Endothelial dysfunction and nutraceutical approaches: In vitro system to study the modulation of metabolic markers on human aortic endothelial cells

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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In Vitro Effects of Hollow Gold Nanoshells on Human Aortic Endothelial Cells

Nanoscale Research Letters ◽

10.1186/s11671-016-1620-5 ◽

2016 ◽

Vol 11 (1) ◽

Cited By ~ 5

Author(s):

Chunrong Gu ◽

Hengfang Wu ◽

Gaoyuan Ge ◽

Xiongzhi Li ◽

Zhirui Guo ◽

...

Keyword(s):

Endothelial Cells ◽

Gold Nanoshells ◽

Aortic Endothelial Cells ◽

Hollow Gold Nanoshells ◽

In Vitro Effects ◽

Human Aortic Endothelial Cells ◽

Aortic Endothelial

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Vitamin E Inhibits Low-Density Lipoprotein–Induced Adhesion of Monocytes to Human Aortic Endothelial Cells In Vitro

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/01.atv.17.3.429 ◽

1997 ◽

Vol 17 (3) ◽

pp. 429-436 ◽

Cited By ~ 90

Author(s):

Antonio Martin ◽

Thomas Foxall ◽

Jeffrey B. Blumberg ◽

Mohsen Meydani

Keyword(s):

Endothelial Cells ◽

Vitamin E ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Low Density ◽

Aortic Endothelial Cells ◽

Human Aortic Endothelial Cells ◽

Aortic Endothelial

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The protease inhibitor E64d improves ox-LDL-induced endothelial dysfunction in human aortic endothelial cells

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2017-0016 ◽

2018 ◽

Vol 96 (2) ◽

pp. 120-127 ◽

Cited By ~ 5

Author(s):

Min Chen ◽

Lina Ren ◽

Yanyan Meng ◽

Liye Shi ◽

Ling Chen ◽

...

Keyword(s):

Endothelial Cells ◽

Endothelial Dysfunction ◽

Protease Inhibitor ◽

Cysteine Protease Inhibitor ◽

Intercellular Adhesion Molecule ◽

Matrix Remodeling ◽

Migration Ability ◽

Aortic Endothelial Cells ◽

Human Aortic Endothelial Cells ◽

Aortic Endothelial

Oxidized low-density lipoprotein (ox-LDL)-induced endothelial dysfunction in human vascular endothelial cells contributes to the development of atherosclerosis. E64d, a cysteine protease inhibitor, blocks the elastolytic activity of cathepsin essential for vascular matrix remodeling and reduces neurovascular endothelial apoptosis. The objective of this study was to investigate the effects and the underling mechanisms of E64d on ox-LDL-induced endothelial dysfunction in human aortic endothelial cells (HAECs). HAECs were treated with various concentrations of ox-LDL (0–200 mg/L) for 24 h with or without E64d. The results showed that E64d attenuated ox-LDL-induced increase in soluble intercellular adhesion molecule-1 (sICAM-1) concentration and reduction in endothelial nitric oxide synthase (eNOS) expression, prevented ox-LDL-induced reduction in cell viability and migration ability of HAECs. E64d decreased the protein expression of cathepsin B (CTSB), Beclin 1, and microtubule-associated protein light chain 3 (LC3)-II, but not p62. LC3 puncta and autophagosome formation were also reduced by E64d in HAECs. Moreover, E64d decreased the production of MDA and increased the activity of SOD. The results showed that E64d ameliorated ox-LDL-induced endothelial dysfunction in HAECs.

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