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1
Cardell, LO, R. Uddman, and L. Edvinsson. "Endothelins: A Role in Cerebrovascular Disease?" Cephalalgia 14, no. 4 (August 1994): 259–65. http://dx.doi.org/10.1046/j.1468-2982.1994.1404259.x.
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Vasoactive factors produced and released by the endothelium exert a powerful influence on vascular tone in the cerebral circulation. Impaired endothelium-dependent responses, such as decreased production of endothelium-derived relaxing factors, and/or release of endothelium-derived contractile factors may give rise to different pathophysiological conditions. Among the endothelium-derived contractile factors the endothelins have recently received particular attention. Endothelin-1 is the major isoform in the endothelin family, which also includes endothelin-2 and endothelin-3. Endothelin-1 is synthesized within the endothelium of cerebral vessels, whereas both endothelin-1 and endothelin-3 in addition have been identified in neurons and glia. Recent electrophysiological work has suggested a neuromodulatory role for these peptides, but at present the general interest is mainly focused on their vasoactive role. Physiological stimuli such as hypoxia, anoxia, and hemodynamic shear stress will stimulate the endothelial endothelin production. In the brain, at least two types of specific subreceptors have been cloned; ETA receptors, exclusively associated with blood vessels and ETB receptors also found on glial, epithelial, and ependymal cells. The endothelins seem so far to be the most potent vasoconstrictors yet identified. The circulating plasma levels of immunoreactive endothelin are low. Since more than 80% of the total amount released from endothelial cells seems to be secreted towards the underlying smooth muscle, endothelins have been ascribed a local vasoregulatory role. Endothelins are believed to be involved in several of our most common cerebrovascular diseases and the present review comments on their possible pathophysiological role in subarachnoid haemorrhage, cerebral ischemia, and migraine.
2
Westerweel, Peter E., та Marianne C. Verhaar. "Protective Actions of PPAR-γActivation in Renal Endothelium". PPAR Research 2008 (2008): 1–9. http://dx.doi.org/10.1155/2008/635680.
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Renal endothelial damage is pivotal in the initiation and progression of renal disease. Damaged renal endothelium may be regenerated through proliferation of local endothelium and circulation-derived endothelial progenitor cells. Activation of the PPAR-γ-receptors present on endothelial cells affects their cellular behavior. Proliferation, apoptosis, migration, and angiogenesis by endothelial cells are modulated, but may involve both stimulation and inhibition depending on the specific circumstances. PPAR-γ-receptor activation stimulates the production of nitric oxide, C-type natriuretic peptide, and superoxide dismutase, while endothelin-1 production is inhibited. Together, they augment endothelial function, resulting in blood pressure lowering and direct renoprotective effects. The presentation of adhesion molecules and release of cytokines recruiting inflammatory cells are inhibited by PPAR-γ-agonism. Finally, PPAR-γ-receptors are also found on endothelial progenitor cells and PPAR-γ-agonists stimulate progenitor-mediated endothelial repair. Together, the stimulatory effects of PPAR-γ-agonism on endothelium make an important contribution to the beneficial actions of PPAR-γ-agonists on renal disease.
3
Mebazaa, A., E. Mayoux, K. Maeda, L. D. Martin, E. G. Lakatta, J. L. Robotham, and A. M. Shah. "Paracrine effects of endocardial endothelial cells on myocyte contraction mediated via endothelin." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 5 (November 1, 1993): H1841—H1846. http://dx.doi.org/10.1152/ajpheart.1993.265.5.h1841.
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Endocardial endothelium is reported to modulate myocardial contraction by releasing diffusible factors, but the nature of the agent(s) responsible is unknown. In the present study we investigated the potential role of endothelin in these effects. Cultured sheep endocardial endothelial cells were found to express endothelin-1 mRNA and to release endothelin-1 into superfusing solution. This superfusate induced positive inotropic effects in isolated rat cardiac myocytes, associated with an increase in the cytosolic Ca2+ transient. Similar positive inotropic effects were induced by vascular endothelial cell superfusate as well as by synthesized endothelin-1, administered at concentrations similar to those present in the superfusate. Incubation of endocardial endothelial cell superfusate with endothelin-1-specific antiserum reduced the free endothelin-1 concentration to undetectable levels and abolished both the positive inotropic effect and the rise in cytosolic Ca2+. These findings indicate that endocardial endothelial cells may modulate myocardial contraction in part through the release of endothelin-1 and suggest that endocardial as well as vascular endothelium could exert potent paracrine effects on myocardium.
4
Saenz de Tejada, I., M. P. Carson, A. de las Morenas, I. Goldstein, and A. M. Traish. "Endothelin: localization, synthesis, activity, and receptor types in human penile corpus cavernosum." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 4 (October 1, 1991): H1078—H1085. http://dx.doi.org/10.1152/ajpheart.1991.261.4.h1078.
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The localization, synthesis, and activity of endothelin and the receptor types mediating its effects in penile corpus cavernosum were investigated in whole tissue and in cultured cells derived from this tissue. With immunocytochemistry, utilizing an antiendothelin 1 (ET-1) monoclonal antibody, endothelin-like immunoreactivity was localized intensely in the endothelium and to a lesser degree in the trabecular smooth muscle. Human corpus cavernosum endothelial cells in culture expressed preproendothelin 1 mRNA, as determined by Northern blot analysis. Significant amounts of endothelin-like immunoreactivity were measured by radioimmunoassay in the supernatants of corpus cavernosum endothelial cells in culture. Endothelins are potent constrictors and caused long-lasting contractions of corporeal strips in organ chambers. Equilibrium binding analysis of endothelins to their receptor sites revealed high-affinity, specific, and saturable binding of labeled endothelins to corporeal membranes. Competition binding experiments demonstrated receptors with high affinity for ET-1 and -2 and low affinity for ET-3 and another, less abundant, set of receptors with high affinity for ET-1, -2, and -3. Affinity labeling of endothelins to corporeal membranes, followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis, revealed that ET-1 and -2 cross-linked specifically to three different molecular mass components (75, 52, and 34 kDa). ET-3 bound only to the 34-kDa component. It is concluded that human corpus cavernosum endothelium has the ability to synthesize and release endothelin, that endothelins contract corporeal smooth muscle, and that at least two distinct endothelin receptors may exist and are differentiated by their affinity for ET-3.
5
Rosolowsky, L. J., and W. B. Campbell. "Endothelial cells stimulate aldosterone release from bovine adrenal zona glomerulosa cells." American Journal of Physiology-Endocrinology and Metabolism 266, no. 1 (January 1, 1994): E107—E117. http://dx.doi.org/10.1152/ajpendo.1994.266.1.e107.
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Intra-adrenal factors promote basal as well as adrenocorticotropic hormone (ACTH)-, angiotensin-, and flow-induced steroid secretion. Because endothelial cells respond to changes in flow and are in a close anatomical relationship to steroidogenic cells, we examined the effect of endothelial cells on the secretion of aldosterone from zona glomerulosa (ZG) cells. Endothelial cells and endothelial cell-conditioned medium (EC-CM) stimulated the release of aldosterone from ZG cells. The stimulatory effect was related to the concentration of endothelial cells or EC-CM. The maximal stimulatory effect was 60-70% of the maximal effect of ACTH. Endothelial cells alone did not produce aldosterone. Human fibroblasts were ineffective in promoting aldosterone release. Endothelial cells and EC-CM failed to stimulate cortisol release from zona fasciculata cells. Treatment of the EC-CM with trypsin and pronase abolished the activity, indicating that a protein mediated the effect. However, the EC-CM activity could be distinguished from angiotensin, endothelin-1, and bradykinin. The factor stimulated the formation of pregnenolone but not the conversion of corticosterone to aldosterone. This endothelium-derived steroidogenic factor appeared to be a novel stimulus to aldosterone secretion. This study represents the first demonstration that endothelial cells alter endocrine function in vitro.
6
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.
7
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.
8
CPK, Cheung. "T Cells, Endothelial Cell, Metabolism; A Therapeutic Target in Chronic Inflammation." Open Access Journal of Microbiology & Biotechnology 5, no. 2 (2020): 1–6. http://dx.doi.org/10.23880/oajmb-16000163.
