Journal articles on the topic 'Blood endothelial cells'
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1
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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Dehouck, Marie-Pierre, Paul Vigne, Gérard Torpier, Jean Philippe Breittmayer, Roméo Cecchelli, and Christian Frelin. "Endothelin-1 as a Mediator of Endothelial Cell–Pericyte Interactions in Bovine Brain Capillaries." Journal of Cerebral Blood Flow & Metabolism 17, no. 4 (April 1997): 464–69. http://dx.doi.org/10.1097/00004647-199704000-00012.
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Endothelial cells and pericytes are closely associated in brain capillaries. Together with astrocytic foot processes, they form the blood–brain barrier. Capillaries were isolated from bovine brain cortex. Pure populations of endothelial cells and pericytes were isolated and cultured in vitro. Polarized monolayers of endothelial cells preferentially secreted immunoreactive endothelin-1 (Et-1) at their abluminal (brain-facing) membrane. They did not express receptors for Et-1. Pericytes expressed BQ-123-sensitive ETA receptors for endothelins as evidenced by 125I-Et-1 binding experiments. These receptors were coupled to phospholipase C as demonstrated by intracellular calcium measurements using indo-1-loaded cells. Addition of Et-1 to pericytes induced marked changes in the cell morphology that were associated with a reorganization of F-actin and intermediate filaments. It is concluded that Et-1 is a paracrine mediator at the bovine blood–brain barrier and that capillary pericytes are target cells for endothelium-derived Et-1.
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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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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.
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Speck, Nancy, Qin Zhu, Peng Gao, Joanna Tober, Laura Bennett, Changya Chen, Yasin Uzun, Yan Li, and Kai Tan. "Developmental Biology of the Blood System." Blood 134, Supplement_1 (November 13, 2019): SCI—29—SCI—29. http://dx.doi.org/10.1182/blood-2019-121283.
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Hematopoietic stem and progenitor cells (HSPCs) in the bone marrow are derived from a small population of hemogenic endothelial (HE) cells located in the yolk sac and major caudal arteries of the mammalian embryo. HE cells undergo an endothelial to hematopoietic cell transition, giving rise to HSPCs that accumulate in intra-arterial clusters before colonizing the fetal liver. To examine the molecular transitions between endothelial cells, HE, and intra-arterial cluster cells, and the heterogeneity of HSPCs within the intra-arterial clusters, we profiled ~40,000 cells from the caudal arteries (dorsal aorta, umbilical, vitelline) of embryonic day 9.5 to 11.5 mouse embryos by single-cell RNA sequencing (scRNA-seq) and single-cell chromatin accessibility sequencing (scATAC-Seq). A continuous developmental trajectory leads from endothelial cells to intra-arterial cluster cells, with identifiable intermediate stages between endothelial cells and HE. The intermediate endothelial stages most proximal to HE are characterized by elevated expression of genes regulated by GATA and SOX transcription factors. Developmental bottlenecks separate endothelial cells from HE cells, with the efficiency of transit through one of the last bottleneck regulated by RUNX1 dosage. Distinct developmental trajectories within intra-arterial cluster cells result in two populations of CD45+HSPCs; an initial wave of multi-lineage committed progenitors followed by precursors of hematopoietic stem cells (pre-HSCs). These and other insights gained from single cell analyses of HSPC formation from arterial endothelium will be presented. Disclosures No relevant conflicts of interest to declare.
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Westerweel, Peter E., and 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.
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Tissot Van Patot, M. C., S. MacKenzie, A. Tucker, and N. F. Voelkel. "Endotoxin-induced adhesion of red blood cells to pulmonary artery endothelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 270, no. 1 (January 1, 1996): L28—L36. http://dx.doi.org/10.1152/ajplung.1996.270.1.l28.
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Cell-cell interactions are important in intravascular inflammation. Neutrophils and monocytes adhere to the vascular endothelium and release mediators, such as tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1 beta, and reactive oxygen species. Red blood cells (RBC) from patients with malaria, sickle cell anemia, and diabetes also adhere to endothelial cells. The objectives of this investigation were to develop a bovine system of RBC adhesion to endothelial cells and to begin to investigate the mechanisms involved in the RBC adhesion. We show that 51Cr-RBC adhere to bovine pulmonary artery endothelial cells (BPAEC) after stimulation of both cell types with endotoxin (ETX; 50 micrograms/ml). RBC adhesion to BPAEC depended on the ETX concentration and the presence of divalent cations. TNF-alpha, IL-1 beta, and antioxidants (superoxide dismutase; catalase; and dimethyl sulfoxide) all induced RBC adhesion to BPAEC. Phosphatidylserine, which has been implicated in adhesion of sickle cells and aged RBC to endothelium, reduced RBC adhesion to BPAEC, whether ETX-treated or not. In conclusion, ETX, proinflammatory cytokines and, surprisingly, antioxidants increase RBC adherence to BPAEC monolayers. RBC adhesion to endothelium is decreased by phosphatidylserine.
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Iruela-Arispe, M. Luisa. "Pumping blood with self-reliance and cooperation." Journal of Experimental Medicine 215, no. 10 (September 18, 2018): 2480–82. http://dx.doi.org/10.1084/jem.20181537.
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In this issue of JEM, Singhal et al. (https://doi.org/10.1084/jem.20180008) explore the cellular mechanisms involved in endothelial cell regeneration in the liver. Using a combination of myeloablative and nonmyeloablative approaches, the authors found that repair of the endothelium is mediated by endothelial cells themselves, but when injured, endothelial cells enlist myeloid counterparts that aid in vascular repair.
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Smiljic, Sonja, Sladjana Savic, Zvezdan Milanovic, and Goran Grujic. "Endocardial endothelium as a blood-heart barrier." Medical review 71, no. 1-2 (2018): 60–64. http://dx.doi.org/10.2298/mpns1802060s.
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Introduction. Endocardial endothelium is formed from a single layer of closely related cells with complex interrelationships and extensive overlap at the junctional edges. Morphological characteristics of blood-heart barrier. Endocardium is composed of three layers: endocardial endothelium, subendothelial loose connective tissue and subendocardium. The fibrous component of the subendothelium consists of small amount of collagen and elastic fibers. Several cell types are present in subendocardium: telocytes, fibroblasts and nerve endings. Intercellular bonds between the endocardial endothelial cells. Endocardial endothelial cells are attached to one another via sets of binding proteins forming solid, adherent and communicating connections. Communicating connections form transmembrane channels between the neighboring cells, while solid and adherent connections form pericellular structures like stitches. The maintenance of the presumed transendocardial electrochemical potential difference provides a high gradient for certain ions as well as a selective boundary barrier, basal lamina, preventing ionic leakage. The negatively charged glycocalyx also modulates endothelial permeability. Electrophysiological characteristics of heart-blood barrier. Electrophysiological studies have shown the existence of a large number of membrane ion channels in the endocardial endothelial cells: inward rectifying K+ channels, Ca2+ dependent K+channels, voltage-dependent Cl-channels, volume-activated Cl-channels, stretch-activated cation channels and one carrier mediated transport mechanism - Na+K+adenosine triphosphatase. Conclusion. Numerous diseases of the cardiovascular system may be a consequence, but also the cause of the endocardial endothelium dysfunction. Selective damage to the endocardial endothelium and subendocardium is found in arrhythmia, atrial fibrillation, ischemia/reperfusion injury and heart failure. Typical lesions of endocardial and microvascular endothelium have also been described in sepsis, myocardial infarction, inflammation and thrombosis. The result of endothelial dysfunction is the weakening of the endothelial barrier regulation and electrolyte imbalance of the subendocardial interstitium.
