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Cited by 85

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Aspirin reduces endothelial cell senescence

Bode-Böger, Stefanie M., Martens-Lobenhoffer, Jens, Täger, Michael, Schröder, Henning, Scalera, Fortunato·2005·Biochemical and Biophysical Research Communications
DOI 10.1016/j.bbrc.2005.07.014
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Abstract

We report here the effect of aspirin on the onset of replicative senescence. Endothelial cells that were cultured until cumulative population doublings 40 showed clear signs of aging. Incubation with aspirin inhibited senescence-associated beta-galactosidase activity and increased telomerase activity. Along with the delayed onset of senescence, aspirin decreased reactive oxygen species and increased nitric oxide (NO) and cGMP levels. Furthermore, aspirin reduced the elaboration of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NO synthase, and up-regulated the activity of dimethylarginine dimethylaminohydrolase, the enzyme that degrades ADMA. These effects were specific in that other nonsteroidal anti-inflammatory drugs, such as ibuprofen or acetaminophen, did not prevent the onset of endothelial senescence. The NO synthase inhibitor l-NAME, but not its inactive d-enantiomer, led to complete inhibition of aspirin-delayed senescence. These findings demonstrate that aspirin delays the onset of endothelial senescence by preventing a decrease in NO formation/generation. This might provide a therapeutic strategy aimed at blocking aging-induced NO inhibition.

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Cited by

Metadata

Authors
Bode-Böger, S. M., Martens-Lobenhoffer, J., Täger, M., Schröder, H., & Scalera, F.
Venue
Biochemical and Biophysical Research Communications
Publisher
Elsevier BV
Published
2005-09
Volume
334
Issue
4
Pages
1226-1232
ISSN
0006-291X
DOI
10.1016/j.bbrc.2005.07.014
Cited by
85
References
2
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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