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The role of metabolic reprogramming in the coordination of the immune response has gained increasing consideration in recent years. Indeed, it has become clear that changes in the metabolic status of immune cells can alter their functional properties. During inflammation, stimulated immune cells need to generate sufficient energy and biomolecules to support growth, proliferation and effector functions, including migration, cytotoxicity and production of cytokines. Thus, immune cells switch from oxidative phosphorylation to aerobic glycolysis, increasing their glucose uptake. A similar metabolic reprogramming has been described in endothelial cells which have the ability to interact with and modulate the function of immune cells and vice versa. Nonetheless, this complicated interplay between local environment, endothelial and immune cells metabolism, and immune functions remains incompletely understood. We analyze the metabolic reprogramming of endothelial and T cells during inflammation and we highlight some key components of this metabolic switch that can lead to the development of new therapeutics in chronic inflammatory disease.
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Jaffredo, T., R. Gautier, A. Eichmann, and F. Dieterlen-Lievre. "Intraaortic hemopoietic cells are derived from endothelial cells during ontogeny." Development 125, no. 22 (November 15, 1998): 4575–83. http://dx.doi.org/10.1242/dev.125.22.4575.
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We have investigated the developmental relationship of the hemopoietic and endothelial lineages in the floor of the chicken aorta, a site of hemopoietic progenitor emergence in the embryo proper. We show that, prior to the onset of hemopoiesis, the aortic endothelium uniformly expresses the endothelium-specific membrane receptor VEGF-R2. The onset of hemopoiesis can be determined by detecting the common leukocyte antigen CD45. VEGF-R2 and CD45 are expressed in complementary fashion, namely the hemopoietic cluster-bearing floor of the aorta is CD45(+)/VEGF-R2(−), while the rest of the aortic endothelium is CD45(−)/VEGF-R2(+). To determine if the hemopoietic clusters are derived from endothelial cells, we tagged the E2 endothelial tree from the inside with low-density lipoproteins (LDL) coupled to DiI. 24 hours later, hemopoietic clusters were labelled by LDL. Since no CD45(+) cells were inserted among endothelial cells at the time of vascular labelling, hemopoietic clusters must be concluded to derive from precursors with an endothelial phenotype.
10
Faivre-Fiorina, Béatrice, Alexis Caron, Céline Fassot, Isabelle Fries, Patrick Menu, Pierre Labrude, and Claude Vigneron. "Presence of hemoglobin inside aortic endothelial cells after cell-free hemoglobin administration in guinea pigs." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 2 (February 1, 1999): H766—H770. http://dx.doi.org/10.1152/ajpheart.1999.276.2.h766.
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The endothelium is the production site of several potent vasoactive factors that contribute to the modulation of the vascular tone. Because hemoglobin-based oxygen carriers (HBOC) have been demonstrated to cause vasoconstriction and thereby increase arterial pressure by interacting with endothelium-derived factors such as nitric oxide and endothelin-1, we hypothesized that hemoglobin could penetrate into the endothelial cells. Therefore, we investigated the presence of hemoglobin into guinea pig aortic endothelial cells by immunohistochemical staining after exchange transfusion with a hemoglobin-based oxygen carrier. Despite the large molecular size of HBOC due to chemical modifications designed to prevent hemoglobin subunit dissociation and extravascular leakage, hemoglobin was detectable by immunohistochemical staining into the endothelial cells. These findings suggest that the vascular endothelial cells could uptake hemoglobin by endocytosis mechanisms or could help hemoglobin to cross the endothelial barrier toward media by transcytosis mechanisms. These findings are very important to lead future investigations to the mechanisms by which HBOC cause vasoconstriction.
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Hendrickx, Jan, Kris Doggen, Ellen O. Weinberg, Pascale Van Tongelen, Paul Fransen, and Gilles W. De Keulenaer. "Molecular diversity of cardiac endothelial cells in vitro and in vivo." Physiological Genomics 19, no. 2 (October 4, 2004): 198–206. http://dx.doi.org/10.1152/physiolgenomics.00143.2004.
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In addition to a number of common features, cardiovascular endothelium displays structural, functional, and genetic differences according to its position in the cardiovascular tree. In the heart, endocardial and cardiac microvascular endothelia (CMVE) interact directly with surrounding cardiomyocytes, whereas the endothelium within blood vessels interacts with smooth muscle cells. In this study, we investigated whether cardiac endothelial cells were distinct from aortic endothelial (AE) cells at the transcriptional level. Using Affymetrix microarray technology and subsequent real-time PCR analyses for validation, we identified sets of genes with marked preferential expression in cultured endocardial endothelium (EE) compared with cultured AE and vice versa. Among the genes preferentially expressed in EE, some were also expressed in cultured CMVE. Immunohistochemical staining of cardiac and aortic tissue revealed that the endothelial genetic diversity observed in culture reflects, in part, a physiological diversity existing in vivo. The identification of a set of genes preferentially expressed in EE provides new insights in the functional adaptations of this endothelial subtype to its intracavitary localization and to its role in the control of ventricular performance.
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Inoue, Hajime, Nagaoki Wakisaka, Nobuhiro Tane, Kazumasa Ando, Emiko Isono, Miwa Yamanaka, Masaki Aihara, and Hirotomo Ishida. "Endothelin-1 Production by Normal Human Cultured Keratinocytes and its Regulation." Mediators of Inflammation 3, no. 6 (1994): 433–37. http://dx.doi.org/10.1155/s096293519400061x.
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The possibility that cultured keratinocytes produce endothelins were investigated. The results showed that cultured keratinocytes derived from normal human skin produce endothelin-1. Moreover, keratinocyte endothelin-1 production was completely inhibited by the presence of actinomycin D in the medium. As in the case of endothelial cells, recombinant interleukin-1β was capable of promoting endothelin-1 production in keratinocytes, whereas herapin inhibited it. Thrombin also inhibited endothelin-1 production. These results indicate that the mechanism of endothelin-1 production in keratinocytes is slightly different from the mechanism in vascular endothelial cells.
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Stewart, D. J., D. Langleben, P. Cernacek, and K. Cianflone. "Endothelin release is inhibited by coculture of endothelial cells with cells of vascular media." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 6 (December 1, 1990): H1928—H1932. http://dx.doi.org/10.1152/ajpheart.1990.259.6.h1928.
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Endothelin is a potent vasoconstrictor peptide and a smooth muscle mitogen produced in large amounts by endothelial cells in culture. To determine whether other cellular elements of the vessel wall modify the release or clearance of endothelin, we studied the effect of coculture of endothelial cells with vascular smooth muscle cells or fibroblasts on endothelin release. Endothelial cells were grown to confluence on microcarrier beads and transferred to dishes containing confluent cultures of smooth muscle cells or fibroblasts or control media only. In parallel experiments, endothelial cells on microcarrier beads were incubated in media conditioned by 48-h exposure to smooth muscle cells or fibroblasts. Endothelin concentration was determined by radioimmunoassay (rabbit anti-endothelin-1 serum). Endothelial cells alone released large amounts of endothelin: 169 +/- 60 and 982 +/- 237 pg/10(6) endothelial cells at 4 and 24 h, respectively. Endothelin accumulation was markedly reduced in coculture with smooth muscle cells or fibroblasts by 81 +/- 10 and 49 +/- 5% (P less than 0.05), respectively, at 24 h. This difference could not be explained by smooth muscle cell binding or degradation of endothelin. Furthermore, smooth muscle cell- or fibroblast-conditioned media significantly reduced endothelin release, and twofold concentration of smooth muscle cell-conditioned media fully reproduced the inhibition of endothelin release found in coculture, confirming the presence of a transferable inhibitor. Therefore, we propose that endothelin secretion from endothelial cells may be regulated by an inhibitory factor produced by the vascular media. This mechanism might limit the production of endothelin in intact vessels and thereby protect against excessive vasoconstriction or proliferation of vascular target cells.
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Mariassy, A. T., M. K. Glassberg, M. Salathe, F. Maguire, and A. Wanner. "Endothelial and epithelial sources of endothelin-1 in sheep bronchi." American Journal of Physiology-Lung Cellular and Molecular Physiology 270, no. 1 (January 1, 1996): L54—L61. http://dx.doi.org/10.1152/ajplung.1996.270.1.l54.
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Airway smooth muscle tone and growth is regulated by endothelin-1 (ET-1), but the sources of ET-1 in the airway wall have not been clearly defined. We therefore wished to estimate the relative contributions of the epithelium and endothelium to ET-1 production in the bronchi (mean ID 1.7-4.9 mm) of mature normal sheep. Morphometric assessment of bronchial cross-sections revealed a number of epithelial cells three times greater than endothelial cells by direct cell count. In contrast, the overall cell surface density was five to six times greater, and the airway smooth muscle-centered cell surface density was three to four times greater for endothelial cells than for epithelial cells. The expression of preproendothelin-1 mRNA was detected in cultured aortic endothelial cells (as a substitute for bronchial endothelial cells) but not in cultured bronchial epithelial cells, and the former secreted seven times more immunoreactive ET-1 than the latter. These findings show that topographically the endothelium is better positioned for the regulation of ovine bronchial smooth muscle than the epithelium. Furthermore, the findings suggest greater constitutive ET-1 secretion by cultured endothelium than by epithelium.