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Barcia Durán, José Gabriel. "Endothelial JAK3 Expression Enhances Pro-Hematopoietic Angiocrine Function of Sinusoidal Endothelial Cells." Blood 134, Supplement_1 (November 13, 2019): 2488. http://dx.doi.org/10.1182/blood-2019-122449.
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Unlike Jak1, Jak2, and Tyk2, Jak3 is the only member of the Jak family of secondary messengers that signals exclusively by binding the common gamma chain of interleukin receptors IL2, IL4, IL7, IL9, IL15, and IL21. Jak3-null mice display defective T and NK cell development, which results in a mild SCID phenotype. Still, functional Jak3 expression outside the hematopoietic system remains unreported. Our data show that Jak3 is expressed in endothelial cells across hematopoietic and non-hematopoietic organs, with heightened expression in the bone marrow and spleen. Increased arterial zonation in the bone marrow of Jak3-null mice further suggests that Jak3 is a marker of sinusoidal endothelium, which is confirmed by fluorescent microscopy staining and single-cell RNA-sequencing. We also show that the Jak3-null niche is deleterious for the maintenance of long-term repopulating hematopoietic stem and progenitor cells (LT-HSCs) and that Jak3-overexpressing endothelial cells have increased potential to expand LT-HSCs in vitro. In addition, we identify the soluble factors downstream of Jak3 that provide endothelial cells with this functional advantage and show their localization to the bone marrow sinusoids in vivo. Our work serves to identify a novel function for a non-promiscuous tyrosine kinase in the bone marrow vascular niche and further characterize the hematopoietic stem cell niche of sinusoidal endothelium. Disclosures No relevant conflicts of interest to declare.
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Läubli, Heinz, Katharina-Susanne Spanaus, and Lubor Borsig. "Selectin-mediated activation of endothelial cells induces expression of CCL5 and promotes metastasis through recruitment of monocytes." Blood 114, no. 20 (November 12, 2009): 4583–91. http://dx.doi.org/10.1182/blood-2008-10-186585.
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Abstract Hematogenous metastasis is promoted by interactions of tumor cells with leukocytes, platelets, and the endothelium in the local intravascular microenvironment. Here we show that the activation of the microvascular endothelium results in recruitment of monocytes to metastatic tumor cells and promotes the establishment of the metastatic microenvironment. This inflammatory-like endothelial response was observed in microvascular endothelial cells only. Microarray analysis of microvascular endothelial cells cocultured with tumor cells in the presence of leukocytes and platelets revealed a specific gene expression profile. Selectin-mediated interactions of tumor cells with platelets and leukocytes activated endothelial cells and induced production of C-C chemokine ligand 5 (CCL5). Inhibition of CCL5-dependent monocyte recruitment during the early phase of metastasis by a CCL5 receptor antagonist strongly reduced tumor cell survival and attenuated metastasis. Collectively, these findings demonstrate that the endothelial expression of CCL5 contributes to the formation of a permissive metastatic microenvironment.
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Williams, Cassin Kimmel, Ji-Liang Li, Matilde Murga, Adrian L. Harris, and Giovanna Tosato. "Up-regulation of the Notch ligand Delta-like 4 inhibits VEGF-induced endothelial cell function." Blood 107, no. 3 (February 1, 2006): 931–39. http://dx.doi.org/10.1182/blood-2005-03-1000.
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AbstractDelta-like 4 (Dll4), a membrane-bound ligand for Notch1 and Notch4, is selectively expressed in the developing endothelium and in some tumor endothelium, and it is induced by vascular endothelial growth factor (VEGF)-A and hypoxia. Gene targeting studies have shown that Dll4 is required for normal embryonic vascular remodeling, but the mechanisms underlying Dll4 regulatory functions are currently not defined. In this study, we generated primary human endothelial cells that overexpress Dll4 protein to study Dll4 function and mechanism of action. Human umbilical vein endothelial cells retrovirally transduced with Dll4 displayed reduced proliferative and migratory responses selectively to VEGF-A. Expression of VEGF receptor-2, the principal signaling receptor for VEGF-A in endothelial cells, and coreceptor neuropilin-1 was significantly decreased in Dll4-transduced endothelial cells. Consistent with Dll4 signaling through Notch, expression of HEY2, one of the transcription factors that mediates Notch function, was significantly induced in Dll4-overexpressing endothelial cells. The γ-secretase inhibitor L-685458 significantly reconstituted endothelial cell proliferation inhibited by immobilized extracellular Dll4 and reconstituted VEGFR2 expression in Dll4-overerexpressing endothelial cells. These results identify the Notch ligand Dll4 as a selective inhibitor of VEGF-A biologic activities down-regulating 2 VEGF receptors expressed on endothelial cells and raise the possibility that Dll4 may be exploited therapeutically to modulate angiogenesis.
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El Nemer, Wassim, Marie-Paule Wautier, Cécile Rahuel, Pierre Gane, Patricia Hermand, Frédéric Galactéros, Jean-Luc Wautier, Jean-Pierre Cartron, Yves Colin, and Caroline Le Van Kim. "Endothelial Lu/BCAM glycoproteins are novel ligands for red blood cell α4β1integrin: role in adhesion of sickle red blood cells to endothelial cells." Blood 109, no. 8 (December 7, 2006): 3544–51. http://dx.doi.org/10.1182/blood-2006-07-035139.
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Abstract The Lutheran (Lu) blood group and basal cell adhesion molecule (BCAM) antigens are both carried by 2 glycoprotein isoforms of the immunoglobulin superfamily representing receptors for the laminin α5 chain. In addition to red blood cells, Lu/BCAM proteins are highly expressed in endothelial cells. Abnormal adhesion of red blood cells to the endothelium could potentially contribute to the vaso-occlusive episodes in sickle cell disease. Considering the presence of integrin consensus-binding sites in Lu/BCAM proteins, we investigated their potential interaction with integrin α4β1, the unique integrin expressed on immature circulating sickle red cells. Using cell adhesion assays under static and flow conditions, we demonstrated that integrin α4β1 expressed on transfected cells bound to chimeric Lu-Fc protein. We showed that epinephrine-stimulated sickle cells, but not control red cells, adhered to Lu-Fc via integrin α4β1 under flow conditions. Antibody-mediated activation of integrin α4β1 induced adhesion of sickle red cells to primary human umbilical vein endothelial cells; this adhesion was inhibited by soluble Lu-Fc and vascular cell adhesion molecule-1 (VCAM-1)–Fc proteins. This novel interaction between integrin α4β1 in sickle red cells and endothelial Lu/BCAM proteins could participate in sickle cell adhesion to endothelium and potentially play a role in vaso-occlusive episodes.
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Dudley, Andrew C., Taturo Udagawa, Juan M. Melero-Martin, Shou-Ching Shih, Adam Curatolo, Marsha A. Moses, and Michael Klagsbrun. "Bone marrow is a reservoir for proangiogenic myelomonocytic cells but not endothelial cells in spontaneous tumors." Blood 116, no. 17 (October 28, 2010): 3367–71. http://dx.doi.org/10.1182/blood-2010-02-271122.
