[Effect of soluble epoxide hydrolase inhibitor on the function of endothelial progenitor cells in patients with coronary heart disease].
OBJECTIVE
To investigate the effect of soluble epoxide hydrolase inhibitor (sEHi) tAUCB on the function of endothelial progenitor cells (EPCs) and expression of vascular endothelial growth factor (VEGF) in EPCs in patients with coronary heart disease (CHD).


METHODS
Mononuclear cells, from the peripheral blood of CHD patients, were isolated by ficoll density gradient centrifugation and cultured. After 7 days of culture in vitro, EPCs were identified by double staining and flow cytometry. EPCs were then stimulated by 0, 10(-6), 10(-5), and 10(-4) mol/L of tAUCB for 24 h. Migration assay was performed in transwell chamber and tube formation assay was performed by Matrigel-Matrix in vitro model. The expression of VEGF in EPCs was measured by Western blot. EPCs from age and gender matched healthy subjects were also cultured as controls.


RESULTS
The migration and tube formation activities of EPCs from CHD patients were obviously damaged compared with those from healthy controls (P<0.05). The tAUCB could dose-dependently increase the migration and tube formation activities and increase the expression of VEGF in EPCs compared with those from CHD patients without treatment. The 10(-6) mol/L tAUCB increased those activities of EPCs and the expression of VEGF with statistical difference.


CONCLUSIONS
sEHi can positively modulate the function of EPCs from CHD patients, suggesting the potential predictive significance of sEHi in the therapy of CHD.
Xu
Danyan
D
Department of Cardiology, Second Xiangya Hospital, Central South University, Changsha 410011, China. xudanyan02@sina.com
Chen
Chen
C
Jiang
Yun
Y
Zhao
Shuiping
S
Liu
Zheliang
Z
Xie
Xiaomei
X
Liu
Ling
L
D000368:Aged; D002454:Cell Differentiation / Q000187:drug effects; D002465:Cell Movement / Q000187:drug effects; D002478:Cells, Cultured; D003327:Coronary Disease / Q000473:pathology*; D042783:Endothelial Cells / Q000378:metabolism / Q000473:pathology / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D004851:Epoxide Hydrolases / Q000037:antagonists & inhibitors*; D005260:Female; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000473:pathology; D008297:Male; D008875:Middle Aged; D012995:Solubility; D013234:Stem Cells / Q000378:metabolism / Q000473:pathology / Q000502:physiology*; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics / Q000378:metabolism
D004791:Enzyme Inhibitors; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D004851:Epoxide Hydrolases