scholarly journals Synergic fabrication of succimer coated titanium dioxide nanomaterials delivery for in vitro proliferation and in vivo examination on human aortic endothelial cells

Drug Delivery ◽  
2021 ◽  
Vol 28 (1) ◽  
pp. 1785-1794
Author(s):  
Ming Qi ◽  
Chunfang Li ◽  
Ze Song ◽  
Lei Wang
1992 ◽  
Vol 262 (4) ◽  
pp. H1088-H1095 ◽  
Author(s):  
H. W. Farber ◽  
A. S. Antonov ◽  
Y. A. Romanov ◽  
V. N. Smirnov ◽  
L. M. Scarfo ◽  
...  

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.


2002 ◽  
Vol 165 (1) ◽  
pp. 69-77 ◽  
Author(s):  
Rosa A Rabini ◽  
Arianna Vignini ◽  
Eleonora Salvolini ◽  
Roberto Staffolani ◽  
Daniela Martarelli ◽  
...  

1997 ◽  
Vol 185 (12) ◽  
pp. 2069-2077 ◽  
Author(s):  
Leslie M. McEvoy ◽  
Hailing Sun ◽  
Philip S. Tsao ◽  
John P. Cooke ◽  
Judith A. Berliner ◽  
...  

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.


Author(s):  
Rahul Mittal ◽  
Vasanti M. Jhaveri ◽  
Sae-In Samantha Kay ◽  
Patricia Blackwelder ◽  
Kunal Patel

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.


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