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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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Wilkes, B. M., M. Susin, and P. F. Mento. "Localization of endothelin-1-like immunoreactivity in human placenta." Journal of Histochemistry & Cytochemistry 41, no. 4 (April 1993): 535–41. http://dx.doi.org/10.1177/41.4.8450193.
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We examined the distribution of endothelin-1-like immunoreactivity in human placenta, using the immunoperoxidase technique. A specific polyclonal antibody to endothelin-1 was raised in rabbits, which recognized endothelin-1 and its precursor molecule, big endothelin. Immunoperoxidase staining revealed that endothelin-1-like immunoreactivity was widely distributed in the placenta. Endothelin-1-like immunoreactivity was present in endothelial cells of capillaries of the microvilli and in small- and medium-sized arteries and veins. The distribution of endothelin-1-like immunoreactivity was similar to the distribution of Factor VIII-related antigen, which stains endothelial cells. The nature of endothelin in the human placenta was further examined with cultured umbilical vein endothelial cells. Endothelial cells released endothelin-like material into the culture medium. The amount of endothelin-like material varied directly with time of incubation and the amount of fetal calf serum in the culture medium. Fractionation of the endothelin-1-like material by reversed-phase high-performance liquid chromatography (HPLC) and quantitation by radioimmunoassay (RIA) revealed that endothelin-like immunoreactivity co-eluted with endothelin-1 but not with big endothelin-1. We conclude that endothelin-1-like immunoreactivity is widely distributed in vascular endothelium of the human placenta. These data are compatible with a role for endothelin as an autocrine or paracrine modulator of vascular tone in the human placenta.
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Uchida, K., and B. J. Ballermann. "Sustained activation of PGE2 synthesis in mesangial cells cocultured with glomerular endothelial cells." American Journal of Physiology-Cell Physiology 263, no. 1 (July 1, 1992): C200—C209. http://dx.doi.org/10.1152/ajpcell.1992.263.1.c200.
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Glomerular endothelial cells synthesize and release endothelin-1 (ET-1), and mesangial cells, normally closely apposed to endothelial cells in vivo, respond to ET-1 with contraction, proliferation, and prostaglandin E2 (PGE2) release. This study sought to determine whether chronic coculture of mesangial cells with glomerular endothelial cells alters mesangial cell PGE2 synthesis. Mesangial cells cocultured with endothelial cells were found to release PGE2 at rates much greater than those observed in mesangial cells not cocultured with endothelial cells. This effect persisted for at least 24 h after the mesangial cells were removed from coculture with endothelial cells. The increase in basal mesangial cell PGE2 synthesis was dependent on endothelial cell-derived ET-1. Despite the increase in basal PGE2 synthesis after coculture with endothelial cells, acute ET-1-stimulated PGE2 release was markedly blunted in mesangial cells that had been cocultured with endothelial cells when compared with mesangial cells in solo-culture. This lack of responsiveness was specific for ET-1 and resulted from a profound downregulation of mesangial cell endothelin receptors. Thus coculture with endothelial cells produces two apparently opposing and ET-1-dependent effects in mesangial cells, namely a sustained increase in basal PGE2 synthesis by the cells and a loss of responsiveness to further stimulation with ET-1. It is postulated that the induction of sustained PGE2 synthesis may also occur in vivo if endothelin release from endothelial cells is stimulated and may explain, in part, the extraordinary sensitivity of some patients with glomerular disease to cyclooxygenase inhibitors.
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Kasuya, Hidetoshi, Bryce K. A. Weir, David M. White, and Kari Stefansson. "Mechanism of oxyhemoglobin-induced release of endothelin-1 from cultured vascular endothelial cells and smooth-muscle cells." Journal of Neurosurgery 79, no. 6 (December 1993): 892–98. http://dx.doi.org/10.3171/jns.1993.79.6.0892.
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✓ Release of endothelin-1 from cultured endothelial cells can be induced with oxyhemoglobin (oxyHb). The present study was conducted to explore whether oxyHb affects the release of endothelin-1 and the induction of endothelin-1 messenger ribonucleic acid (mRNA) and to examine the mechanism whereby oxyHb induces endothelin-1 production in cultured vascular smooth-muscle cells as well as in cultured endothelial cells. Oxyhemoglobin produces concentration-dependent (0.1 to 10 µM) and time-dependent (0 to 24 hours) increases in immunoreactive endothelin-1 in conditioned medium from bovine arterial endothelial cells. Oxyhemoglobin induces immunoreactive endothelin-1 in rat aortic smooth-muscle cells in the same fashion, although the rate is 30-fold less than that of endothelial cells. This promoting effect is much higher than that of other stimulators such as thrombin and phorbol 12-myristate 13-acetate. Northern blot analysis of total RNA from endothelial cells also showed endothelin-1 mRNA induction. Staurosporine, a protein kinase C (PKC) inhibitor inhibited oxyHb-induced endothelin-1 production in both vascular endothelial and smooth-muscle cells, whereas an increase of intracellular cyclic adenosine monophosphate (cAMP) by forskolin or an addition of 8-bromo-cAMP only inhibited this effect in smooth-muscle cells. These findings suggest that oxyHb-induced endothelin-1 production in endothelial cells is regulated by PKC, and in smooth-muscle cells by both PKC and the cAMP-dependent pathway. The production of endothelin, the most potent vasoconstrictor, in both vascular endothelial and smooth-muscle cells by oxyHb may have significance in the pathogenesis of cerebral vasospasm.
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Lew, R. A., and A. J. Baertschi. "Endothelium-dependent ANF secretion in vitro." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 4 (October 1, 1992): H1071—H1077. http://dx.doi.org/10.1152/ajpheart.1992.263.4.h1071.
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Coculture of endothelial cells with atrial cells (R. A. Lew and A. J. Baertschi. Biochem. Biophys. Res. Commun. 163: 701-709, 1989) increased atrial natriuretic factor (ANF) release to 205 +/- 15% (n = 33 experiments) of basal secretion (2.02 +/- 0.33 ng/ml). Stimulation of ANF release by endothelial cells was significantly reduced (P < 0.05) by addition of the calcium channel antagonist nicardipine (Nic, 100 nM; by 69 +/- 4%), the guanylate cyclase activator sodium nitroprusside (SNP, 1 microM; by 97 +/- 27%), or acetylcholine (ACh, 10 microM; by 55 +/- 13%). Endothelial cell-conditioned medium elicited a 62 +/- 10% (n = 10) increase in ANF release. Rat and porcine endothelin (0.1-100 nM) each elicited a dose-dependent increase in ANF release [up to 84 +/- 14% (n = 18) over baseline]. The activity of conditioned medium was not affected by heat or trypsin treatment, but was significantly reduced by addition of Nic or SNP and was attenuated by ACh. Stimulation of ANF by 1 nM synthetic rat or porcine endothelin was also unaffected by heat or trypsin but was significantly reduced by Nic, SNP, and ACh. Addition of endothelin-specific antiserum abolished the ANF stimulatory activity of endothelial cell-conditioned medium. Neither inhibition of superoxide anion by superoxide dismutase nor inhibition of endothelium-derived nitric oxide production by NG-monomethyl-L-arginine affected the ANF release from coculture. Thus endothelial cells release a heat-stable, diffusible ANF stimulatory factor, which is not endothelium-derived relaxing factor or superoxide anion but is biologically and immunologically similar to endothelin.
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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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Flowers, M. A., Y. Wang, R. J. Stewart, B. Patel, and P. A. Marsden. "Reciprocal regulation of endothelin-1 and endothelial constitutive NOS in proliferating endothelial cells." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 6 (December 1, 1995): H1988—H1997. http://dx.doi.org/10.1152/ajpheart.1995.269.6.h1988.