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Abstract The hypothesis that bone marrow–derived, circulating endothelial cells incorporate into tumor blood vessels is unresolved. We have measured the numbers of bone marrow–derived versus resident endothelial cells in spontaneous prostate cancers during different stages of tumor progression and in age-matched normal prostates. Bone marrow–derived endothelial cells were rare in dysplasia and in well differentiated cancers representing between 0 and 0.04% of the total tumor mass. Instead, approximately 99% of all tumor-associated bone marrow–derived cells were CD45+ hematopoietic cells, including GR-1+, F4-80+, and CD11b+ myeloid cells. Similar to peripheral blood mononuclear cells, these tumor-associated myeloid cells expressed matrix metalloproteinases (MMPs), consistent with their proposed catalytic role during tumor angiogenesis. Furthermore, freshly isolated CD11b+ cells stimulated tumor endothelial cell cord formation by 10-fold in an in vitro angiogenesis assay. The bone marrow is, therefore, a reservoir for cells that augment tumor angiogenesis, but the tumor endothelium is derived primarily from the local environment.
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Atkinson, Ben T., Reema Jasuja, Vivien M. Chen, Prathima Nandivada, Bruce Furie, and Barbara C. Furie. "Laser-induced endothelial cell activation supports fibrin formation." Blood 116, no. 22 (November 25, 2010): 4675–83. http://dx.doi.org/10.1182/blood-2010-05-283986.
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Laser-induced vessel wall injury leads to rapid thrombus formation in an animal thrombosis model. The target of laser injury is the endothelium. We monitored calcium mobilization to assess activation of the laser-targeted cells. Infusion of Fluo-4 AM, a calcium-sensitive fluorochrome, into the mouse circulation resulted in dye uptake in the endothelium and circulating hematopoietic cells. Laser injury in mice treated with eptifibatide to inhibit platelet accumulation resulted in rapid calcium mobilization within the endothelium. Calcium mobilization correlated with the secretion of lysosomal-associated membrane protein 1, a marker of endothelium activation. In the absence of eptifibatide, endothelium activation preceded platelet accumu-lation. Laser activation of human umbilical vein endothelial cells loaded with Fluo-4 resulted in a rapid increase in calcium mobilization associated cell fluorescence similar to that induced by adenosine diphosphate (10μM) or thrombin (1 U/mL). Laser activation of human umbilical vein endothelial cells in the presence of corn trypsin inhibitor treated human plasma devoid of platelets and cell microparticles led to fibrin for-mation that was inhibited by an inhibitory monoclonal anti–tissue factor antibody. Thus laser injury leads to rapid endothelial cell activation. The laser activated endothelial cells can support formation of tenase and prothrombinase and may be a source of activated tissue factor as well.
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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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Shang, Dezhi, X. Wu Zheng, Masami Niiya, and X. Long Zheng. "Apical sorting of ADAMTS13 in vascular endothelial cells and Madin-Darby canine kidney cells depends on the CUB domains and their association with lipid rafts." Blood 108, no. 7 (October 1, 2006): 2207–15. http://dx.doi.org/10.1182/blood-2006-02-002139.
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Abstract ADAMTS13 biosynthesis appeared to occur mainly in hepatic stellate cells, but detection of ADAMTS13 mRNA in many other tissues suggests that vascular endothelium may also produce ADAMTS13. We showed that ADAMTS13 mRNA and protein were detectable in human umbilical vein endothelial cells, aortic endothelial cells, and endothelium-derived cell line (ECV304). ADAMTS13 in cell lysate or serum-free conditioned medium cleaved von Willebrand factor (VWF) specifically. ADAMTS13 and VWF were localized to the distinct compartments of endothelial cells. Moreover, ADAMTS13 was preferentially sorted into apical domain of ECV304 and Madin-Darby canine kidney (MDCK) cells. Apical sorting of ADAMTS13 depended on the CUB domains and their association with lipid rafts. A mutation in the second CUB domain of ADAMTS13 (4143-4144insA), naturally occurring in patients with inherited thrombotic thrombocytopenic purpura, resulted in a significant reduction of ADAMTS13 secretion and a reversal of its polarity in MDCK cells. These data demonstrated that ADAMTS13 is synthesized and secreted from endothelial cells; the apically secreted ADAMTS13 from endothelial cells may contribute significantly to plasma ADAMTS13 proteases. The data also suggest a critical role of the CUB domains and a novel cargo-selective mechanism for apical sorting of a soluble ADAMTS protease in polarized cells.
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Nordling, Sofia, Jaan Hong, Karin Fromell, Fredrik Edin, Johan Brännström, Rolf Larsson, Bo Nilsson, and Peetra U. Magnusson. "Vascular repair utilising immobilised heparin conjugate for protection against early activation of inflammation and coagulation." Thrombosis and Haemostasis 113, no. 06 (2015): 1312–22. http://dx.doi.org/10.1160/th14-09-0724.
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SummaryIschaemia-reperfusion injury (IRI) poses a major challenge in many thrombotic conditions and in whole organ transplantation. Activation of the endothelial cells and shedding of the protective vascular glycocalyx during IRI increase the risk of innate immune activation, cell infiltration and severe thrombus formation, promoting damage to the tissue. Here, we present a novel one-step strategy to protect the vasculature by immobilisation of a unique multi-arm heparin conjugate to the endothelium. Applying a new in vitro blood endothelial cell chamber model, the heparin conjugate was found to bind not only to primary human endothelial cells but also directly to the collagen to which the cells adhered. Incubation of hypoxic endothelial cells with freshly drawn human blood in the blood chambers elicited coagulation activation reflected by thrombin anti-thrombin formation and binding of platelets and neutrophils. Immobilisation of the heparin conjugate to the hypoxic endothelial cells created a protective coating, leading to a significant reduction of the recruitment of blood cells and coagulation activation compared to untreated hypoxic endothelial cells. This novel approach of immobilising multi-arm heparin conjugates on the endothelial cells and collagen of the basement membrane ensures to protect the endothelium against IRI in thrombotic disorders and in transplantation.
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Claesson-Welsh, Lena. "Endothelial cells in line." Blood 109, no. 4 (February 15, 2007): 1343–44. http://dx.doi.org/10.1182/blood-2006-11-059592.
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Gehling, Ursula M., Süleyman Ergün, Udo Schumacher, Christoph Wagener, Klaus Pantel, Marcus Otte, Gunter Schuch, et al. "In vitro differentiation of endothelial cells from AC133-positive progenitor cells." Blood 95, no. 10 (May 15, 2000): 3106–12. http://dx.doi.org/10.1182/blood.v95.10.3106.
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Abstract Recent findings support the hypothesis that the CD34+-cell population in bone marrow and peripheral blood contains hematopoietic and endothelial progenitor and stem cells. In this study, we report that human AC133+ cells from granulocyte colony-stimulating factor–mobilized peripheral blood have the capacity to differentiate into endothelial cells (ECs). When cultured in the presence of vascular endothelial growth factor (VEGF) and the novel cytokine stem cell growth factor (SCGF), AC133+ progenitors generate both adherent and proliferating nonadherent cells. Phenotypic analysis of the cells within the adherent population reveals that the majority display endothelial features, including the expression of KDR, Tie-2, Ulexeuropaeus agglutinin-1, and von Willebrand factor. Electron microscopic studies of these cells show structures compatible with Weibel-Palade bodies that are found exclusively in vascular endothelium. AC133-derived nonadherent cells give rise to both hematopoietic and endothelial colonies in semisolid medium. On transfer to fresh liquid culture with VEGF and SCGF, nonadherent cells again produce an adherent and a nonadherent population. In mice with severe combined immunodeficiency, AC133-derived cells form new blood vessels in vivo when injected subcutaneously together with A549 lung cancer cells. These data indicate that the AC133+-cell population consists of progenitor and stem cells not only with hematopoietic potential but also with the capacity to differentiate into ECs. Whether these hematopoietic and endothelial progenitors develop from a common precursor, the hemangioblast will be studied at the single-cell level.
