Abstract: Abstract： Objective To investigate the effects of asymmetric dimethylarginine (ADMA) on apoptosis and phosphorylation of c-jun N-terminal kinase (JNK) in endothelial outgrowth cells (EOCs). Methods The mononuclear cells were harvested from umbilical cord blood by ficoll density gradient centrifugation, and induced into EOCs and then expanded in vitro. The identified EOCs were treated with different concentrations of ADMA (0, 1, 5, 10, 20 µmol/L) for 48 h.The adherent cells were treated with 10 µmol/L ADMA， then different concentrations of JNK specific inhibitor SP600125 (0，5， 10， 20 and 40 µmol /L) were added and incubated for 48 hours. Caspase-3 activity was measured by microplate reader.Apoptotic incidences of EOCs were quantitatively determined by flow cytometry. The expression of Caspase- 3 and phosphorylase- JNK (p- JNK) were detected by Western blot assay. Results The treatment of ADMA (1- 20 µmol/L)significantly induced apoptosis in EOCs by enhancing Caspase- 3 express and also induced phosphorylation of JNK (P＜0.05). Meantime, the JNK specific inhibitor SP600125 could attenuate the apoptosis induced by ADMA during this process(F=6.733， P＜0.05) and inhibit the expression of Caspase- 3 and p- JNK. Conclusion ADMA can induce apoptosis in EOC, which may be achieved by activating JNK signal transduction pathway.

Key words: arginine, apoptosis, protein kinases, JNK mitogen-activated protein kinases, asyrmetric dimethylarginine, endothelial outgrowth cells