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The expression of endothelin-1 (ET-1) and endothelial constitutive nitric oxide synthase (ecNOS) was assessed in two independent in vitro models: asynchronously differentially proliferating cultures and wounded endothelial cell monolayers. Northern blot analysis of RNA isolated from preconfluent, confluent, and postconfluent cells revealed a fourfold rise in ET-1 mRNA transcripts, whereas levels of ecNOS mRNA transcripts were reduced twofold in proliferating cells. Nuclear run-off analysis demonstrated that increased steady-state ET-1 mRNA content in proliferating cells was mediated, in part, by increased gene transcription. In contrast, ecNOS transcription rates in proliferating cells were not decreased compared with quiescent nonproliferating cells, indicating that mRNA destabilization mediated the decreased ecNOS mRNA levels in proliferating endothelium. Concordant changes in protein expression were documented for both ET-1 and ecNOS. In injured endothelial cell monolayers, in situ cRNA hybridization demonstrated increased mRNA transcript levels for ET-1 in growth fronts of injured endothelial monolayers. These data are taken to indicate that expression of ET-1 and ecNOS is reciprocally regulated in two different models of endothelial cell proliferation.
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Ghoneim, Shams, Zsuzsa Fabry, Judy Keiner, and Michael Hart. "Behavior and Cell-to-Cell Interaction of Cultured Endothelia and Smooth Muscle Cells Seeded on Nucleopore Filter." Proceedings, annual meeting, Electron Microscopy Society of America 48, no. 3 (August 12, 1990): 160–61. http://dx.doi.org/10.1017/s0424820100158340.
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Vascular endothelia and smooth muscle cultures, derived from small vessels may retain some of their in vivo characteristics. It has been demonstrated by other investigators that there exists in-vivo a close relationship between endothelia cells and smooth muscle cells of most vascular beds. The myo-endothelial junction has functional implications which could explain a humoral transmition of substances between the two cell population. Rhodin demonstrated that arteriolar endothelium exhibited foot-like processes which penetrated the endothelial basement membrane and extended into smooth muscle cells of the media(1). Fawcett, believed that a pathway exists between endothelia and smooth muscle cells for the exchange of metabolites (2).The objective of this in-vitro study was to examine the possible relationship between smooth muscle and endothelia cells in culture. Nucleopore filters with both 0.4μ and 3.0μ pores were used. They were seeded for 6 days with mouse brain endothelia cells on the top side of the filter and for 7 days with smooth muscle cells on the bottom side.
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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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Garner, Omai B., Hector Aguilar, Jennifer Fulcher, Ernest Levroney, Benhur Lee, and Linda Baum. "A novel mechanism for Galectin-1 inhibition of endothelial cell fusion in Nipah virus infection; a critical component of vascular mediated innate immunity and host defense (128.3)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 128.3. http://dx.doi.org/10.4049/jimmunol.182.supp.128.3.
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Abstract The vascular endothelium plays a critical role in the pathogenesis of many viral infections, either via direct infection of endothelial cells, or via damage to endothelia by the immune system. Nipah virus (NiV) is an emerging viral pathogen, of the genus Paramyxoviridae, but little is known about NiV biology or the immune response to NiV. The virus targets endothelial cells, with endothelial syncytia formation being the pathogenic hallmark of infection. Endothelial cell fusion requires expression of NiV-F and NiV-G envelope glycoproteins, and specific N-glycans on NiV-F regulate the extent of endothelial cell fusion. We have found that galectin-1, an endogenous lectin expressed by activated endothelia, inhibits NiV mediated endothelial cell fusion and syncytia formation by a direct effect on NiV-F. Specifically, galectin-1 regulates endothelial cell fusion triggered by NiV-F by binding glycans on NiV-F and thus retaining immature NiV-F on the cell surface, restricting endocytosis necessary for NiV-F maturation, and inhibiting the mature NiV-F protein from fusing endothelial cell membranes. This suggests that endogenous galectin-1 may regulate the extent of endothelial cell damage in Nipah virus infection. These findings may be broadly applicable to other vascular diseases in which endothelial damage and syncytia formation occur.
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Jacques, Danielle, Sawsan Sader, Claudine Perreault, Dima Abdel-Samad, and Chantale Provost. "Roles of nuclear NPY and NPY receptors in the regulation of the endocardial endothelium and heart functionThis paper is one of a selection of papers published in this Special issue, entitled Second Messengers and Phosphoproteins—12th International Conference." Canadian Journal of Physiology and Pharmacology 84, no. 7 (July 2006): 695–705. http://dx.doi.org/10.1139/y05-162.
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It is now well accepted that the heart is a multifunctional organ in which endothelial cells, and more particularly endocardial endothelial cells (EECs), seem to play an important role in regulating and maintaining cardiac excitation–contraction coupling. Even if major differences exist between vascular endothelial cells (VECs) and EECs, all endothelial cells including EECs release a variety of auto- and paracrine factors such as nitric oxide, endothelin-1, angiotensin II, and neuropeptide Y. All these factors were reported to affect cardiomyocyte contractile performance and rhythmicity. In this review, findings on the morphology of EECs, differences between EECs and other types of endothelial cells, interactions between EECs and the adjacent cardiomyocytes, and effects of NPY on the heart will be presented. We will also show evidence on the presence and localization of NPY and the Y1 receptor in the endocardial endothelium and discuss their role in the regulation of cytosolic and nuclear free calcium.
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Mathiesen, Allison, Tyree Hamilton, Nigeste Carter, Michael Brown, William McPheat, and Anca Dobrian. "Endothelial Extracellular Vesicles: From Keepers of Health to Messengers of Disease." International Journal of Molecular Sciences 22, no. 9 (April 28, 2021): 4640. http://dx.doi.org/10.3390/ijms22094640.
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Endothelium has a rich vesicular network that allows the exchange of macromolecules between blood and parenchymal cells. This feature of endothelial cells, along with their polarized secretory machinery, makes them the second major contributor, after platelets, to the particulate secretome in circulation. Extracellular vesicles (EVs) produced by the endothelial cells mirror the remarkable molecular heterogeneity of their parent cells. Cargo molecules carried by EVs were shown to contribute to the physiological functions of endothelium and may support the plasticity and adaptation of endothelial cells in a paracrine manner. Endothelium-derived vesicles can also contribute to the pathogenesis of cardiovascular disease or can serve as prognostic or diagnostic biomarkers. Finally, endothelium-derived EVs can be used as therapeutic tools to target endothelium for drug delivery or target stromal cells via the endothelial cells. In this review we revisit the recent evidence on the heterogeneity and plasticity of endothelial cells and their EVs. We discuss the role of endothelial EVs in the maintenance of vascular homeostasis along with their contributions to endothelial adaptation and dysfunction. Finally, we evaluate the potential of endothelial EVs as disease biomarkers and their leverage as therapeutic tools.
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Brutsaert, Dirk L. "Cardiac Endothelial-Myocardial Signaling: Its Role in Cardiac Growth, Contractile Performance, and Rhythmicity." Physiological Reviews 83, no. 1 (January 1, 2003): 59–115. http://dx.doi.org/10.1152/physrev.00017.2002.
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Experimental work during the past 15 years has demonstrated that endothelial cells in the heart play an obligatory role in regulating and maintaining cardiac function, in particular, at the endocardium and in the myocardial capillaries where endothelial cells directly interact with adjacent cardiomyocytes. The emerging field of targeted gene manipulation has led to the contention that cardiac endothelial-cardiomyocytal interaction is a prerequisite for normal cardiac development and growth. Some of the molecular mechanisms and cellular signals governing this interaction, such as neuregulin, vascular endothelial growth factor, and angiopoietin, continue to maintain phenotype and survival of cardiomyocytes in the adult heart. Cardiac endothelial cells, like vascular endothelial cells, also express and release a variety of auto- and paracrine agents, such as nitric oxide, endothelin, prostaglandin I2, and angiotensin II, which directly influence cardiac metabolism, growth, contractile performance, and rhythmicity of the adult heart. The synthesis, secretion, and, most importantly, the activities of these endothelium-derived substances in the heart are closely linked, interrelated, and interactive. It may therefore be simplistic to try and define their properties independently from one another. Moreover, in relation specifically to the endocardial endothelium, an active transendothelial physicochemical gradient for various ions, or blood-heart barrier, has been demonstrated. Linkage of this blood-heart barrier to the various other endothelium-mediated signaling pathways or to the putative vascular endothelium-derived hyperpolarizing factors remains to be determined. At the early stages of cardiac failure, all major cardiovascular risk factors may cause cardiac endothelial activation as an adaptive response often followed by cardiac endothelial dysfunction. Because of the interdependency of all endothelial signaling pathways, activation or disturbance of any will necessarily affect the others leading to a disturbance of their normal balance, leading to further progression of cardiac failure.