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Gehling, Ursula M., Süleyman Ergün, Udo Schumacher, Christoph Wagener, Klaus Pantel, Marcus Otte, Gunter Schuch, et al. "In vitro differentiation of endothelial cells from AC133-positive progenitor cells." Blood 95, no. 10 (May 15, 2000): 3106–12. http://dx.doi.org/10.1182/blood.v95.10.3106.010k08_3106_3112.
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Recent findings support the hypothesis that the CD34+-cell population in bone marrow and peripheral blood contains hematopoietic and endothelial progenitor and stem cells. In this study, we report that human AC133+ cells from granulocyte colony-stimulating factor–mobilized peripheral blood have the capacity to differentiate into endothelial cells (ECs). When cultured in the presence of vascular endothelial growth factor (VEGF) and the novel cytokine stem cell growth factor (SCGF), AC133+ progenitors generate both adherent and proliferating nonadherent cells. Phenotypic analysis of the cells within the adherent population reveals that the majority display endothelial features, including the expression of KDR, Tie-2, Ulexeuropaeus agglutinin-1, and von Willebrand factor. Electron microscopic studies of these cells show structures compatible with Weibel-Palade bodies that are found exclusively in vascular endothelium. AC133-derived nonadherent cells give rise to both hematopoietic and endothelial colonies in semisolid medium. On transfer to fresh liquid culture with VEGF and SCGF, nonadherent cells again produce an adherent and a nonadherent population. In mice with severe combined immunodeficiency, AC133-derived cells form new blood vessels in vivo when injected subcutaneously together with A549 lung cancer cells. These data indicate that the AC133+-cell population consists of progenitor and stem cells not only with hematopoietic potential but also with the capacity to differentiate into ECs. Whether these hematopoietic and endothelial progenitors develop from a common precursor, the hemangioblast will be studied at the single-cell level.
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Vanhoutte, PM. "Endothelium and the Control of Vascular Tissue." Physiology 2, no. 1 (February 1, 1987): 18–22. http://dx.doi.org/10.1152/physiologyonline.1987.2.1.18.
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Endothelial cells contribute more than an inside lining of blood vessels. They react to mechanical forces and to a number of substances, either locally produced or circulating in blood, that cause the release of one or more as yet unidentified endothelium-derived relaxing factors. Other agents, including stretch and blood pressure, evoke endothelium-dependent contraction of blood vessels. Such mechanisms make endothelial cells ideal sensors to monitor changes in the flow and composition of the blood.
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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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Bailey, Alexis S., Shuguang Jiang, Michael Afentoulis, Christina I. Baumann, David A. Schroeder, Susan B. Olson, Melissa H. Wong, and William H. Fleming. "Transplanted adult hematopoietic stems cells differentiate into functional endothelial cells." Blood 103, no. 1 (January 1, 2004): 13–19. http://dx.doi.org/10.1182/blood-2003-05-1684.
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Abstract During early embryogenesis, blood vessels and hematopoietic cells arise from a common precursor cell, the hemangioblast. Recent studies have identified endothelial progenitor cells in the peripheral blood, and there is accumulating evidence that a subset of these cells is derived from precursors in the bone marrow. Here we show that adult bone marrow–derived, phenotypically defined hematopoietic stem cells (c-kit+, Sca-1+, lineage–) give rise to functional endothelial cells. With the exception of the brain, donor-derived cells are rapidly integrated into blood vessels. Durably engrafted endothelial cells express CD31, produce von Willebrand factor, and take up low-density lipoprotein. Analysis of DNA content indicates that donor-derived endothelial cells are not the products of cell fusion. Self-renewal of stem cells with hematopoietic and endothelial cell potential was revealed by serial transplantation studies. The clonal origin of both hematopoietic and endothelial cell outcomes was established by the transfer of a single cell. These results suggest that adult bone marrow–derived hematopoietic stem cells may serve as a reservoir for endothelial cell progenitors.
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Rohde, Eva, Christina Malischnik, Daniela Thaler, Theresa Maierhofer, Werner Linkesch, Gerhard Lanzer, Christian Guelly, and Dirk Strunk. "Blood Monocytes Mimic Endothelial Progenitor Cells." Stem Cells 24, no. 2 (February 2006): 357–67. http://dx.doi.org/10.1634/stemcells.2005-0072.
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Rodrigues, Stephen F., and D. Neil Granger. "Blood cells and endothelial barrier function." Tissue Barriers 3, no. 1-2 (January 14, 2015): e978720. http://dx.doi.org/10.4161/21688370.2014.978720.
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Hebbel, Robert P. "Blood endothelial cells: utility from ambiguity." Journal of Clinical Investigation 127, no. 5 (May 1, 2017): 1613–15. http://dx.doi.org/10.1172/jci93649.
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Chang, Vivian Y., Christina M. Termini, and John P. Chute. "Young endothelial cells revive aging blood." Journal of Clinical Investigation 127, no. 11 (October 16, 2017): 3921–22. http://dx.doi.org/10.1172/jci97707.
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Sehgal, Tushar, Shano Naseem, and Neelam Varma. "Endothelial cells in peripheral blood film." Hematology/Oncology and Stem Cell Therapy 7, no. 4 (December 2014): 165. http://dx.doi.org/10.1016/j.hemonc.2014.06.004.
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Gornikiewicz, Alexander, Anna Zommer, Raimund Jakesz, Michael Gnant, and Christine Brostjan. "Retroviral targeting of proliferating endothelial cells." Acta Biochimica Polonica 52, no. 3 (September 30, 2005): 731–35. http://dx.doi.org/10.18388/abp.2005_3438.
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Tumor growth requires the formation of new blood vessels by endothelial cells. Thus, surface molecules -- such as angiogenin receptors -- that are selectively expressed on growing endothelium represent an attractive target for directed delivery of compounds to tumor tissue. We attempted to obtain genetically engineered retroviral vectors targeted to the endothelium by inserting the human angiogenin sequence into Moloney murine leukemia virus envelope glycoprotein. Abundant expression of the chimeric protein could be verified. However, while being selective for proliferating human endothelial cells, the recombinant retroviral particles displayed low transduction efficiencies and thus have to be further improved.
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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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Canu, Giovanni, and Christiana Ruhrberg. "First blood: the endothelial origins of hematopoietic progenitors." Angiogenesis 24, no. 2 (March 30, 2021): 199–211. http://dx.doi.org/10.1007/s10456-021-09783-9.
