Fluid shear stress upregulated endothelial nitric oxide synthase gene expression and nitric oxide formation in human endothelial progenitor cells.
- Author:
Zhen YANG
1
;
Jun TAO
;
Jie-Mei WANG
;
Chang TU
;
Ming-Guo XU
;
Yan WANG
;
Long CHEN
;
Chu-Fan LUO
;
An-Li TANG
;
Hong MA
Author Information
- Publication Type:Journal Article
- MeSH: Cell Differentiation; Cells, Cultured; Endothelial Cells; cytology; metabolism; secretion; Humans; Nitric Oxide; metabolism; Nitric Oxide Synthase Type III; genetics; metabolism; Stem Cells; cytology; metabolism; secretion; Stress, Mechanical
- From: Chinese Journal of Cardiology 2007;35(4):359-362
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of fluid shear stress on the eNOS gene expression and NO production in endothelial progenitor cells (EPCs).
METHODSThe peripheral blood mononuclear cells from healthy volunteers were inducted into EPCs and divided into stationary group (0 dyn/cm(2), 1 dyn/cm(2) = 0.1 Pa), low-flow shear stress group (5 dyn/cm(2)), medium-flow shear stress group (15 dyn/cm(2)) and high-flow shear stress group (25 dyn/cm(2)). The effects of shear stress on the endothelial nitric oxide synthase (eNOS) gene expression and nitric oxide (NO) production in human EPCs were measured.
RESULTSTypical "spindle-shaped" appearance was shown in EPCs derived from peripheral blood mononuclear cells and were positively labeled by acetylated-LDL, lectin, FLK-1 and vWF. After 4 hours treatment with various shear stresses, the ratio of eNOS/beta-actin mRNA expression by human EPCs in low, medium and high-flow shear stress group was 0.364, 0.505 and 0.548 respectively, which was significantly higher than that in stationary group (0.183, all P < 0.05) and the NO secretion in human EPCs in low, medium and high-flow shear stress group was also significantly higher than that in stationary group (all P < 0.05).
CONCLUSIONFluid shear stress enhances the eNOS mRNA expression and NO secretion in human EPCs, therefore, shear stress could potentiate the repair efficacy of EPCs for endothelial injury.
