oxLDL reduced endothelial progenitor cells survival and function via regulating Akt/eNOS signal pathway.
- Author:
Feng-xia MA
1
;
Qian REN
;
Zhong-chao HAN
Author Information
- Publication Type:Journal Article
- MeSH: Cells, Cultured; Endothelial Cells; cytology; metabolism; Humans; Lipoproteins, LDL; metabolism; Nitric Oxide Synthase Type III; metabolism; Phosphorylation; Proto-Oncogene Proteins c-akt; metabolism; Signal Transduction; Stem Cells; cytology; metabolism; Umbilical Veins; cytology
- From: Chinese Journal of Cardiology 2007;35(2):173-177
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo 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.
METHODSAfter 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.
RESULTSIncubation 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.
CONCLUSIONoxLDL reduced EPC survival and function via regulating Akt/eNOS signal pathway.