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AbstractHematopoiesis in vertebrate embryos occurs in temporally and spatially overlapping waves in close proximity to blood vascular endothelial cells. Initially, yolk sac hematopoiesis produces primitive erythrocytes, megakaryocytes, and macrophages. Thereafter, sequential waves of definitive hematopoiesis arise from yolk sac and intraembryonic hemogenic endothelia through an endothelial-to-hematopoietic transition (EHT). During EHT, the endothelial and hematopoietic transcriptional programs are tightly co-regulated to orchestrate a shift in cell identity. In the yolk sac, EHT generates erythro-myeloid progenitors, which upon migration to the liver differentiate into fetal blood cells, including erythrocytes and tissue-resident macrophages. In the dorsal aorta, EHT produces hematopoietic stem cells, which engraft the fetal liver and then the bone marrow to sustain adult hematopoiesis. Recent studies have defined the relationship between the developing vascular and hematopoietic systems in animal models, including molecular mechanisms that drive the hemato-endothelial transcription program for EHT. Moreover, human pluripotent stem cells have enabled modeling of fetal human hematopoiesis and have begun to generate cell types of clinical interest for regenerative medicine.
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Rafii, Shahin, Christopher C. Kloss, Jason M. Butler, Michael Ginsberg, Eric Gars, Raphael Lis, Qiansheng Zhan, et al. "Human ESC-derived hemogenic endothelial cells undergo distinct waves of endothelial to hematopoietic transition." Blood 121, no. 5 (January 31, 2013): 770–80. http://dx.doi.org/10.1182/blood-2012-07-444208.
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Key PointsLive imaging of endothelial to hematopoietic conversion identifies distinct subpopulations of hESC-derived hemogenic endothelium. Expression of the Notch ligand DII4 on vascular ECs drives induction of myeloid fate from hESC-derived hematopoietic progenitors.
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Elsheikh, Elzafir, Mehmet Uzunel, Zhong He, Jan Holgersson, Grzegorz Nowak, and Suchitra Sumitran-Holgersson. "Only a specific subset of human peripheral-blood monocytes has endothelial-like functional capacity." Blood 106, no. 7 (October 1, 2005): 2347–55. http://dx.doi.org/10.1182/blood-2005-04-1407.
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Abstract The monocyte population in blood is considered a possible source of endothelial precursors. Because endothelial-specific receptor tyrosine kinases act as regulators of endothelial cell function, we investigated whether expression of the vascular endothelial growth factor receptor-2 (VEGFR-2) on monocytes is important for their endothelial-like functional capacity. Peripheral-blood monocytes expressing vascular endothelial growth factor receptor-2 (VEGFR-2), or CD14+/VEGFR-2+, were isolated, and their phenotypic, morphologic, and functional capacities were compared with those of monocytes negative for this marker (CD14+/VEGFR-2-). CD14+/VEGFR-2+ cells constituted approximately 2% ± 0.5% of the total population of monocytes and 0.08% ± 0.04% of mononuclear cells in blood. CD14+/VEGFR-2+ cells exhibited the potential to differentiate in vitro into cells with endothelial characteristics. The cells were efficiently transduced by a lentiviral vector driving expression of the green fluorescence protein (GFP). Transplantation of GFP-transduced cells into balloon-injured femoral arteries of nude mice significantly contributed to efficient reendothelialization. CD14+/VEGFR-2- did not exhibit any of these characteristics. These data demonstrate that the expression of VEGFR-2 on peripheral blood monocytes is essential for their endothelial-like functional capacity and support the notion of a common precursor for monocytic and endothelial cell lineage. Our results help clarify which subpopulations may restore damaged endothelium and may participate in the maintenance of vascular homeostasis.
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Osterud, Bjarne. "Tissue factor in blood cells and endothelial cells." Frontiers in Bioscience E4, no. 1 (2012): 289–99. http://dx.doi.org/10.2741/e376.
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Oberlin, Estelle, Manuela Tavian, Istvàn Blazsek, and Bruno Péault. "Blood-forming potential of vascular endothelium in the human embryo." Development 129, no. 17 (September 1, 2002): 4147–57. http://dx.doi.org/10.1242/dev.129.17.4147.
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Hematopoietic cells arise first in the third week of human ontogeny inside yolk sac developing blood vessels, then, one week later and independently, from the wall of the embryonic aorta and vitelline artery. To address the suggested derivation of emerging hematopoietic stem cells from the vessel endothelium, endothelial cells have been sorted by flow cytometry from the yolk sac and aorta and cultured in the presence of stromal cells that support human multilineage hematopoiesis. Embryonic endothelial cells were most accurately selected on CD34 or CD31 surface expression and absence of CD45, which guaranteed the absence of contaminating hematopoietic cells. Yet, rigorously selected endothelial cells yielded a progeny of myelo-lymphoid cells in culture. The frequency of hemogenic endothelial cells in the yolk sac and aorta reflected the actual blood-forming activity of these tissues, as a function of developmental age. Even less expected, a subset of endothelial cells sorted similarly from the embryonic liver and fetal bone marrow also exhibited blood-forming potential. These results suggest that a part at least of emerging hematopoietic cells in the human embryo and fetus originate in vascular walls.
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Tso, C., K. Rye, and P. Barter. "Generation of Endothelial-like Cells from Endothelium-adherent Blood Monocytes." Heart, Lung and Circulation 19 (January 2010): S14. http://dx.doi.org/10.1016/j.hlc.2010.06.695.
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Natarajan, M., MM Udden, and LV McIntire. "Adhesion of sickle red blood cells and damage to interleukin-1 beta stimulated endothelial cells under flow in vitro." Blood 87, no. 11 (June 1, 1996): 4845–52. http://dx.doi.org/10.1182/blood.v87.11.4845.bloodjournal87114845.
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Two factors that are hypothesized to contribute to vasoocclusive crises in sickle cell anemia are increased sickle red blood cell-endothelial cell interactions and damage to endothelium. Despite considerable study, the mechanisms by which erythrocyte-endothelial interactions occur and the role of endothelial damage have not yet been fully elucidated. In this report, we demonstrate that adhesion and damage may be related in a model of vasoocclusion in sickle cell anemia. Phase contrast microscopy coupled to digital image processing was used to determine the adhesion of sickle red blood cells to 1-, 4-, and 24-hour interleukin-I beta (IL-1 beta) stimulated endothelial calls in a parallel plate flow chamber. Morphological alterations to activated endothelial cells after the perfusion of sickle erythrocytes were also identified. Pretreatment of monolayers with 50 pg/mL of IL-1 beta for 1, 4, and 24 hours caused approximately 16-fold increases in adhesion of sickle cells to activated endothelium at all time points. Results with an Arginine-glycine aspartic acid (RGD) peptide and monoclonal antibodies indicated a role for three different endothelial cell receptors: alpha v beta 3 after 1 hour of IL-1 beta stimulation; E- selectin after 4 hours of IL-1 beta stimulation; and vascular cell adhesion molecule-1 after prolonged exposure to cytokines. Perfusion of sickle, but not normal, erythrocytes resulted in alteration of endothelial morphology. Approximately 6% to 8% damage was observed on 4- and 24-hour IL-1 beta stimulated endothelial cells after the perfusion of sickle cells. Damage to 24-hour activated endothelial cells showed a positive correlation (r = .899) with the number of adherent sickle erythrocytes.
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Shilkina, N. P., I. E. Yunonin, S. V. Butusova, E. V. Mikhailova, and A. A. Vinogradov. "Endothelial damage and circadian blood pressure profile in rheumatoid arthritis." Terapevticheskii arkhiv 91, no. 5 (May 15, 2019): 89–95. http://dx.doi.org/10.26442/00403660.2019.05.000052.
