scholarly journals Salvianolic acid B protects human endothelial cells from oxidative stress damage: a possible protective role of glucose-regulated protein 78 induction

2008 ◽  
Vol 81 (1) ◽  
pp. 148-158 ◽  
Author(s):  
H.-L. Wu ◽  
Y.-H. Li ◽  
Y.-H. Lin ◽  
R. Wang ◽  
Y.-B. Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Protective Role ◽  
Salvianolic Acid B ◽  
Human Endothelial Cells ◽  
Salvianolic Acid ◽  
Stress Damage ◽  
Glucose Regulated Protein

scholarly journals Cytoprotection of human endothelial cells from oxidative stress by polyphenols: the role of gene expression versus direct antioxidant effect

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Xinyu Wang ◽  
James Bynum ◽  
Salomon Stavchansky ◽  
Michael Dubick ◽  
Robert Hackman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Endothelial Cells ◽  
Antioxidant Effect ◽  
Human Endothelial Cells

The role of oxidative stress in pro-inflammatory activation of human endothelial cells on Ti6Al4V alloy

Biomaterials ◽  
2013 ◽  
Vol 34 (33) ◽  
pp. 8075-8085 ◽  
Author(s):  
Roman Tsaryk ◽  
Kirsten Peters ◽  
Susanne Barth ◽  
Ronald E. Unger ◽  
Dieter Scharnweber ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Ti6al4v Alloy ◽  
Human Endothelial Cells ◽  
Inflammatory Activation

scholarly journals Lp(a) and LDL induce apoptosis in human endothelial cells and in rabbit aorta: Role of oxidative stress

1999 ◽  
Vol 55 (4) ◽  
pp. 1450-1461 ◽  
Author(s):  
Jan Galle ◽  
Reinhard Schneider ◽  
Alexandra Heinloth ◽  
Christoph Wanner ◽  
Peter R. Galle ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Rabbit Aorta ◽  
Human Endothelial Cells

scholarly journals Sirt1 Inhibits Oxidative Stress in Vascular Endothelial Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Weijin Zhang ◽  
Qiaobing Huang ◽  
Zhenhua Zeng ◽  
Jie Wu ◽  
Yaoyuan Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Protective Role ◽  
Vascular Endothelial ◽  
Protective Effects ◽  
Beneficial Effects ◽  
Key Factor ◽  
Antioxidative Stress

The vascular endothelium is a layer of cells lining the inner surface of vessels, serving as a barrier that mediates microenvironment homeostasis. Deterioration of either the structure or function of endothelial cells (ECs) results in a variety of cardiovascular diseases. Previous studies have shown that reactive oxygen species (ROS) is a key factor that contributes to the impairment of ECs and the subsequent endothelial dysfunction. The longevity regulator Sirt1 is a NAD+-dependent deacetylase that has a potential antioxidative stress activity in vascular ECs. The mechanisms underlying the protective effects involve Sirt1/FOXOs, Sirt1/NF-κB, Sirt1/NOX, Sirt1/SOD, and Sirt1/eNOs pathways. In this review, we summarize the most recent reports in this field to recapitulate the potent mechanisms involving the protective role of Sirt1 in oxidative stress and to highlight the beneficial effects of Sirt1 on cardiovascular functions.

scholarly journals Inhibition of miR‐155 Attenuates Detrimental Vascular Effects of Tobacco Cigarette Smoking

2020 ◽  
Vol 9 (24) ◽  
Author(s):  
Giacomo Frati ◽  
Maurizio Forte ◽  
Flavio di Nonno ◽  
Antonella Bordin ◽  
Isotta Chimenti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Cigarette Smoking ◽  
Cigarette Smoke ◽  
Healthy Subjects ◽  
Cigarette Smoke Condensate ◽  
Human Endothelial Cells ◽  
Vascular Effects ◽  
Tobacco Cigarette

Background The role of microRNAs dysregulation in tobacco cigarette smoking–induced vascular damage still needs to be clarified. We assessed the acute effects of tobacco cigarette smoking on endothelial cell‐related circulating microRNAs in healthy subjects. In addition, we investigated the potential role of microRNAs in smoking‐dependent endothelial cell damage. Methods and Results A panel of endothelial‐related microRNAs was quantified in healthy subjects before and after smoking 1 tobacco cigarette. Serum levels of miR‐155 were found to be significantly increased shortly after smoking. We also observed a progressive and significant miR‐155 accumulation in culture media of human endothelial cells after 30 minutes and up to 4 hours of cigarette smoke condensate treatment in vitro without evidence of cell death, indicating that miR‐155 can be released by endothelial cells in response to smoking stress. Cigarette smoke condensate appeared to enhance oxidative stress and impair cell survival, angiogenesis, and NO metabolism in human endothelial cells. Notably, these effects were abrogated by miR‐155 inhibition. We also observed that miR‐155 inhibition rescued the deleterious effects of cigarette smoke condensate on endothelial‐mediated vascular relaxation and oxidative stress in isolated mouse mesenteric arteries. Finally, we found that exogenous miR‐155 overexpression mimics the effects of smoking stress by inducing the upregulation of inflammatory markers, impairing angiogenesis and reducing cell survival. These deleterious effects were associated with downregulation of vascular endothelial growth factor and endothelial NO synthetase. Conclusions Our results suggest that miR‐155 dysregulation may contribute to the deleterious vascular effects of tobacco smoking.

scholarly journals Potentiation of complement regulator factor H protects human endothelial cells from complement attack in aHUS sera

2019 ◽  
Vol 3 (4) ◽  
pp. 621-632 ◽  
Author(s):  
Richard B. Pouw ◽  
Mieke C. Brouwer ◽  
Marlon de Gast ◽  
Anna E. van Beek ◽  
Lambertus P. van den Heuvel ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Complement Activation ◽  
Protective Role ◽  
Human Cells ◽  
Factor H ◽  
Human Endothelial Cells ◽  
Complement Regulation ◽  
Wide Range ◽  
Complement Regulator

Abstract Mutations in the gene encoding for complement regulator factor H (FH) severely disrupt its normal function to protect human cells from unwanted complement activation, resulting in diseases such as atypical hemolytic uremic syndrome (aHUS). aHUS presents with severe hemolytic anemia, thrombocytopenia, and renal disease, leading to end-stage renal failure. Treatment of severe complement-mediated disease, such as aHUS, by inhibiting the terminal complement pathway, has proven to be successful but at the same time fails to preserve the protective role of complement against pathogens. To improve complement regulation on human cells without interfering with antimicrobial activity, we identified an anti-FH monoclonal antibody (mAb) that induced increased FH-mediated protection of primary human endothelial cells from complement, while preserving the complement-mediated killing of bacteria. Moreover, this FH-activating mAb restored complement regulation in sera from aHUS patients carrying various heterozygous mutations in FH known to impair FH function and dysregulate complement activation. Our data suggest that FH normally circulates in a less active conformation and can become more active, allowing enhanced complement regulation on human cells. Antibody-mediated potentiation of FH may serve as a highly effective approach to inhibit unwanted complement activation on human cells in a wide range of hematological diseases while preserving the protective role of complement against pathogens.

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