scholarly journals Inhibitory effect of serotonin derivatives on high glucose-induced adhesion and migration of monocytes on human aortic endothelial cells

2009 ◽  
Vol 102 (2) ◽  
pp. 264-272 ◽  
Author(s):  
Rosaria Piga ◽  
Yuji Naito ◽  
Satoshi Kokura ◽  
Osamu Handa ◽  
Toshikazu Yoshikawa
Keyword(s):  
Endothelial Cells ◽  
High Glucose ◽  
Atherosclerotic Lesion ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Aortic Endothelial Cells ◽  
Serotonin Derivatives ◽  
And Migration ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

Previous reports have shown that safflower-seed extract and its major antioxidant constituents, serotonin hydroxycinnamic amides, attenuated atherosclerotic lesion formation in apoE-deficient mice, as well as inflammation and aortic stiffness in human subjects. In the present report, we examined a still unknown cell-based mechanism of serotonin derivatives against the development of atherosclerosis, focusing our attention on their action against the increase of adhesion molecules and the release of chemotactic factors on human aortic endothelial cells, phenomena that represent the key events in the early stages of atherosclerogenesis. Serotonin derivatives N-(p-coumaroyl)serotonin and N-feruloylserotonin exerted an inhibitory effect on short-term high glucose-induced up-regulation of mRNA and protein of adhesion and migration factors, and the consequent adhesion and migration of monocytes to endothelial cells; they inhibited the activation of transcription factors such as NF-κB, and the overproduction of the mitochondrial superoxide by acting as scavengers of the superoxide radical. In addition, serotonin derivative concentration inside the cells and inside the mitochondria was increased in a time-dependent manner. These results identify a mechanism of action of serotonin derivatives against endothelial damage at a cellular level, and underline their benefits against the disorders and complications related to reactive oxygen species.

De novo emergence of insulin-stimulated glucose uptake in human aortic endothelial cells incubated with high glucose

2006 ◽  
Vol 290 (3) ◽  
pp. E516-E522 ◽  
Author(s):  
Aidar R. Gosmanov ◽  
Frankie B. Stentz ◽  
Abbas E. Kitabchi
Keyword(s):  
Endothelial Cells ◽  
Insulin Receptor ◽  
Glucose Uptake ◽  
Insulin Signaling ◽  
High Glucose ◽  
Time Dependent ◽  
Dependent Manner ◽  
Aortic Endothelial Cells ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

Elevated glucose concentrations have profound effects on cell function. We hypothesized that incubation of human aortic endothelial cells (HAEC) with high glucose increases insulin signaling and develops the appearance of insulin-stimulated glucose uptake by the cells. Compared with 5 mM glucose, incubation of HAEC with 30 mM glucose for up to 48 h increased in a time-dependent manner expression of insulin receptor, insulin receptor substrate (IRS)-1, IRS-2, and GLUT1 proteins. High glucose also increased the specific binding of 125I-labeled insulin in HAEC accompanied by accelerated production of interleukin (IL)-6 and IL-8. Short-term stimulation by 50 μU/ml insulin did not activate [14C]glucose uptake by HAEC incubated in 5 mM glucose. However, an addition of insulin to high glucose-exposed endothelial cells led to a significant increase in [14C]glucose uptake in a glucose concentration- and time-dependent fashion, reaching a plateau at 48 h of incubation. Furthermore, incubation of HAEC with 30 mM glucose resulted in a new insulin-stimulated extracellular signal-regulated kinase-1/2 mitogen-activated protein kinase phosphorylation and increased lipid peroxidation and production of reactive oxygen species. These studies show for the first time that high glucose increases expression of insulin receptors and downstream elements of the insulin-signaling pathway and transforms “insulin-resistant” aortic endothelial cells into “insulin-sensitive” tissue regarding glucose uptake.

Modulation of tissue factor and thrombomodulin expression in human aortic endothelial cells incubated with high glucose

2010 ◽  
Vol 49 (2) ◽  
pp. 125-130 ◽  
Author(s):  
Huang-Joe Wang ◽  
Huey-Chun Huang ◽  
Yi-Ching Chuang ◽  
Pei-Ju Liao ◽  
Den-Mei Yang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tissue Factor ◽  
High Glucose ◽  
Aortic Endothelial Cells ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

scholarly journals Insulin Inhibits NFκB and MCP-1 Expression in Human Aortic Endothelial Cells

2001 ◽  
Vol 86 (1) ◽  
pp. 450-453 ◽  
Author(s):  
Ahmad Aljada ◽  
Husam Ghanim ◽  
Rana Saadeh ◽  
Paresh Dandona
Keyword(s):  
Endothelial Cells ◽  
Nuclear Factor Κb ◽  
Inhibitory Effect ◽  
Binding Activity ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Monocyte Chemoattractant Protein 1 ◽  
Aortic Endothelial Cells ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

In view of our recent demonstration that insulin inhibits the expression of intercellular adhesion molecule-1 (ICAM-1) and the fact that ICAM-1 expression is known to be modulated by nuclear factor-κB (NFκB), we have now investigated whether insulin inhibits intranuclear NFκB binding activity. We have also investigated whether insulin inhibits the pro-inflammatory chemokine, monocyte chemoattractant protein-1 (MCP-1), which attracts leucocytes to the inflamed sites and is also regulated by NFκB. Insulin was incubated with cultured human aortic endothelial cells (HAEC) at 0, 100 and 1000μ U/mL. Intranuclear NFκB binding activity was suppressed by approximately 45% at 100 μU/mL and by 60% at 1000 μU/mL (p< 0.05). MCP-1 mRNA expression was also suppressed by 47% at 100μ U/mL and by 79% at 1000 μU/mL (p < 0.05). We conclude that insulin at physiologically relevant concentrations exerts an inhibitory effect on the cardinal pro-inflammatory transcription factor NFκB and the pro-inflammatory chemokine MCP-1; these effects suggest an anti-inflammatory and potential anti-atherogenic effects of insulin.

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