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Göthert, Joachim R., Sonja E. Gustin, J. Anke M. van Eekelen, Uli Schmidt, Mark A. Hall, Stephen M. Jane, Anthony R. Green, Berthold Göttgens, David J. Izon, and C. Glenn Begley. "Genetically tagging endothelial cells in vivo: bone marrow-derived cells do not contribute to tumor endothelium." Blood 104, no. 6 (September 15, 2004): 1769–77. http://dx.doi.org/10.1182/blood-2003-11-3952.
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Abstract Tumor growth is dependent in part on “neoangiogenesis.” Functional involvement of bone marrow (BM)-derived cells in this process has been demonstrated. However, it remains controversial as to whether tumor endothelium itself is BM derived. Here we sought to address this issue with an endothelial-specific, inducible transgenic model. We generated Cretransgenic mice (endothelial-SCL-Cre-ERT) using the tamoxifen-inducible Cre-ERT recombinase driven by the 5′ endothelial enhancer of the stem cell leukemia (SCL) locus. These mice were intercrossed with Cre reporter strains in which β-galactosidase (LacZ) or enhanced yellow fluorescent protein (EYFP) are expressed upon Cre-mediated recombination. After tamoxifen administration, endothelial LacZ staining was observed in embryonic and adult tissues. Cre-mediated recombination was also observed in newly generated tumor endothelium. In adult BM cells we could only detect trace amounts of recombination by flow cytometry. Subsequently, BM from endothelial-SCL-Cre-ERT;R26R mice was transplanted into irradiated recipients. When tumors were grown in recipient mice, which received tamoxifen, no tumor LacZ staining was detected. However, when tumors were grown in endothelial-SCL-Cre-ERT;R26R mice 3 weeks after the cessation of tamoxifen treatment, there was widespread endothelial LacZ staining present. Thus, this genetic model strongly suggests that BM cells do not contribute to tumor endothelium and demonstrates the lineage relation between pre-existing endothelium and newly generated tumor endothelial cells. (Blood. 2004;104:1769-1777)
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Segal, Mark S., Azra Bihorac, and Mehmet Koç. "Circulating endothelial cells: tea leaves for renal disease." American Journal of Physiology-Renal Physiology 283, no. 1 (July 1, 2002): F11—F19. http://dx.doi.org/10.1152/ajprenal.00008.2002.
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Fully differentiated endothelial cells and their precursors circulate in the bloodstream. Since their initial description more than 30 years ago, circulating endothelial cells have been quantified in a number of different clinical conditions that affect the endothelium. Only recently, however, have investigators begun to examine the protein expression and functionality of these cells. Because a number of diseases prevalent in the field of nephrology affect endothelial cells, the study of circulating endothelial cells may allow the direct examination of the state of the endothelium in these conditions. This review will discuss the endothelium and renal disease, the methods to quantify these circulating endothelial cells, their origins, and their therapeutic potential.
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Williams, Stuart K. "Endothelial Cell Transplantation." Cell Transplantation 4, no. 4 (July 1995): 401–10. http://dx.doi.org/10.1177/096368979500400411.
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Endothelial cells line the lumenal surface of al) elements of the vascular system. These cells exhibit numerous metabolic functions necessary for the maintenance of homeostasis. The critical role of endothelium in maintaining normal blood vessel function is exemplified by the poor clinical performance of small diameter polymeric vascular grafts which fail due, in part, to the lack of a functional endothelium on the lumenal surface. Extensive research has explored the potentiality of transplanting endothelial cells onto polymeric vascular grafts to improve graft function. Several critical issues have been explored including the source of endothelial cells for transplantation, the interaction of endothelium with polymers and the healing process of endothelial cell transplanted grafts. The future of endothelial cell transplantation will also include the use of these cells as vehicles for genetic engineering.
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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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Lansdell, Theresa A., Laura C. Chambers, and Anne M. Dorrance. "Endothelial Cells and the Cerebral Circulation." Comprehensive Physiology 12, no. 3 (June 29, 2022): 3449–508. https://doi.org/10.1002/j.2040-4603.2022.tb00220.x.
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AbstractEndothelial cells form the innermost layer of all blood vessels and are the only vascular component that remains throughout all vascular segments. The cerebral vasculature has several unique properties not found in the peripheral circulation; this requires that the cerebral endothelium be considered as a unique entity. Cerebral endothelial cells perform several functions vital for brain health. The cerebral vasculature is responsible for protecting the brain from external threats carried in the blood. The endothelial cells are central to this requirement as they form the basis of the blood‐brain barrier. The endothelium also regulates fibrinolysis, thrombosis, platelet activation, vascular permeability, metabolism, catabolism, inflammation, and white cell trafficking. Endothelial cells regulate the changes in vascular structure caused by angiogenesis and artery remodeling. Further, the endothelium contributes to vascular tone, allowing proper perfusion of the brain which has high energy demands and no energy stores. In this article, we discuss the basic anatomy and physiology of the cerebral endothelium. Where appropriate, we discuss the detrimental effects of high blood pressure on the cerebral endothelium and the contribution of cerebrovascular disease endothelial dysfunction and dementia. © 2022 American Physiological Society. Compr Physiol 12:3449‐3508, 2022.
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Kirsch, Torsten, Alexander Woywodt, Michaela Beese, Kristin Wyss, Joon-Keun Park, Uta Erdbruegger, Barbara Hertel, Hermann Haller, and Marion Haubitz. "Engulfment of apoptotic cells by microvascular endothelial cells induces proinflammatory responses." Blood 109, no. 7 (November 21, 2006): 2854–62. http://dx.doi.org/10.1182/blood-2006-06-026187.
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AbstractCirculating endothelial cells (CECs) have been detected in a variety of vascular disorders, but their interactions with healthy endothelium remain unknown. The aim of this study was to evaluate the response of human endothelial cells (ECs) to apoptotic or necrotic ECs in an in vitro model and to delineate pathogenetic pathways. Here we show that incubation of the human microvascular endothelial cell line (HMEC-1) with apoptotic ECs resulted in increased expression of chemokines and enhanced binding of leukocytes to HMEC-1 cells, whereas exposure of HMEC-1 cells to necrotic ECs caused no changes in leukocyte-binding affinity. Both apoptotic and necrotic cells were bound and engulfed by HMEC-1 cells and primary human umbilical vein endothelial cells (HUVECs). We therefore suggest that exposures to apoptotic and necrotic ECs induce different patterns of chemokine synthesis and leukocyte adhesion in healthy ECs. These data indicate that CECs are not only markers of vascular damage but may induce proinflammatory signals in the endothelium.
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Onitsuka, Izumi, Masaki Takeuchi, Tomoya Okabe, Yoshiko Kamiya, Ayami Hirata, Ichiro Yahara, and Atsushi Miyajima. "Two Distinct Precursors of Hematopoietic Stem Cells and Endothelial Progenitors Characterized by the PCLP1 Expression." Blood 106, no. 11 (November 16, 2005): 2274. http://dx.doi.org/10.1182/blood.v106.11.2274.2274.
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Abstract Blood cells and endothelia are believed to arise from their common progenitor hemangioblast. However, it still remains unknown how these lineages develop. Here we report the existence of two distinct precursors for hematopoietic stem cells (HSCs) and endothelial progenitors in murine fetal liver (FL). Podocalyxin-like protein 1 (PCLP1) is a member of the sialomucin family and was shown to be expressed in hemangioblasts in the aorta-gonad-mesonephros region in murine embryo. To further analyze the fates of hematopoietic/endothelial cells, we focused on embryonic day 14.5 (E14.5) FL, since it is a major hematopoietic organ during embryonic period. Based on the PCLP1 expression levels, E14.5 FL cells could be fractionated into four distinct populations. In vitro colony-forming assay and in vivo transplantation analysis revealed that lineage-committed progenitors with colony-forming activities and long-term repopulating hematopoietic stem cells (LTR-HSCs) were in PCLP1neg cells. PCLP1dull cells contained erythroid lineage-committed cells. Interestingly, while PCLP1med cells lacked colony-forming activities, they showed LTR-HSC activity in vivo. To further characterize these cell populations, we cultured them with OP9 stromal cells, since OP9 cells have been used to induce hematopoietic and endothelial lineages from embryonic stem cells. In co-culture with OP9 cells, PCLP1neg cells immediately generated blood cells with colony-forming activity but lacking in vivo hematopoietic activity, indicating that OP9 cells failed to support hematopoietic progenitor/HSCs. However, PCLP1med generated colony-forming hematopoietic progenitors with LTR-HSC activities in the presence of OP9 cells. These results indicated that PCLP1med cells contained stromal cell-dependent immature precursors for HSCs. PCLP1high cells did not express the hematopoietic markers or endothelial cell markers such as PECAM1 and VE-cadherin. However, they formed endothelia-like cell colonies which were highly proliferative and serially transferable in OP9 co-culture. Interestingly, the addition of vascular endothelial growth factor (VEGF) to the culture strongly induced the expression of PECAM1 and VE-cadherin in these colonies. PCLP1high cells contributed to PECAM1+ endothelium in several organs in vivo when transplanted to conditioned neonatal liver. Therefore, PCLP1high cells contained immature precursors for endothelial progenitors. These results indicate that PCLP1 expression levels distinguish previously unrecognized early precursors for HSCs and endothelial progenitors, which are distinct from hemangioblasts.
