Cytokine secretion by human aortic endothelial cells is related to degree of atherosclerosis

1992 ◽  
Vol 262 (4) ◽  
pp. H1088-H1095 ◽  
Author(s):  
H. W. Farber ◽  
A. S. Antonov ◽  
Y. A. Romanov ◽  
V. N. Smirnov ◽  
L. M. Scarfo ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cytokine Secretion ◽  
Aortic Endothelial Cells ◽  
Monocyte Migration ◽  
Morphological Heterogeneity ◽  
Human T Cell ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

We have previously described a 13- to 15-kDa T-lymphocyte-specific chemotactic protein (endothelial cell-derived lymphocyte chemoattractant activity, ED-LCA) secreted by serotonin-stimulated bovine aortic endothelial cells. In the current study, we have identified a similar serotonin-induced chemotaxin secreted by human aortic endothelial cells (HAEC). Like the bovine ED-LCA, secretion of this human T-cell chemotaxin peaked at 10(-5) M serotonin, was blocked by 5-HT2-receptor antagonists, and was not induced by other vasoactive amines, such as histamine or angiotensin II. In addition, human ED-LCA had no effect on neutrophil or monocyte migration. Using HAEC and human pulmonary arterial endothelial cells (HPAEC) from the same individual, we found that serotonin-stimulated HAEC, but not HPAEC, secreted ED-LCA. Because human vascular endothelium affected by atherosclerosis is morphologically, ultrastructurally, and phenotypically distinct from unaffected areas, we evaluated the secretion of this cytokine from cultured HAEC derived from areas of aorta differentially affected by atherosclerosis. We found that the degree of atherosclerotic involvement of an individual vessel was associated with a decrease in the uptake of serotonin and a reduction in serotonin-induced ED-LCA secretion. In response to serotonin, HAEC derived from atherosclerotic plaques did not secrete ED-LCA, whereas HAEC derived from fatty streaks secreted lesser amounts of ED-LCA than HAEC derived from normal areas. These studies demonstrate that in vivo morphological heterogeneity of HAEC is maintained in vitro and is associated with alterations in function, as measured by cytokine secretion.

Activation of human aortic endothelial cells by LDL from Type 1 diabetic patients: an in vitro study

2002 ◽  
Vol 165 (1) ◽  
pp. 69-77 ◽  
Author(s):  
Rosa A Rabini ◽  
Arianna Vignini ◽  
Eleonora Salvolini ◽  
Roberto Staffolani ◽  
Daniela Martarelli ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
In Vitro Study ◽  
Vitro Study ◽  
Diabetic Patients ◽  
Aortic Endothelial Cells ◽  
Type 1 Diabetic Patients ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

scholarly journals Novel Vascular Molecule Involved in Monocyte Adhesion to Aortic Endothelium in Models of Atherogenesis

1997 ◽  
Vol 185 (12) ◽  
pp. 2069-2077 ◽  
Author(s):  
Leslie M. McEvoy ◽  
Hailing Sun ◽  
Philip S. Tsao ◽  
John P. Cooke ◽  
Judith A. Berliner ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Ex Vivo ◽  
Critical Role ◽  
Constitutive Expression ◽  
Monocyte Adhesion ◽  
Aortic Endothelial Cells ◽  
Aortic Endothelium ◽  
Aortic Endothelial

Adhesion of monocytes to the endothelium in lesion-prone areas is one of the earliest events in fatty streak formation leading to atherogenesis. The molecular basis of increased monocyte adhesion is not fully characterized. We have identified a novel vascular monocyte adhesion-associated protein, VMAP-1, that plays a role in adhesion of monocytes to activated endothelium. Originally selected for its ability to block binding of a mouse monocyte-like cell line (WEHI78/24) to cytokine- or LPS-stimulated cultured mouse endothelial cells in vitro, antiVMAP-1 mAb LM151 cross-reacts with rabbit endothelium and blocks binding of human monocytes to cultured rabbit aortic endothelial cells stimulated with minimally modified low density lipoprotein, thought to be a physiologically relevant atherogenic stimulus. Most importantly, LM151 prevents adhesion of normal monocytes and monocytoid cells to intact aortic endothelium from cholesterol-fed rabbits in an ex vivo assay. VMAP-1 is a 50-kD protein. Immunohistology of vessels reveals focal constitutive expression in aorta and other large vessels. VMAP-1 is thus a novel vascular adhesion-associated protein that appears to play a critical role in monocyte adhesion to aortic endothelial cells in atherogenesis in vivo.

Pseudomonas aeruginosa Invades Human Aortic Endothelial Cells and Induces Cell Damage in vitro

2019 ◽  
Vol 19 (1) ◽  
pp. 45-50
Author(s):  
Rahul Mittal ◽  
Vasanti M. Jhaveri ◽  
Sae-In Samantha Kay ◽  
Patricia Blackwelder ◽  
Kunal Patel
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Endothelial Cells ◽  
Cell Damage ◽  
Severe Infection ◽  
Enzyme Linked Immunosorbent Assay ◽  
Mortality And Morbidity ◽  
Aortic Endothelial Cells ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

Background:Cardiovascular diseases such as endocarditis are the second most common cause of death worldwide. Infective Endocarditis (IE) is the most severe infection of the heart associated with significant mortality and morbidity. The binding and invasion of Human Aortic Endothelial Cells (HAECs) by pathogenic microbes can play an important role in the pathogenesis of IE.Objective:Pseudomonas aeruginosa is an emerging pathogen that has been associated with IE. However, it is not known whether P. aeruginosa can bind and interact with HAECs. The aim of this study was to determine whether P. aeruginosa can bind and colonize HAECs.Methods:The invasion of HAECs by P. aeruginosa was assessed by gentamicin protection assay. Cytokine levels were determined by enzyme-linked Immunosorbent Assay (ELISA) kits. Cell damage was determined by Lactate Dehydrogenase (LDH) assay.Results:P. aeruginosa can bind and invade HAECs. Infection of HAECs with P. aeruginosa induces TNF-α IL-1β, IL-6 and IL-8 cytokine production leading to the generation of inflammatory milieu that can cause tissue damage as observed in human clinical cases of IE. We also observed that P. aeruginosa induces cell damage in HAECs.Conclusion:In this study, we demonstrate for first time that P. aeruginosa can invade and survive inside HAECs. This cell culture model can be of immense importance to determine the efficacy of drug targets against IE.

Secretion of SPARC by endothelial cells transformed by polyoma middle T oncogene inhibits the growth of normal endothelial cells in vitro

1992 ◽  
Vol 70 (7) ◽  
pp. 579-592 ◽  
Author(s):  
E. Helene Sage
Keyword(s):  
Cell Cycle ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Conditioned Media ◽  
Capillary Endothelium ◽  
Aortic Endothelial Cells ◽  
Cells Cultured ◽  
Aortic Endothelial

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

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