Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10765730 | Biochemical and Biophysical Research Communications | 2009 | 6 Pages |
Abstract
We have recently shown that inhibition of nitric oxide (NO) synthesis by asymmetrical dimethylarginine (ADMA) accelerated endothelial cell (EC) senescence which was prevented by coincubation with l-arginine; however the effect of long-term treatment of l-arginine alone on senescence of ECs have not been investigated. Human ECs were cultured in medium containing different concentrations of l-arginine until senescence. l-Arginine paradoxically accelerated senescence indicated by inhibiting telomerase activity. Moreover, l-arginine decreased NO metabolites, increased peroxynitrite, and 8-iso-prostaglandin F2α formation. In old cells, the mRNA expression of human amino acid transporter (hCAT)2B, the activity and protein expression of arginase II were upregulated indicated by enhanced urea, l-ornithine, and l-arginine consumption. Inhibition of arginase activity, or transfection with arginase II siRNA prevented l-arginine-accelerated senescence. The most possible explanation for the paradoxical acceleration of senescence by l-arginine so far may be the translational and posttranslational activation of arginase II.
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Authors
Fortunato Scalera, Ellen I. Closs, Eva Flick, Jens Martens-Lobenhoffer, Jean P. Boissel, Uwe Lendeckel, Anke Heimburg, Stefanie M. Bode-Böger,