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Marsden, P. A., M. S. Goligorsky, and B. M. Brenner. "Endothelial cell biology in relation to current concepts of vessel wall structure and function." Journal of the American Society of Nephrology 1, no. 7 (January 1991): 931–48. http://dx.doi.org/10.1681/asn.v17931.
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Vascular endothelium is now appreciated to modulate vessel wall structure and function in health and disease. Strategically located between the intravascular space and vessel wall proper, the endothelium has a broad capacity to modify the functional state of adjacent or trafficking cells. Furthermore, recent findings indicate that the endothelium is an interactive tissue capable of responding to numerous mechanical, chemical, and cellular stimuli. The focus of this review will be a discussion of endothelial cell biology in relation to vascular structure and function, with particular emphasis on endothelial modulation of vasomotor tone. It is evident that endothelial cells contribute to the local control of vascular tone by releasing potent vasodilatory mediators, such as endothelium-derived relaxing factor, and vasoconstrictor mediators such as endothelin-1. The endothelium also serves to modify blood-borne signals to which vascular tissues respond. The kidney shares, directly and indirectly, in these events, making this emerging new area a focus of major interest for nephrologists.
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Nogueras, Sonia, Ana Merino, Raquel Ojeda, Julia Carracedo, Mariano Rodriguez, Alejandro Martin-Malo, Rafael Ramírez, and Pedro Aljama. "Coupling of endothelial injury and repair: an analysis using an in vivo experimental model." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 2 (February 2008): H708—H713. http://dx.doi.org/10.1152/ajpheart.00466.2007.
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The repair of the endothelium after inflammatory injury is essential to maintaining homeostasis. The link between inflammation-induced endothelial damage and repair has not been fully characterized in vivo. We have developed a rat model to evaluate the coupling of lipopolysaccharide (LPS)-induced endothelial injury and repair. Aortic endothelium injury was analyzed by both inmunohistochemistry and flow cytometry to quantify the number of endothelial cells and the percentage of apoptotic endothelial cells. We have also identified the percentage of circulating angiogenic cells capable of repairing the damaged endothelium. Erythropoietin was administered to inhibit LPS-induced endothelial apoptosis. Loss of the normal endothelial structure was observed in the aorta of the animals treated with LPS. Eight hours after LPS administration, the number of endothelial cells decreased by 40%, returning to normal after 24 h. There was a threefold increase in the percentage of circulating angiogenic cells, which did not return to normal levels until 48 h after LPS administration. Circulating angiogenic cell levels did not change when LPS-induced endothelial damage was prevented by erythropoietin. The endothelial injury caused by inflammation activates the mobilization of circulating angiogenic cells, thus completing endothelial repair. Inflammation without endothelial injury does not trigger the mobilization of circulating angiogenic cells.
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Brandt, R. R., D. M. Heublein, M. T. Mattingly, M. R. Pittelkow, and J. C. Burnett. "Presence and secretion of atrial natriuretic peptide from cultured human aortic endothelial cells." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 2 (February 1, 1995): H921—H925. http://dx.doi.org/10.1152/ajpheart.1995.268.2.h921.
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The endothelium is the production site of several potent vasoactive substances that modulate vascular tone and growth. The present study was undertaken to investigate the presence and secretion of atrial natriuretic peptide (ANP) immunoreactivity from vascular endothelial cells. ANP immunoreactivity was present in cultured human aortic endothelial cells by both immunohistochemical staining and radioimmunoassay. ANP immunoreactivity was also detectable in culture medium from human aortic endothelial cells in low picogram concentrations. These findings suggest that vascular endothelium is a site of ANP production and secretion of ANP. There was a differential distribution of ANP and endothelin-1 (ET-1), with a higher ANP concentration in cell extracts and a higher ET-1 concentration in cell culture media. Although ANP has been conceived as a circulating endocrine hormone, these findings are consistent with ANP functioning also as an autocrine and paracrine modulator in the regulation of vascular tone and growth.
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Ochoa, Cristhiaan D., Troy Stevens, and Ron Balczon. "Cold exposure reveals two populations of microtubules in pulmonary endothelia." American Journal of Physiology-Lung Cellular and Molecular Physiology 300, no. 1 (January 2011): L132—L138. http://dx.doi.org/10.1152/ajplung.00185.2010.
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Microtubules are composed of α-tubulin and β-tubulin dimers. Microtubules yield tubulin dimers when exposed to cold, which reassemble spontaneously to form microtubule fibers at 37°C. However, mammalian neurons, glial cells, and fibroblasts have cold-stable microtubules. While studying the microtubule toxicity mechanisms of the exotoxin Y from Pseudomonas aeruginosa in pulmonary microvascular endothelial cells, we observed that some endothelial microtubules were very difficult to disassemble in the cold. As a consequence, we designed studies to test the hypothesis that microvascular endothelium has a population of cold-stable microtubules. Pulmonary microvascular endothelial cells and HeLa cells (control) were grown under regular cell culture conditions, followed by exposure to an ice-cold water bath and a microtubule extraction protocol. Polymerized microtubules were detected by immunofluorescence confocal microscopy and Western blot analyses. After cold exposure, immunofluorescence revealed that the majority of HeLa cell microtubules disassembled, whereas a smaller population of endothelial cell microtubules disassembled. Immunoblot analyses showed that microvascular endothelial cells express the microtubule cold-stabilizing protein N-STOP (neuronal stable tubule-only polypeptides), and that N-STOP binds to endothelial microtubules after cold exposure, but not if microtubules are disassembled with nocodazole before cold exposure. Hence, pulmonary endothelia have a population of cold-stable microtubules.
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Six, Isabelle, Nicolas Guillaume, Valentine Jacob, Romuald Mentaverri, Said Kamel, Agnès Boullier, and Michel Slama. "The Endothelium and COVID-19: An Increasingly Clear Link Brief Title: Endotheliopathy in COVID-19." International Journal of Molecular Sciences 23, no. 11 (May 31, 2022): 6196. http://dx.doi.org/10.3390/ijms23116196.
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The endothelium has a fundamental role in the cardiovascular complications of coronavirus disease 2019 (COVID-19). Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) particularly affects endothelial cells. The virus binds to the angiotensin-converting enzyme 2 (ACE-2) receptor (present on type 2 alveolar cells, bronchial epithelial cells, and endothelial cells), and induces a cytokine storm. The cytokines tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6 have particular effects on endothelial cells—leading to endothelial dysfunction, endothelial cell death, changes in tight junctions, and vascular hyperpermeability. Under normal conditions, apoptotic endothelial cells are removed into the bloodstream. During COVID-19, however, endothelial cells are detached more rapidly, and do not regenerate as effectively as usual. The loss of the endothelium on the luminal surface abolishes all of the vascular responses mediated by the endothelium and nitric oxide production in particular, which results in greater contractility. Moreover, circulating endothelial cells infected with SARS-CoV-2 act as vectors for viral dissemination by forming clusters that migrate into the circulation and reach distant organs. The cell clusters and the endothelial dysfunction might contribute to the various thromboembolic pathologies observed in COVID-19 by inducing the formation of intravascular microthrombi, as well as by triggering disseminated intravascular coagulation. Here, we review the contributions of endotheliopathy and endothelial-cell-derived extracellular vesicles to the pathogenesis of COVID-19, and discuss therapeutic strategies that target the endothelium in patients with COVID-19.
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Kulovic-Sissawo, Azra, Carolina Tocantins, Mariana S. Diniz, Elisa Weiss, Andreas Steiner, Silvija Tokic, Corina T. Madreiter-Sokolowski, Susana P. Pereira, and Ursula Hiden. "Mitochondrial Dysfunction in Endothelial Progenitor Cells: Unraveling Insights from Vascular Endothelial Cells." Biology 13, no. 2 (January 23, 2024): 70. http://dx.doi.org/10.3390/biology13020070.
