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1

Cardell, LO, R. Uddman, and L. Edvinsson. "Endothelins: A Role in Cerebrovascular Disease?" Cephalalgia 14, no. 4 (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 s
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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 pepti
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3

Mebazaa, A., E. Mayoux, K. Maeda, et al. "Paracrine effects of endocardial endothelial cells on myocyte contraction mediated via endothelin." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 5 (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 endoth
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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 (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 immun
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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 (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
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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 (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
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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 (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 endothel
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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 metaboli
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9

Faivre-Fiorina, Béatrice, Alexis Caron, Céline Fassot, et al. "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 (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 hemoglob
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10

Jaffredo, T., R. Gautier, A. Eichmann, and F. Dieterlen-Lievre. "Intraaortic hemopoietic cells are derived from endothelial cells during ontogeny." Development 125, no. 22 (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 en
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11

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 (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 anal
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12

Inoue, Hajime, Nagaoki Wakisaka, Nobuhiro Tane, et al. "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 i
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13

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 (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 surfa
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14

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 (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
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15

Szczesny-Malysiak, Ewa, Marta Stojak, Roberto Campagna, et al. "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 potent
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16

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 (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 simila
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17

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 (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
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18

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 (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
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19

Lew, R. A., and A. J. Baertschi. "Endothelium-dependent ANF secretion in vitro." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 4 (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 m
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20

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 rec
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21

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 (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 c
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22

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 (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,
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23

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 (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)
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24

Czerniak, Jakub, and Dorota Olszewska-Słonina. "Laboratory markers of endothelial activation, dysfunctionand damage." Diagnostyka Laboratoryjna 61, no. 2 (2025): 1–14. https://doi.org/10.5604/01.3001.0055.1348.

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Activation, dysfunction and damage to the vascular endothelium play a key role in pathogenesis ofcardiovasculatory diseases and inflammatory diseases of the blood vessels. Disturbances in the functioningand structure of the endothelium also occur in hypertension, infectious diseases, cancers and some bleedingdisorders. Endothelial activation is expressed with an increase of its permeability to water, lipoproteins andplasma proteins as well as an increased expression of adhesion molecules on the surface of endothelial cells.Expression of adhesion molecules on the endothelium allows the leukocyt
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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 (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 th
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26

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 (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 e
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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 (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 endothelia
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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 (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, va
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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 (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 con
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Göthert, Joachim R., Sonja E. Gustin, J. Anke M. van Eekelen, et al. "Genetically tagging endothelial cells in vivo: bone marrow-derived cells do not contribute to tumor endothelium." Blood 104, no. 6 (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-galac
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31

Williams, Stuart K. "Endothelial Cell Transplantation." Cell Transplantation 4, no. 4 (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 issue
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Takahashi, M., K. Fukuda, K. Shimada, et al. "Localization of rat endothelin-converting enzyme to vascular endothelial cells and some secretory cells." Biochemical Journal 311, no. 2 (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-leve
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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 (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 b
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Kirsch, Torsten, Alexander Woywodt, Michaela Beese, et al. "Engulfment of apoptotic cells by microvascular endothelial cells induces proinflammatory responses." Blood 109, no. 7 (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 n
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Onitsuka, Izumi, Masaki Takeuchi, Tomoya Okabe, et al. "Two Distinct Precursors of Hematopoietic Stem Cells and Endothelial Progenitors Characterized by the PCLP1 Expression." Blood 106, no. 11 (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, si
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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 (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 o
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Nogueras, Sonia, Ana Merino, Raquel Ojeda, et al. "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 (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 repairi
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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 (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 endotheliu
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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 (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
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Six, Isabelle, Nicolas Guillaume, Valentine Jacob, et al. "The Endothelium and COVID-19: An Increasingly Clear Link Brief Title: Endotheliopathy in COVID-19." International Journal of Molecular Sciences 23, no. 11 (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 d
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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 (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 pree
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42

Kulovic-Sissawo, Azra, Carolina Tocantins, Mariana S. Diniz, et al. "Mitochondrial Dysfunction in Endothelial Progenitor Cells: Unraveling Insights from Vascular Endothelial Cells." Biology 13, no. 2 (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 endothelia
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Cameron, IT, and AP Davenport. "Endothelins in reproduction." Reproductive Medicine Review 1, no. 1 (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 (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), th
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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 (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
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Isales, Carlos M., Bauer Sumpio, Roni J. Bollag, 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 (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 concentra
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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 (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 mechanis
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Brock, Thomas, Elisabeth Boudriot, Anke Klawitter, et al. "The Influence of VE-Cadherin on Adhesion and Incorporation of Breast Cancer Cells into Vascular Endothelium." International Journal of Molecular Sciences 22, no. 11 (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,
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Bochenek, Magdalena L., Christiane Leidinger, Nico S. Rosinus та ін. "Activated Endothelial TGFβ1 Signaling Promotes Venous Thrombus Nonresolution in Mice Via Endothelin-1". Circulation Research 126, № 2 (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
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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 (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 a
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