Effect of L-arginine on asymmetric dimethylarginine (ADMA) or homocysteine-accelerated endothelial cell aging |
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Authors: | Scalera Fortunato Martens-Lobenhoffer Jens Täger Michael Bukowska Alicja Lendeckel Uwe Bode-Böger Stefanie M |
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Institution: | Institute of Clinical Pharmacology, University Hospital Otto-von-Guericke University, Magdeburg, Germany. |
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Abstract: | We investigated here the effect of l-arginine on asymmetric dimethylarginine (ADMA) or homocysteine-accelerated endothelial aging. Endothelial cells were cultured in medium containing 70micromol/L arginine until fourteenth passage. ADMA, dl-homocysteine, and l-arginine were replaced every 48h starting at the fourth passage. ADMA or homocysteine inhibited significantly the population doublings (PD) and accelerated the process of aging. Co-incubation with l-arginine enhanced PD, inhibited senescence associated beta-galactosidase activity, and increased telomerase activity. This effect was associated with an increase in NO synthesis and NO synthase protein expression. Furthermore, l-arginine-induced NO formation was accompanied by a reduction in oxidative stress and an increase in protein expression and enzyme activity of heme oxygenase (HO)-1. The NO synthase inhibitor l-NAME completely abolished the effect of l-arginine on ADMA or homocysteine-accelerated aging. These findings demonstrate that l-arginine prevents the onset of endothelial aging in ADMA or homocysteine-treated cells by increasing NO formation and consequently the induction of HO-1. This might provide a new strategy to delay ADMA or homocysteine-accelerated aging. |
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Keywords: | Arginine Aging Nitric oxide Heme oxygenase-1 Asymmetric dimethylarginine Homocysteine Oxidative stress Telomerase Senescence l-NAME" target="_blank">l-NAME |
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