[oxLDL reduced endothelial progenitor cells survival and function via regulating Akt/eNOS signal pathway].

Objective: To investigate the association between Akt/eNOS signal pathway changes and the survival/function of endothelial progenitor cells (EPC) in the presence of oxLDL, L-NAME or triciribine.

Methods: After 14 d culture, EPC was stimulated with different concentrations of oxLDL, L-NAME or triciribine for 48 h. In one group, EPC was preincubated with L-arginine for 24 h and then exposed to 50 microg/ml oxLDL for 48 h. The survival and the ability of adhesion, migration and tube structure formation of EPC were observed and the level of phosphorylated Akt protein expression, eNOS protein and mRNA expression were assayed.

Results: Incubation with oxLDL at concentration 25 microg/ml or higher resulted EPC apoptosis, significantly reduced migratory rate, reduced adhesion to fibronectin and impaired ability of EPC to form tube structure in a dose-dependent manner. A simultaneous dose-dependent NO generation and Akt phosphorylation decrease as well as eNOS expression reduction at protein and mRNA levels were also observed. Pretreatment of EPC with L-arginine could attenuate these changes.

Conclusion: oxLDL reduced EPC survival and function via regulating Akt/eNOS signal pathway.