specific RT-PCR." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 1 (July 1, 1999): H413—H416. http://dx.doi.org/10.1152/ajpheart.1999.277.1.h413.

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A simple method for analyzing the differential gene expression of coronary endothelial cells and cardiac muscle cells was developed. Cells were isolated from guinea pig hearts by collagenase digestion. In the diluted cell suspension, single cardiomyocytes and capillary fragments containing 6–15 endothelial cells could be identified morphologically. A simple “cell picker” was constructed using a polyethylene pipette with a tip diameter of ∼150 μm that was attached to a micromanipulator and connected to an electric miniature valve. Intermittent suction pulses (1- to 2-cm water column) were applied by opening the valve for 100–200 ms at 1-s intervals. Cardiomyocytes (800–1,000) or capillary fragments (150) were picked under visual control using an inverted microscope. The cells were transferred to a reaction tube for RNA extraction, reverse transcription (RT), and DNA amplification (RT-PCR) with gene-specific and intron-spanning primers. All PCR products were verified by sequencing. Troponin T and endothelin-1 were found to be specific markers for guinea-pig cardiac muscle cells and coronary endothelial cells, respectively.

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Nagashima, Tatsuya, Shijing Wu, Michio Yamaguchi, and Norihiko Tamaki. "Reoxygenation Injury of Human Brain Capillary Endothelial Cells." Cellular and Molecular Neurobiology 19, no. 1 (February 1999): 151–61. http://dx.doi.org/10.1023/a:1006980911551.

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Anderson, Christopher R., Nicole E. Hastings, Brett R. Blackman, and Richard J. Price. "Capillary Sprout Endothelial Cells Exhibit a CD36low Phenotype." American Journal of Pathology 173, no. 4 (October 2008): 1220–28. http://dx.doi.org/10.2353/ajpath.2008.071194.

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Wang, Hua, Shengfu Chen, Buddy D. Ratner, E. Helene Sage, and Shaoyi Jiang. "Capillary Differentiation of Endothelial Cells on Microgrooved Surfaces." Journal of Physical Chemistry C 111, no. 40 (October 2007): 14602–6. http://dx.doi.org/10.1021/jp075746z.

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Schupp, Jonas C., Taylor S. Adams, Carlos Cosme, Micha Sam Brickman Raredon, Yifan Yuan, Norihito Omote, Sergio Poli, et al. "Integrated Single-Cell Atlas of Endothelial Cells of the Human Lung." Circulation 144, no. 4 (July 27, 2021): 286–302. http://dx.doi.org/10.1161/circulationaha.120.052318.

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Background: Cellular diversity of the lung endothelium has not been systematically characterized in humans. We provide a reference atlas of human lung endothelial cells (ECs) to facilitate a better understanding of the phenotypic diversity and composition of cells comprising the lung endothelium. Methods: We reprocessed human control single-cell RNA sequencing (scRNAseq) data from 6 datasets. EC populations were characterized through iterative clustering with subsequent differential expression analysis. Marker genes were validated by fluorescent microscopy and in situ hybridization. scRNAseq of primary lung ECs cultured in vitro was performed. The signaling network between different lung cell types was studied. For cross-species analysis or disease relevance, we applied the same methods to scRNAseq data obtained from mouse lungs or from human lungs with pulmonary hypertension. Results: Six lung scRNAseq datasets were reanalyzed and annotated to identify >15 000 vascular EC cells from 73 individuals. Differential expression analysis of EC revealed signatures corresponding to endothelial lineage, including panendothelial, panvascular, and subpopulation-specific marker gene sets. Beyond the broad cellular categories of lymphatic, capillary, arterial, and venous ECs, we found previously indistinguishable subpopulations; among venous EC, we identified 2 previously indistinguishable populations: pulmonary–venous ECs (COL15A1 neg ) localized to the lung parenchyma and systemic–venous ECs (COL15A1 pos ) localized to the airways and the visceral pleura; among capillary ECs, we confirmed their subclassification into recently discovered aerocytes characterized by EDNRB , SOSTDC1 , and TBX2 and general capillary EC. We confirmed that all 6 endothelial cell types, including the systemic–venous ECs and aerocytes, are present in mice and identified endothelial marker genes conserved in humans and mice. Ligand-receptor connectome analysis revealed important homeostatic crosstalk of EC with other lung resident cell types. scRNAseq of commercially available primary lung ECs demonstrated a loss of their native lung phenotype in culture. scRNAseq revealed that endothelial diversity is maintained in pulmonary hypertension. Our article is accompanied by an online data mining tool ( www.LungEndothelialCellAtlas.com ). Conclusions: Our integrated analysis provides a comprehensive and well-crafted reference atlas of ECs in the normal lung and confirms and describes in detail previously unrecognized endothelial populations across a large number of humans and mice.

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Gamble, J. R., L. J. Matthias, G. Meyer, P. Kaur, G. Russ, R. Faull, M. C. Berndt, and M. A. Vadas. "Regulation of in vitro capillary tube formation by anti-integrin antibodies." Journal of Cell Biology 121, no. 4 (May 15, 1993): 931–43. http://dx.doi.org/10.1083/jcb.121.4.931.