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Endothelial dysfunction is associated with several lifestyle-related diseases, including cardiovascular and neurodegenerative diseases, and it contributes significantly to the global health burden. Recent research indicates a link between cardiovascular risk factors (CVRFs), excessive production of reactive oxygen species (ROS), mitochondrial impairment, and endothelial dysfunction. Circulating endothelial progenitor cells (EPCs) are recruited into the vessel wall to maintain appropriate endothelial function, repair, and angiogenesis. After attachment, EPCs differentiate into mature endothelial cells (ECs). Like ECs, EPCs are also susceptible to CVRFs, including metabolic dysfunction and chronic inflammation. Therefore, mitochondrial dysfunction of EPCs may have long-term effects on the function of the mature ECs into which EPCs differentiate, particularly in the presence of endothelial damage. However, a link between CVRFs and impaired mitochondrial function in EPCs has hardly been investigated. In this review, we aim to consolidate existing knowledge on the development of mitochondrial and endothelial dysfunction in the vascular endothelium, place it in the context of recent studies investigating the consequences of CVRFs on EPCs, and discuss the role of mitochondrial dysfunction. Thus, we aim to gain a comprehensive understanding of mechanisms involved in EPC deterioration in relation to CVRFs and address potential therapeutic interventions targeting mitochondrial health to promote endothelial function.
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Lee, Dennis K., and Ori Nevo. "Microvascular endothelial cells from preeclamptic women exhibit altered expression of angiogenic and vasopressor factors." American Journal of Physiology-Heart and Circulatory Physiology 310, no. 11 (June 1, 2016): H1834—H1841. http://dx.doi.org/10.1152/ajpheart.00083.2016.
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Preeclampsia (PE) is a severe complication of pregnancy associated with maternal and fetal morbidity and mortality. The underlying pathophysiology involves maternal systemic vascular and endothelial dysfunction associated with circulating antiangiogenic factors, although the specific etiology of the disease remains elusive. Our aim was to investigate the maternal endothelium in PE by exploring the expression of genes involved with endothelial function in a novel platform of maternal primary endothelial cells. Adipose tissue was sampled at the time of caesarean section from both normal and preeclamptic patients. Maternal microvascular endothelial cells were isolated by tissue digestion and CD31 magnetic Dynabeads. Cell purity was confirmed by immunofluorescence microscopy and flow cytometry. Western analyses revealed VEGF activation of VEGF receptor 2 (VEGFR2) and ERK in primary cells. Quantitative PCR analyses revealed significantly altered mRNA levels of various genes involved with angiogenesis and blood pressure control in preeclamptic cells, including soluble fms-like tyrosine kinase-1, endoglin, VEGFR2, angiotensin receptor 1, and endothelin compared with cells isolated from normal pregnancies. Overall, maternal endothelial cells from preeclamptic patients exhibit extensive alteration of expression of factors associated with antiangiogenic and vasoconstrictive phenotypes, shedding light on the underlying mechanisms associated with the vascular dysfunction characteristic of PE.
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Cameron, IT, and AP Davenport. "Endothelins in reproduction." Reproductive Medicine Review 1, no. 1 (March 1992): 99–113. http://dx.doi.org/10.1017/s0962279900000466.
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Endothelin-1 (ET-1) is a 21 amino acid peptide, first isolated in 1988 from porcine aortic endothelial cells in tissue culture (Figure 1). The peptide was shown to be the most potent known vasoconstrictor of porcine coronary arteries. A powerful endothelium-derived vasoconstrictor had been predicted for some time, but it was when Yanagisawa and his colleagues elucidated the structure, and provided information about the molecular biology and mode of action of the peptide that an unprecedented interest was stimulated in the endothelins.
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Franke, Werner W., Lisa M. Domke, Yvette Dörflinger, and Ralf Zimbelmann. "The cell–cell junctions of mammalian testes. III. Absence of an endothelial cell layer covering the peritubular wall of the seminiferous tubules—an immunocytochemical correction of a 50-year-old error in the literature." Cell and Tissue Research 379, no. 1 (November 12, 2019): 75–92. http://dx.doi.org/10.1007/s00441-019-03116-5.
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Abstract In the molecular biological and ultrastructural studies of the peritubular wall cells encasing the seminiferous tubules of mammalian testes, we found it necessary to characterize the outermost cell layer bordering on the interstitial space in detail. For half a century, the extremely thin cells of this monolayer have in the literature been regarded as part of a lymphatic endothelium, in particular in rodents. However, our double-label immunofluorescence microscopical results have shown that in all six mammalian species examined, including three rodent ones (rat, mouse, guinea pig), this classification is not correct: the very attenuated cells of this monolayer are not of lymphatic endothelial nature as they do not contain established endothelial marker molecules. In particular, they do not contain claudin-5-positive tight junctions, VE-cadherin-positive adherens junctions, “lymph vessel endothelium hyaluronan receptor 1” (LYVE-1), podoplanin, protein myozap and “von Willebrand Factor” (vWF). By contrast and as controls, all these established marker molecules for the lymphatic endothelial cell type are found in the endothelia of the lymph and—partly also—blood vessels located nearby in the interstitial space. Thus, our results provide evidence that the monolayer cells covering the peritubular wall do not contain endothelial marker molecules and hence are not endothelial cells. We discuss possible methodological reasons for the maintenance of this incorrect cell type classification in the literature and emphasize the value of molecular analyses using multiple cell type–specific markers, also with respect to physiology and medical sciences.
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Little, Peter J., Christopher D. Askew, Suowen Xu, and Danielle Kamato. "Endothelial Dysfunction and Cardiovascular Disease: History and Analysis of the Clinical Utility of the Relationship." Biomedicines 9, no. 6 (June 20, 2021): 699. http://dx.doi.org/10.3390/biomedicines9060699.
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The endothelium is the single-cell monolayer that lines the entire vasculature. The endothelium has a barrier function to separate blood from organs and tissues but also has an increasingly appreciated role in anti-coagulation, vascular senescence, endocrine secretion, suppression of inflammation and beyond. In modern times, endothelial cells have been identified as the source of major endocrine and vaso-regulatory factors principally the dissolved lipophilic vosodilating gas, nitric oxide and the potent vascular constricting G protein receptor agonists, the peptide endothelin. The role of the endothelium can be conveniently conceptualized. Continued investigations of the mechanism of endothelial dysfunction will lead to novel therapies for cardiovascular disease. In this review, we discuss the impact of endothelial dysfunction on cardiovascular disease and assess the clinical relevance of endothelial dysfunction.
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Isales, Carlos M., Bauer Sumpio, Roni J. Bollag, Qing Zhong, Ke-Hong Ding, Wei Du, Jose Rodriguez-Commes, et al. "Functional parathyroid hormone receptors are present in an umbilical vein endothelial cell line." American Journal of Physiology-Endocrinology and Metabolism 279, no. 3 (September 1, 2000): E654—E662. http://dx.doi.org/10.1152/ajpendo.2000.279.3.e654.
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Acute parathyroid hormone exposure induces vascular smooth muscle relaxation. In contrast, continuous infusion of parathyroid hormone leads to vasoconstriction and an elevation of blood pressure. Despite the known effects of parathyroid hormone on vascular smooth muscle, possible direct effects on the vascular endothelium have not previously been investigated. Using a human umbilical vein endothelial cell line, we found that parathyroid hormone increased both intracellular calcium and cellular cAMP content in these endothelial cells. Furthermore, exposure of these cells to increasing concentrations of parathyroid hormone stimulated both [3H]thymidine incorporation and endothelin-1 secretion. Parathyroid hormone/parathyroid hormone-related peptide receptor mRNA could be detected at low levels in these cells. In summary, these data demonstrate that endothelium-derived cells contain functional parathyroid hormone receptors. The potential physiological role of these receptors remains to be determined.
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Lopez-Ongil, S., M. Saura, D. Rodriguez-Puyol, M. Rodriguez-Puyol, and S. Lamas. "Regulation of endothelial NO synthase expression by cyclosporin A in bovine aortic endothelial cells." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 3 (September 1, 1996): H1072—H1078. http://dx.doi.org/10.1152/ajpheart.1996.271.3.h1072.
