The effect of experimental hyperglycaemia on endothelial function and mitochondrial activity in human aortic endothelial cells

2018 ◽  
Vol 275 ◽  
pp. e122
Author(s):  
A. Strembitska ◽  
I.P. Salt ◽  
G. Baillie
Keyword(s):  
Endothelial Cells ◽  
Endothelial Function ◽  
Mitochondrial Activity ◽  
Aortic Endothelial Cells ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

scholarly journals Glyoxalase 1-knockdown in human aortic endothelial cells – effect on the proteome and endothelial function estimates

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Bernd Stratmann ◽  
Britta Engelbrecht ◽  
Britta C. Espelage ◽  
Nadine Klusmeier ◽  
Janina Tiemann ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Function ◽  
Aortic Endothelial Cells ◽  
Glyoxalase 1 ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

scholarly journals Effect of Hot Water Extracts of Maqui Berry on Human Aortic Endothelial Cells Exposed to a Hyperglycemic Environment

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 435-435
Author(s):  
Keith Martin
Keyword(s):  
Endothelial Cells ◽  
Endothelial Function ◽  
Final Concentration ◽  
Water Soluble ◽  
Hot Water ◽  
No Production ◽  
Aortic Endothelial Cells ◽  
Maqui Berry ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

Abstract Objectives Impaired endothelial function is associated with many chronic vascular-related diseases including cardiovascular disease, inflammation, and diabetes. The antioxidant-rich Maqui berry (Aristotelia chilensis) has received increasing attention due to a variety of bioactivities including reduction of inflammation, control of blood glucose, and improvement of heart health, e.g., aortic endothelium, but corroborative research is needed. In the present study, we investigated the effects of aqueous Maqui berry extract (MBE) on nitric oxide (NO) production and oxidative stress (ROS) generation in human aortic endothelial cells (HAEC) alone or in a hyperglycemic environment with or without insulin. Methods Sterile (0.22 um filtered) MBE was added to endothelial basal medium (5% v/v) alone or containing glucose (final concentration 600 mg/dL; 33.3 mM) and/or insulin (final concentration 100 nM) followed by addition to monolayers and incubation for 24 hours. Monolayers were then assayed for NO production via the Greiss reaction, ROS via the use of DCFH-DA, and viability using MTT. Results We show that MBE may have increased ROS levels by 1.8-fold (P < 0.05) compared to control cultures using the DCFH-DA assay but decreased by ∼13% in the presence of glucose with or without insulin. MBE also increased NO levels by 3-fold (P < 0.05) compared to levels in control cultures. Glucose inclusion reduced NO by 15% and insulin reduced levels to that of control with or without glucose present. Viability, determined by MTT reduction, was not different between any of the groups. Conclusions The results suggest that water-soluble components of MB may modulate NO production in a hyperglycemic and/or hyperinsulinemic microenvironment and potentially improve endothelial function, in part, via the potential vasorelaxation properties of NO. Funding Sources School of Health Studies, University of Memphis.

scholarly journals P773Uric acid regulates multiple interacting major cellular pathways in human aortic endothelial cells: a global proteome approach

2014 ◽  
Vol 103 (suppl 1) ◽  
pp. S142.1-S142
Author(s):  
A Oberbach ◽  
V Adams ◽  
N Schlichting ◽  
N Jehmich ◽  
U Voelker ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Aortic Endothelial Cells ◽  
Cellular Pathways ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

scholarly journals Sensitization of Human Aortic Endothelial Cells to Lipopolysaccharide via Regulation of Toll-Like Receptor 4 by Bacterial Fimbria-Dependent Invasion

2005 ◽  
Vol 73 (12) ◽  
pp. 8050-8059 ◽  
Author(s):  
Hiromichi Yumoto ◽  
Hsin-Hua Chou ◽  
Yusuke Takahashi ◽  
Michael Davey ◽  
Frank C. Gibson ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Periodontal Disease ◽  
Deficient Mutant ◽  
Wild Type ◽  
Microbial Infection ◽  
Monocyte Chemoattractant Protein 1 ◽  
Aortic Endothelial Cells ◽  
E Coli ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

ABSTRACT Toll-like receptors (TLRs) are differentially up-regulated in response to microbial infection and chronic inflammatory diseases such as atherosclerosis. Epidemiological data support the idea that periodontal disease may be a risk factor for acceleration of atherosclerosis. Porphyromonas gingivalis, the etiological agent of periodontal disease, invades endothelium, has been detected in human atheromatous tissue, and accelerates atheroma formation in apolipoprotein E−/− mice with concurrent induction of TLRs in the aorta. As endothelial cells can present antigen via TLRs and play an important role in the development of atherosclerosis, we examined TLR expression in human aortic endothelial cells (HAEC) cultured with wild-type P. gingivalis, a fimbria-deficient mutant, and purified antigens. We observed increased TLR expression in HAEC infected with wild-type P. gingivalis by fluorescence-activated cell sorter, but not with noninvasive, fimbria-deficient mutant or purified P. gingivalis antigens. Following a wild-type P. gingivalis challenge, functional TLR2 and TLR4 activation was assessed by subsequent stimulation with TLR agonists Staphylococcus aureus lipoteichoic acid (SLTA; TLR2 ligand) and Escherichia coli lipopolysaccharide (LPS; TLR4 ligand). Unchallenged HAEC failed to elicit monocyte chemoattractant protein 1 (MCP-1) in response to LPS or SLTA but did so when cultured with wild-type P. gingivalis. P. gingivalis-induced TLR2 and -4 expression on HAEC functionally reacted to SLTA and E. coli LPS as measured by a further increase in MCP-1 production. Furthermore, MCP-1 expression elicited by E. coli LPS was inhibitable with TLR4-specific antibody and polymyxin B. These results indicate that invasive P. gingivalis stimulates TLR expression on the surface of endothelium and these primed cells respond to defined TLR-specific ligands.

scholarly journals Vitamin D3 attenuates doxorubicin-induced senescence of human aortic endothelial cells by upregulation of IL-10 via the pAMPKα/Sirt1/Foxo3a signaling pathway

PLoS ONE ◽  
2021 ◽  
Vol 16 (6) ◽  
pp. e0252816
Author(s):  
Lei Chen ◽  
Rachel Holder ◽  
Charles Porter ◽  
Zubair Shah
Keyword(s):  
Endothelial Cells ◽  
Vitamin D3 ◽  
Protective Effects ◽  
Cardiovascular Toxicity ◽  
Complex Activity ◽  
Aortic Endothelial Cells ◽  
Cardiovascular Damage ◽  
Cycle Arrest ◽  
Human Aortic Endothelial Cells ◽  
Aortic Endothelial

The toxicity of doxorubicin to the cardiovascular system often limits its benefits and widespread use as chemotherapy. The mechanisms involved in doxorubicin-induced cardiovascular damage and possible protective interventions are not well-explored. Using human aortic endothelial cells, we show vitamin D3 strongly attenuates doxorubicin-induced senescence and cell cycle arrest. We further show the protective effects of vitamin D3 are mediated by the upregulation of IL-10 and FOXO3a expression through fine modulation of pAMPKα/SIRT1/FOXO3a complex activity. These results have great significance in finding a target for mitigating doxorubicin-induced cardiovascular toxicity.

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