Effects of asymmetric dimethylarginine on apoptosis and expression of c-Jun N-terminal kinase in endothelial outgrowth cells
10.11958/20161043
- VernacularTitle:ADMA对内皮生长晕细胞凋亡及JNK表达的影响
- Author:
Fuqing ZHANG
;
Xin LI
;
Yahui HU
;
Zhanquan JIAO
;
Xiaolin TIAN
;
Jie LIU
- Keywords:
arginine;
apoptosis;
protein kinases;
JNK mitogen-activated protein kinases;
asyrmetric dimethylarginine;
endothelial outgrowth cells
- From:
Tianjin Medical Journal
2017;45(3):254-257,前插3
- CountryChina
- Language:Chinese
-
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.