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Aim. To study the influence of the state of endothelium on the daily profile of arterial pressure (AP) in patients with rheumatoid arthritis (RA). Materials and methods. In 70 RA pts carried out C-reactive protein (CRP), vascular endothelial adhesion molecule type 1 (sVCAM-1), antigen von Willebrand Factor (AG WF), interleukin-8 (Il-8), rheumatoid factor (RF), IgG, endotheline-1 (ET-1), number of desquamated endotheliocytes cells (DE), VS, activity of renin by immunoenzyme analysis. The dysfunction of endothelium was evaluated by calculation of DE. The functional methods included the daily monitoring of arterial pressure (AP). Results. Arterial hypertension (AH) occurred in 40 (57.1%) pts. RA pts are revealed the signs of endothelial dysfunction, about which significant differences among the indices of activation of endothelium in comparison with control group testify. ET-1, sVCAM-1, vWF AG, Il-8, CRP content was higher in RA pts. Reliably above there was a number of DE. Reliable differences according to these indices depending of RA activity were discovered. With conducting of correlation analysis it is revealed, that markers of the activation of endothelium: sVCAM-1, vWF AG positively correlated with increasing RF IgG and indices of the immune inflammation: CRP, and DE number. In patients suffering from RA, showed signs of endothelial dysfunction. The positive correlation between endothelial damage and daily profile of AP show the relationship of these processes. Conclusion. Positive correlations between the damage of endothelium and disturbance of AP daily profile testify about the interrelation of these processes.
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Fiuza, Carmen, Michael Bustin, Shefali Talwar, Margaret Tropea, Eric Gerstenberger, James H. Shelhamer, and Anthony F. Suffredini. "Inflammation-promoting activity of HMGB1 on human microvascular endothelial cells." Blood 101, no. 7 (April 1, 2003): 2652–60. http://dx.doi.org/10.1182/blood-2002-05-1300.
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Systemic inflammation because of sepsis results in endothelial cell activation and microvascular injury. High-mobility group protein-1 (HMGB1), a novel inflammatory molecule, is a late mediator of endotoxin shock and is present in the blood of septic patients. The receptor for advanced glycation end products (RAGE) is expressed on endothelium and is a receptor for HMGB1. Here we examine the effects of HMGB1 on human endothelial cell function. Recombinant human HMGB1 (rhHMGB1) was cloned and expressed in Escherichia coli and incubated with human microvascular endothelium. rhHMGB1 caused a dose- and time-dependent increase in the expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and RAGE. rhHMGB1 induced the secretion of tumor necrosis factor-α (TNFα), interleukin 8 (IL-8), monocyte chemotactic protein-1 (MCP-1), plasminogen activator inhibitor 1 (PAI-1), and tissue plasminogen activator (tPA) (P < .01). rhHMGB1 stimulation resulted in transient phosphorylation of mitogen-activated protein (MAP) kinases, extracellular signal-related kinase (ERK), Jun N-terminal kinase (JNK), and p38, and in nuclear translocation of transcription factors NF-κB and Sp1. These effects are partially mediated by TNFα autocrine stimulation, as anti-TNFα antibodies significantly decrease chemokine and adhesion molecule responses (P ≤ .002). Thus, rhHMGB1 elicits proinflammatory responses on endothelial cells and may contribute to alterations in endothelial cell function in human inflammation.
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Hara, Yaiko . "Morphological Study on Development of Vascular Endothelium in Chick Embryo." JOURNAL OF MULTIDISCIPLINARY DENTAL RESEARCH 8, no. 2 (December 15, 2022): 57–60. http://dx.doi.org/10.38138/jmdr/v8i2.22.29.
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The vascular endothelium and hematopoietic stem cells are believed to derive from common progenitor cells called hemangioblasts. However, morphological study on the development of vascular endothelial cell has been scarce. The present study is intended to provide more morphological explanation of the differentiation process of the hemangioblast. We performed histological observation, using 10 four-day-old chick embryos. After fixation with 4% concentration paraformaldehyde, hematoxylin eosin staining, toluidine blue staining and immunostaining were performed in that order for observation of morphological changes of the detected cells. Blood corpuscles were aggregated in the dorsal aorta and the heart (that had been observed to beat in its preparation). Some red blood cells showed immunoreactivity to both anti-Flk-1(VEGFR2) and anti-CD31 antibody. Additionally, some blood cells had small vacuoles in the cytoplasm, and they fused to form one larger vacuole ultimately a balloon-like shape that was connected to endothelial cells. These cells were present in close proximity to the vascular endothelium. We reveal that some of the early embryonic blood cells differentiate into vascular endothelial cells. Keywords: Vasculogenesis, Angiogenesis, Hemangioblasts, Vascular endothelial cells
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Uziel, Orit, Lian Lipshtein, Zinab Sarsor, Einat Beery, Shaked Bogen, Meir Lahav, Vitali Kliminski, et al. "CLL-Derived Exosomes Turn Endothelial Cells into IL-6 Producing Cells." Blood 138, Supplement 1 (November 5, 2021): 1547. http://dx.doi.org/10.1182/blood-2021-152236.
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Abstract CLL is characterized by gradual accumulation of mature appearing long-lived lymphocytes that travel in blood and reside in lymph nodes, spleen and bone marrow. In these sites, pro inflammatory humoral factors support the survival and proliferation of the neoplastic cells. Previous studies showed that levels of the proinflammatory cytokine IL-6 are at least 10 folds higher in patients with CLL compared with healthy individuals. Yet, which cells produce and secrete IL-6 and what triggers this cellular activity in CLL is unknown. Secreted by all types of cells, exosomes are nano-scaled particles that travel in blood and carry a cargo that at least partially reflects the molecular makeup of its cell of origin. Exosomes, including those originating from neoplastic cells, function as stable intercellular transport vehicles that deliver their cargo to cells that engulf them. For example, CLL-derived exosomes are taken up by mesenchymal stromal cells, transforming them to cancer associated fibroblasts. Given the appropriate stimulation, endothelial cells produce IL-6 which provides CLL cells with a survival advantage. Therefore, we hypothesized that CLL-exosomes turn endothelial cells into "IL-6-secreting cells". To test this hypothesis, we transfected vein-derived (HUVECs) and arterial-derived (HAOEC) endothelial cells with exosomes that we isolated from the peripheral blood of 45 treatment naïve patients. We found that endothelial cells take-up CLL-exosomes in a dose- and time- dependent manner. Since CLL cells are protected from apoptosis in IL-6 rich environment, we wondered whether CLL-exosomes turn endothelial cells into IL-6-producing cells. To test this, we exposed endothelial cells to CLL-exosomes and found 50% increase in IL-6 levels, suggesting that the endothelial-exposed cells produced and secreted IL-6. Subsequently, we filtered out this growth medium and added CLL cells to this IL-6 enriched medium. After 15 minutes, STAT3 became phosphorylated and there was 40% decrease in the rate of apoptosis, indicating that IL-6 activated STAT3-dependent anti-apoptotic pathway. Phosphor-proteomics analysis of endothelial cells that were loaded with CLL-exosomes revealed 23 phosphor-proteins that were upregulated. Network analysis unraveled the central role of phosphor-b-catenin. To test whether b-catenin induces IL-6 in these cells, we transfected HUVECs with a b-catenin containing plasmid. We found by ELISA 30% increase in the levels of IL-6 in the culture medium and by chromatin immunoprecipitation assay an increased binding of 3 transcription factors (NFkB, LEF/TCF, and CEBP) to the IL-6 promoter. Taken together, we found that CLL cells communicate with endothelial cells through exosomes that they release. Once these exosomes are taken up by endothelial, they turn them into IL-6 producing cells, which in turn contributes to CLL cells' survival. Disclosures No relevant conflicts of interest to declare.
