Senescence-associated cell death of human endothelial cells: the role of oxidative stress

2003 ◽  
Vol 38 (10) ◽  
pp. 1149-1160 ◽  
Author(s):  
H Unterluggauer
2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Xinyu Wang ◽  
James Bynum ◽  
Salomon Stavchansky ◽  
Michael Dubick ◽  
Robert Hackman ◽  
...  

Biomaterials ◽  
2013 ◽  
Vol 34 (33) ◽  
pp. 8075-8085 ◽  
Author(s):  
Roman Tsaryk ◽  
Kirsten Peters ◽  
Susanne Barth ◽  
Ronald E. Unger ◽  
Dieter Scharnweber ◽  
...  

1999 ◽  
Vol 55 (4) ◽  
pp. 1450-1461 ◽  
Author(s):  
Jan Galle ◽  
Reinhard Schneider ◽  
Alexandra Heinloth ◽  
Christoph Wanner ◽  
Peter R. Galle ◽  
...  

2010 ◽  
Vol 45 (7-8) ◽  
pp. 638-644 ◽  
Author(s):  
Thomas Diener ◽  
Michael Neuhaus ◽  
Rafal Koziel ◽  
Lucia Micutkova ◽  
Pidder Jansen-Dürr

2020 ◽  
Vol 9 (24) ◽  
Author(s):  
Giacomo Frati ◽  
Maurizio Forte ◽  
Flavio di Nonno ◽  
Antonella Bordin ◽  
Isotta Chimenti ◽  
...  

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.


2001 ◽  
Vol 59 (s78) ◽  
pp. 120-123 ◽  
Author(s):  
Jan Galle ◽  
Alexandra Heinloth ◽  
Christoph Wanner ◽  
Kathrin Heermeier

2021 ◽  
Vol 165 ◽  
pp. 35
Author(s):  
Rebeca Osca-Verdegal ◽  
Jesús Beltrán-García ◽  
Ana B. Paes ◽  
Elena Nacher-Sendra ◽  
Federico V. Pallardó ◽  
...  

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