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Human endothelial cells are induced to form an anastomosing network of capillary tubes on a gel of collagen I in the presence of PMA. We show here that the addition of mAbs, AK7, or RMAC11 directed to the alpha chain of the major collagen receptor on endothelial cells, the integrin alpha 2 beta 1, enhance the number, length, and width of capillary tubes formed by endothelial cells derived from umbilical vein or neonatal foreskins. The anti-alpha 2 beta 1 antibodies maintained the endothelial cells in a rounded morphology and inhibited both their attachment to and proliferation on collagen but not on fibronectin, laminin, or gelatin matrices. Furthermore, RMAC11 promoted tube formation in collagen gels of increased density which in the absence of RMAC11 did not allow tube formation. Neither RMAC11 or AK7 enhanced capillary formation in the absence of PMA. Lumen structure and size were also altered by antibody RMAC11. In the absence of antibody the majority of lumina were formed intracellularly from single cells, but in the presence of RMAC11, multiple cells were involved and the lumen size was correspondingly increased. Endothelial cells were also induced to undergo capillary formation in fibrin gels after PMA stimulation. The addition of anti-alpha v beta 3 antibodies promoted tube formation in fibrin gels and inhibited EC adhesion to and proliferation on a fibrinogen matrix. The enhancement of capillary formation by the anti-integrin antibodies was matrix specific; that is, anti-alpha v beta 3 antibodies only enhanced tube formation on fibrin gels and not on collagen gels while anti-alpha v beta 1 antibodies only enhanced tubes on collagen and not on fibrin gels. Thus we postulate that changes in the adhesive nature of endothelial cells for their extracellular matrix can profoundly effect their function. Anti-integrin antibodies which inhibit cell-matrix interactions convert endothelial cells from a proliferative phenotype towards differentiation which results in enhanced capillary tube formation.

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Welten, Cassandra M., Emily C. Keats, Lee-Cyn Ang, and Zia A. Khan. "Hemangioblastoma Stromal Cells Show Committed Stem Cell Phenotype." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 39, no. 6 (November 2012): 821–27. http://dx.doi.org/10.1017/s0317167100015675.

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Background:Hemangioblastomas are benign vascular tumors of the central nervous system that occur sporadically or in association with von Hippel-Lindau disease. These tumors are characteristically composed of a dense capillary network with intervening stromal/interstitial cells. To date, the histogenesis of hemangioblastoma remains unclear. We hypothesize that hemangioblastomas arise from a defective mesodermal stem cell, which gives rise to the atypical vasculature.Methods:To test our hypothesis, we have characterized the cellular composition of hemangioblastomas by immunophenotyping pluripotent and committed stem cells and vascular endothelial cells.Results:Our findings show that hemangioblastoma endothelial cells are positive for CD133, a stem and progenitor cell marker. Vascular endothelial cells also expressed nuclear Oct4. In addition to the endothelium, both CD133 and Oct4 were present in stromal and perivascular cells. Interestingly, neither the endothelium nor the stromal cells expressed Sox2 or Nanog suggesting a committed stem cell phenotype.Conclusions:From these findings, we believe that hemangioblastoma stromal cells are committed stem cells producing both vascular cell types. The findings also show an unusual CD133-positive endothelial phenotype in hemangioblastoma.

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Mignatti, P., R. Mazzieri, and D. B. Rifkin. "Expression of the urokinase receptor in vascular endothelial cells is stimulated by basic fibroblast growth factor." Journal of Cell Biology 113, no. 5 (June 1, 1991): 1193–201. http://dx.doi.org/10.1083/jcb.113.5.1193.

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Basic fibroblast growth factor, a potent angiogenesis inducer, stimulates urokinase (uPA) production by vascular endothelial cells. In both basic fibroblast growth factor-stimulated and -nonstimulated bovine capillary endothelial and human umbilical vein endothelial cells single-chain uPA binding is mediated by a membrane protein with a Mr of 42,000. Exposure of bovine capillary or endothelial human umbilical vein endothelial cells to pmolar concentrations of basic fibroblast growth factor results in a dose-dependent, protein synthesis-dependent increase in the number of membrane receptors for uPA (19,500-187,000) and in a parallel decrease in their affinity (KD = 0.144-0.790 nM). With both cells, single-chain uPA binding is competed by synthetic peptides whose sequence corresponds to the receptor-binding sequence in the NH2-terminal domain of uPA. Exposure of bovine capillary endothelial cells to transforming growth factor beta 1, which inhibits uPA production and upregulates type 1 plasminogen activator inhibitor, the major endothelial cell plasminogen activator inhibitor, has no effect on uPA receptor levels. These results show that basic fibroblast growth factor, besides stimulating uPA production by vascular endothelial cells, also increases the production of receptors, which modulates their capacity to focalize this enzyme on the cell surface. This effect may be important in the degradative processes that occur during angiogenesis.

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Journal articles on the topic 'Capillary endothelial cells'

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