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Yoder, Mervin C. "Endothelial stem and progenitor cells (stem cells): (2017 Grover Conference Series)." Pulmonary Circulation 8, no. 1 (November 3, 2017): 204589321774395. http://dx.doi.org/10.1177/2045893217743950.
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The capacity of existing blood vessels to give rise to new blood vessels via endothelial cell sprouting is called angiogenesis and is a well-studied biologic process. In contrast, little is known about the mechanisms for endothelial cell replacement or regeneration within established blood vessels. Since clear definitions exist for identifying cells with stem and progenitor cell properties in many tissues and organs of the body, several groups have begun to accumulate evidence that endothelial stem and progenitor cells exist within the endothelial intima of existing blood vessels. This paper will review stem and progenitor cell definitions and highlight several recent papers purporting to have identified resident vascular endothelial stem and progenitor cells.
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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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Fens, Marcel H. A. M., Enrico Mastrobattista, Anko M. de Graaff, Frits M. Flesch, Anton Ultee, Jan T. Rasmussen, Grietje Molema, Gert Storm, and Raymond M. Schiffelers. "Angiogenic endothelium shows lactadherin-dependent phagocytosis of aged erythrocytes and apoptotic cells." Blood 111, no. 9 (May 1, 2008): 4542–50. http://dx.doi.org/10.1182/blood-2007-06-094763.
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Abstract Angiogenic endothelium plays a crucial role in tumor growth. During angiogenesis, complex alterations in the microenvironment occur. In response, the endothelium undergoes phenotypic changes, for example overexpression of αv-integrins. Here, we show that the overexpression of αv-integrins on angiogenic endothelial cells is engaged in phagocytic actions involving binding (“tethering”) and uptake (“tickling”) of lactadherin (also termed MFG-E8)–opsonized particles. Phosphatidylserine (PS)–exposing multilamellar vesicles, “aged” erythrocytes, and apoptotic melanoma cells incubated with lactadherin were all phagocytosed by angiogenic endothelial cells in vitro. Furthermore, we demonstrated lactadherin expression in and around tumor blood vessels making opsonization in situ plausible. By engineering the surface of erythrocytes with covalently coupled cyclic Arg-Gly-Asp (RGD) peptides—mimicking lactadherin opsonization—we could induce phagocytosis by angiogenic endothelial cells both in vitro and in vivo. In vitro, this was confirmed by cytochalasin D preincubation. When RGD-erythrocytes were administered intravenously in tumor-bearing mice, blood vessel congestion followed by tumor core necrosis was seen. Moreover, RGD-erythrocytes could delay tumor growth in a murine melanoma model, possibly through induction of tumor infarctions. These results reveal that angiogenic endothelial cells have phagocytic properties for lactadherin-opsonized large particles and apoptotic cells. Implications of our findings for diagnostic and therapy of angiogenesis-driven diseases are discussed.
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Choi, Kyung-Dal, Maxim Vodyanik, Shulan Tian, Ron Stewart, James Thomson, and Igor Slukvin. "Identification of Hemogenic Endothelium and Its Direct Precursor in Human Embryonic Stem Cell Differentiation Cultures." Blood 118, no. 21 (November 18, 2011): 1277. http://dx.doi.org/10.1182/blood.v118.21.1277.1277.
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Abstract Abstract 1277 Animal studies demonstrated that the first HSCs are generated in the aorta-gonad-mesonephros from a unique population of endothelial cells, hemogenic endothelium (HE), through endothelial-hematopoietic transition. However, the identity of HE remains obscure and the specific features that distinguish HE from non-HE and the discrete stages of endothelial transition into hematopoietic cells are not characterized. Here we employed hESC differentiation system in coculture with OP9 to define the distinct population of HE, and to develop an experimental system for analysis of endothelial-hematopoietic transition in vitro. Previously, we demonstrated that endothelial cells could be distinguished from hematopoietic progenitors based on the lack of CD43 expression (Vodyanik et al., Blood 2006;108:2095). Here, we analyzed the earliest stages of endothelial development from hESCs before the typical hematopoietic CFCs could be detected. We found that the first CD144+ endothelial cells appear on day 4 of differentiation within a population of APLNR+ cells expressing a high level of KDR. Based on expression of CD235a/CD43, CD73 and CD41a, we identified three major subsets within the emerging CD144+ cells: 1)CD235a/CD43−CD73+, 2)CD235a/CD43−CD73−, and 3)CD235a/CD43+CD41a−. Although all three subsets formed monolayer endothelial cells when grown on fibronectin in endothelial media, only CD235a/CD43+CD41a− cells displayed hematopoietic CFC potential, which required serum-free medium and were dependent on hematopoietic cytokines and FGF2. After culture with OP9, both CD144+CD235a/CD43−CD73− and CD144+CD235a/CD43+CD41a− cells generated CD31+CD43/45− endothelial cells and a significant amount of CD43+ blood cells. In contrast CD144+CD235a/CD43−CD73+ cells formed almost exclusively endothelial cells. Single cell deposition experiments demonstrated that CD144+CD235a/CD43+CD41a− cells formed predominantly hematopoietic cells, while most CD144+CD235a/CD43−CD73− cells gave rise to either hematopoietic or endothelial clusters with approximately 2.5% of cells forming hematoendothelial clusters, indicating the presence of bipotential progenitors within this population. Though all three CD144+ subsets had a very similar molecular signature and expressed typical endothelial genes and genes associated with angiohematopoietic and HSC development, CD235a/CD43+CD41a− showed the higher expression of hematopoietic genes and lower expression of CDH5, CDH2, CAV1, and APOLD1 typical endothelial genes. Based on the functional, phenotypic and molecular properties we designated the identity of subsets as follows: 1) CD144+CD235a/CD43+CD41a− angiogenic blood cells, i.e. cells that possessed primary hematopoietic characteristics but were also capable of generating endothelial cells; 2) CD144+CD235a/CD43−CD73+ endothelial progenitors, i.e. cells that had all functional and molecular features of endothelial cells and endothelial colony-forming potential on OP9; 3) CD144+CD235a/CD43−CD73− HE cells, i.e. cells with primary endothelial characteristics lacking hematopoietic CFC potential and surface markers, but capable of generating blood and endothelial cells after coculture with stromal cells. To find out the direct precursors of HE and blood cells, we analyzed the differentiation potential of major subsets of mesodermal cells isolated on day 4 of hESC coculture with OP9. We found that only APLNR+KDRbrightCD140alow/− mesodermal cells lacking expression of typical hematopoietic (CD43, CD45), endothelial (CD31, CD144), and mesenchymal (CD73, CD105) markers had the potential to generate both blood and endothelium. Moreover, single cell deposition experiments demonstrated that APLNR+KDRbrightCD140alow/− cells formed HE clusters with a high frequency (about 1/10 cells), strongly indicating that these cells represent the direct precursors of HE. Because APLNR+KDRbrightCD140alow/− cells upregulated expression LMO2, TAL1, CBFB, GATA2, and FLI1 transcriptional regulators of hematopoietic and endothelial development, but were lacking expression of primitive streak genes, we designated these cells as angioblasts. Together these studies provide a hESC-based platform for identification of factors required for acquisition of HSC potential by blood cells following transition from endothelium. Disclosures: Thomson: CDI: Consultancy, Equity Ownership, Membership on an entity's Board of Directors or advisory committees. Slukvin:CDI: Consultancy, Equity Ownership.
