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 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 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.

Dual effect of oxidized LDL on cell cycle in human endothelial cells through oxidative stress

2001 ◽  
Vol 59 (s78) ◽  
pp. 120-123 ◽  
Author(s):  
Jan Galle ◽  
Alexandra Heinloth ◽  
Christoph Wanner ◽  
Kathrin Heermeier
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Endothelial Cells ◽  
Oxidized Ldl ◽  
Human Endothelial Cells ◽  
Dual Effect

scholarly journals Peroxiredoxin 6 is required for blood vessel integrity in wounded skin

2007 ◽  
Vol 179 (4) ◽  
pp. 747-760 ◽  
Author(s):  
Angelika Kümin ◽  
Matthias Schäfer ◽  
Nikolas Epp ◽  
Philippe Bugnon ◽  
Christiane Born-Berclaz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Wound Healing ◽  
Endothelial Cells ◽  
Ultrastructural Level ◽  
Peroxiredoxin 6 ◽  
Severe Hemorrhage ◽  
Vessel Integrity ◽  
Knockout Animals

Peroxiredoxin 6 (Prdx6) is a cytoprotective enzyme with largely unknown in vivo functions. Here, we use Prdx6 knockout mice to determine its role in UV protection and wound healing. UV-mediated keratinocyte apoptosis is enhanced in Prdx6-deficient mice. Upon skin injury, we observe a severe hemorrhage in the granulation tissue of knockout animals, which correlates with the extent of oxidative stress. At the ultrastructural level endothelial cells appear highly damaged, and their rate of apoptosis is enhanced. Knock-down of Prdx6 in cultured endothelial cells also increases their susceptibility to oxidative stress, thus confirming the sensitivity of this cell type to loss of Prdx6. Wound healing studies in bone marrow chimeric mice demonstrate that Prdx6-deficient inflammatory and endothelial cells contribute to the hemorrhage phenotype. These results provide insight into the cross-talk between hematopoietic and resident cells at the wound site and the role of reactive oxygen species in this interplay.

scholarly journals LR-90 prevents methylglyoxal-induced oxidative stress and apoptosis in human endothelial cells

APOPTOSIS ◽  
2014 ◽  
Vol 19 (5) ◽  
pp. 776-788 ◽  
Author(s):  
James L. Figarola ◽  
Jyotsana Singhal ◽  
Samuel Rahbar ◽  
Sanjay Awasthi ◽  
Sharad S. Singhal
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Human Endothelial Cells

scholarly journals Vitamin E Analogues Inhibit Angiogenesis by Selective Induction of Apoptosis in Proliferating Endothelial Cells: The Role of Oxidative Stress

2007 ◽  
Vol 67 (24) ◽  
pp. 11906-11913 ◽  
Author(s):  
L.-F. Dong ◽  
E. Swettenham ◽  
J. Eliasson ◽  
X.-F. Wang ◽  
M. Gold ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Vitamin E ◽  
Induction Of Apoptosis
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