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The introduction of cyclosporin A (CsA) is considered a cornerstone advance in immunosuppression. However, serious side effects such as hypertension have fostered an important body of research regarding their pathophysiology. Although the participation of several vasoactive factors in the hypertensive response has been described, recent attention has focused on endothelium-derived vasoactive factors, and several reports describe an overproduction of endothelin-1 and a deficient endothelium-dependent vasodilation. In the case of the latter, no definitive clues for the precise molecular mechanisms have been provided. We demonstrate that endothelial cells in culture synthesize more NO in the presence of CsA for 24 h in a concentration-response manner. This augmentation is correlated with a threefold increase in the endothelial constitutive NO synthase (ecNOS) transcript, which is time dependent and maximal at 24 h. The CsA-induced increase in ecNOS mRNA expression was blocked by actinomycin D but unaltered by cycloheximide. Levels of ecNOS protein were also enhanced by CsA after 24 h. These data establish that NO synthesis is moderately enhanced in endothelial cells exposed to CsA for long periods of time and describe a new mode of regulating ecNOS gene expression.
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Thomas, P. D., F. W. Hampson, and G. W. Hunninghake. "Bacterial adherence to human endothelial cells." Journal of Applied Physiology 65, no. 3 (September 1, 1988): 1372–76. http://dx.doi.org/10.1152/jappl.1988.65.3.1372.
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The adult respiratory distress syndrome (ARDS) is frequently caused by exposure of the lung endothelium to circulating endotoxin (lipopolysaccharide, LPS) and pulmonary infections frequently develop during the course of ARDS. The present studies demonstrate that LPS and interleukin 1 (IL-1, a mediator released by endothelial cells after exposure to LPS) enhance the adherence of Staphylococcus aureus to human umbilical vein endothelial cells. gamma-Interferon, another mediator that induces expression of some cell surface antigens on endothelial cells, had no effect on bacterial adherence. The adherence of bacteria to endothelium was increased by prior opsonization of the bacteria with fresh human serum and was reduced by prior absorption of the serum with bacteria before the use of the serum for opsonization. The capacity of LPS to increase bacterial adherence was time dependent and was maximally expressed after 6 h of exposure; it was blocked by exposure of endothelial cells to LPS in the presence of reduced temperature or dactinomycin (Actinomycin D). These observations suggest that circulating LPS not only can trigger the development of ARDS but also may predispose the lung to the development of pulmonary infections by increasing adherence of bacteria to endothelium.
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Kim, Kyung Wook, and Young Joo Shin. "Interactions of Corneal Endothelial Cells with Stromal Cells during Corneal Endothelial Injury." Journal of the Korean Ophthalmological Society 65, no. 2 (February 15, 2024): 98–107. http://dx.doi.org/10.3341/jkos.2024.65.2.98.
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Purpose: To investigate the interaction of corneal endothelial cells (CECs) with corneal stromal cells (CSCs) on the healing of chemically induced corneal endothelial injury.Methods: Twenty-five rabbits were divided into two groups: rabbits exposed to NaOH and controls. Rabbits were clinically evaluated and sacrificed at 1 day, 1 week, 2 weeks, and 4 weeks after endothelial injury. Corneal endothelial cells and corneal stromal cells were cultured and the wound healing rate of the corneal endothelium and cytokines in the culture medium were analyzed with and without co-culture in the Transwell system.Results: Corneal edema and opacity scores were higher in all rabbits exposed to NaOH than in controls. Corneal endothelial apoptosis with little effect on CSCs was observed in rabbits exposed to NaOH at day 1. Two weeks after injury, CECs migrated from the periphery. CSCs were aligned in parallel to Descemet's membrane, which exhibited the presence of CECs. Transforming factor-β1 and interleukin-6 secretion was lower in the co-culture system than in individual cultures of CECs or CSCs.Conclusions: These results revealed intracameral NaOH injection is a model of corneal endothelial injury with minimal impact on the stroma. Communication between CECs and CSCs during wound healing may lead to the modulation of cytokine production, which is necessary for an enhanced healing process of corneal endothelial injury.
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Brock, Thomas, Elisabeth Boudriot, Anke Klawitter, Marianne Großer, Trang T. P. Nguyen, Sindy Giebe, Erik Klapproth, Achim Temme, Ali El-Armouche, and Georg Breier. "The Influence of VE-Cadherin on Adhesion and Incorporation of Breast Cancer Cells into Vascular Endothelium." International Journal of Molecular Sciences 22, no. 11 (June 3, 2021): 6049. http://dx.doi.org/10.3390/ijms22116049.
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During metastasis, cancer cells that originate from the primary tumor circulate in the bloodstream, extravasate, and form micrometastases at distant locations. Several lines of evidence suggest that specific interactions between cancer cells and endothelial cells, in particular tumor cell adhesion to the endothelium and transendothelial migration, play a crucial role in extravasation. Here we have studied the role of vascular endothelial (VE)-cadherin which is expressed aberrantly by breast cancer cells and might promote such interactions. By comparing different human breast cancer cell lines, we observed that the number of cancer cells that adhered to endothelium correlated with VE-cadherin expression levels. VE-cadherin silencing experiments confirmed that VE-cadherin enhances cancer cell adhesion to endothelial cells. However, in contrast, the number of cancer cells that incorporated into the endothelium was not dependent on VE-cadherin. Thus, it appears that cancer cell adhesion and incorporation are distinct processes that are governed by different molecular mechanisms. When cancer cells incorporated into the endothelial monolayer, they formed VE-cadherin positive contacts with endothelial cells. On the other hand, we also observed tumor cells that had displaced endothelial cells, reflecting either different modes of incorporation, or a temporal sequence where cancer cells first form contact with endothelial cells and then displace them to facilitate transmigration. Taken together, these results show that VE-cadherin promotes the adhesion of breast cancer cells to the endothelium and is involved in the initial phase of incorporation, but not their transmigration. Thus, VE-cadherin might be of relevance for therapeutic strategies aiming at preventing the metastatic spread of breast cancer cells.
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Bochenek, Magdalena L., Christiane Leidinger, Nico S. Rosinus, Rajinikanth Gogiraju, Stefan Guth, Lukas Hobohm, Kerstin Jurk та ін. "Activated Endothelial TGFβ1 Signaling Promotes Venous Thrombus Nonresolution in Mice Via Endothelin-1". Circulation Research 126, № 2 (17 січня 2020): 162–81. http://dx.doi.org/10.1161/circresaha.119.315259.
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Rationale: Chronic thromboembolic pulmonary hypertension (CTEPH) is characterized by defective thrombus resolution, pulmonary artery obstruction, and vasculopathy. TGFβ (transforming growth factor-β) signaling mutations have been implicated in pulmonary arterial hypertension, whereas the role of TGFβ in the pathophysiology of CTEPH is unknown. Objective: To determine whether defective TGFβ signaling in endothelial cells contributes to thrombus nonresolution and fibrosis. Methods and Results: Venous thrombosis was induced by inferior vena cava ligation in mice with genetic deletion of TGFβ1 in platelets (Plt.TGFβ-KO) or TGFβ type II receptors in endothelial cells (End.TGFβRII-KO). Pulmonary endarterectomy specimens from CTEPH patients were analyzed using immunohistochemistry. Primary human and mouse endothelial cells were studied using confocal microscopy, quantitative polymerase chain reaction, and Western blot. Absence of TGFβ1 in platelets did not alter platelet number or function but was associated with faster venous thrombus resolution, whereas endothelial TGFβRII deletion resulted in larger, more fibrotic and higher vascularized venous thrombi. Increased circulating active TGFβ1 levels, endothelial TGFβRI/ALK1 (activin receptor-like kinase), and TGFβRI/ALK5 expression were detected in End.TGFβRII-KO mice, and activated TGFβ signaling was present in vessel-rich areas of CTEPH specimens. CTEPH-endothelial cells and murine endothelial cells lacking TGFβRII simultaneously expressed endothelial and mesenchymal markers and transcription factors regulating endothelial-to-mesenchymal transition, similar to TGFβ1-stimulated endothelial cells. Mechanistically, increased endothelin-1 levels were detected in TGFβRII-KO endothelial cells, murine venous thrombi, or endarterectomy specimens and plasma of CTEPH patients, and endothelin-1 overexpression was prevented by inhibition of ALK5, and to a lesser extent of ALK1. ALK5 inhibition and endothelin receptor antagonization inhibited mesenchymal lineage conversion in TGFβ1-exposed human and murine endothelial cells and improved venous thrombus resolution and pulmonary vaso-occlusions in End.TGFβRII-KO mice. Conclusions: Endothelial TGFβ1 signaling via type I receptors and endothelin-1 contribute to mesenchymal lineage transition and thrombofibrosis, which were prevented by blocking endothelin receptors. Our findings may have relevant implications for the prevention and management of CTEPH.