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‘t Hart, Daan C., Johan van der Vlag, and Tom Nijenhuis. "Laminar flow substantially affects the morphology and functional phenotype of glomerular endothelial cells." PLOS ONE 16, no. 5 (May 5, 2021): e0251129. http://dx.doi.org/10.1371/journal.pone.0251129.
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Shear stress induced by laminar blood flow has a profound effect on the morphology and functional phenotype of macrovascular endothelial cells. The influence of laminar flow on the glomerular microvascular endothelium, however, remains largely elusive. The glomerular endothelium, including its glycocalyx, is a crucial part of the glomerular filtration barrier, which is involved in blood filtration. We therefore investigated the influence of laminar flow-induced shear stress on the glomerular endothelium. Conditionally immortalized mouse glomerular endothelial cells were cultured for 7 days under a laminar flow of 5 dyn/cm2 to mimic the glomerular blood flow. The cells were subsequently analysed for changes in morphology, expression of shear stress-responsive genes, nitric oxide production, glycocalyx composition, expression of anti-oxidant genes and the inflammatory response. Culture under laminar flow resulted in cytoskeletal rearrangement and cell alignment compared to static conditions. Moreover, production of nitric oxide was increased and the expression of the main functional component of the glycocalyx, Heparan Sulfate, was enhanced in response to shear stress. Furthermore, glomerular endothelial cells demonstrated a quiescent phenotype under flow, characterized by a decreased expression of the pro-inflammatory gene ICAM-1 and increased expression of the anti-oxidant enzymes HO-1 and NQO1. Upon exposure to the inflammatory stimulus TNFα, however, glomerular endothelial cells cultured under laminar flow showed an enhanced inflammatory response. In conclusion, laminar flow extensively affects the morphology and functional phenotype of glomerular endothelial cells in culture. Furthermore, glomerular endothelial cells respond differently to shear stress compared to macrovascular endothelium. To improve the translation of future in vitro studies with glomerular endothelial cells to the in vivo situation, it appears therefore crucial to culture glomerular endothelial cells under physiological flow conditions.
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Meissner, Anja, Olaf Zilles, Rosa Varona, Katrin Jozefowski, Uwe Ritter, Gabriel Marquez, Rupert Hallmann, and Heinrich Körner. "CC chemokine ligand 20 partially controls adhesion of naive B cells to activated endothelial cells under shear stress." Blood 102, no. 8 (October 15, 2003): 2724–27. http://dx.doi.org/10.1182/blood-2003-01-0007.
Full textAbstract:
Abstract Chemokines are thought to control lymphocyte recruitment to the inflamed endothelium. To dissect chemokine-mediated adhesion, binding of ex vivo isolated splenocytes to tumor necrosis factor (TNF)–activated endothelial cells was analyzed under shear stress. We observed specific adhesion of naive follicular B cells, which could be blocked by pertussis toxin. This indicated a G protein–mediated binding and pointed at a contribution of chemokine receptors to B-cell adhesion. Analysis of chemokines expressed by TNF-activated endothelial cells showed that CC chemokine ligand 2 (CCL2), CCL17, and CCL20 were up-regulated. Only on follicular B cells was the cognate receptor for CCL20, CC chemokine receptor 6 (CCR6), expressed strongly, and a functional transmigration assay with CCR6-negative B cells demonstrated conclusively the sole signaling of CCL20 through CCR6. Desensitization of CCR6 on naive B cells with CCL20 resulted in receptor down-regulation and reduced B-cell adhesion. We conclude that CCL20 plays a vital role in B-cell adhesion to the inflamed endothelium.
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He, Huanhuan, Jingying Xu, Carmen M. Warren, Dan Duan, Xinmin Li, Lily Wu, and M. Luisa Iruela-Arispe. "Endothelial cells provide an instructive niche for the differentiation and functional polarization of M2-like macrophages." Blood 120, no. 15 (October 11, 2012): 3152–62. http://dx.doi.org/10.1182/blood-2012-04-422758.
Full textAbstract:
Abstract Endothelial cells and macrophages are known to engage in tight and specific interactions that contribute to the modulation of vascular function. Here we show that adult endothelial cells provide critical signals for the selective growth and differentiation of macrophages from several hematopoietic progenitors. The process features the formation of well-organized colonies that exhibit progressive differentiation from the center to the periphery and toward an M2-like phenotype, characterized by enhanced expression of Tie2 and CD206/Mrc1. These colonies are long-lived depending on the contact with the endothelium; removal of the endothelial monolayer results in rapid colony dissolution. We further found that Csf1 produced by the endothelium is critical for the expansion of the macrophage colonies and that blockade of Csf1 receptor impairs colony growth. Functional analyses indicate that these macrophages are capable of accelerating angiogenesis, promoting tumor growth, and effectively engaging in tight associations with endothelial cells in vivo. These findings uncover a critical role of endothelial cells in the induction of macrophage differentiation and their ability to promote further polarization toward a proangiogenic phenotype. This work also highlights some of the molecules underlying the M2-like differentiation, a process that is relevant to the progression of both developmental and pathologic angiogenesis.
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Kaufman, Dan S., Rachel L. Lewis, Eric T. Hanson, Robert Auerbach, Johanna Plendl, and James A. Thomson. "Functional endothelial cells derived from rhesus monkey embryonic stem cells." Blood 103, no. 4 (February 15, 2004): 1325–32. http://dx.doi.org/10.1182/blood-2003-03-0799.
Full textAbstract:
Abstract We have used rhesus monkey embryonic stem (ES) cells to study endothelial cell development. Rhesus ES cells (R366.4 cell line) exposed to medium containing vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), insulin-like growth factor (IGF), and epidermal growth factor (EGF) assumed a relatively uniform endothelial cell morphology and could be propagated and expanded with a consistent phenotype and normal karyotype. When placed in Matrigel, these rhesus ES cell–derived endothelial cells (RESDECs) formed capillary-like structures characteristic of endothelial cells. Immunohistochemical and flow cytometric analysis of RESDECs showed that they take up acetylated low-density lipoprotein (LDL), express CD146, von Willebrand factor, and the integrin αvβ3, and bind the lectin ulex europaeus agglutinin-1. These cells also express the VEGF receptor Flk-1 and secrete VEGF. When introduced in a Matrigel plug implanted subcutaneously in mice, RESDECs formed intact vessels and recruited new endothelial cell growth. In vivo function was demonstrated by coinjection of RESDECs with murine tumor cells subcutaneously into immunocompromised adult mice. RESDECs injected alone did not form measurable tumors. Tumor cells grew more rapidly and had increased vascularization when coinjected with the RESDECs. Immunohistochemical staining demonstrated that the RESDECs participated in forming the tumor neovasculature. RESDECs provide a novel means to examine the mechanisms of endothelial cell development, and may open up new therapeutic strategies.