[Promoting effect of granulocyto-colony stimulating factor on neovascularization in rats with myocardial infarction].
OBJECTIVE
To investigate the effects of granulocyto-colony stimulating factor (G-CSF) on the mobilization of endothelial progenitor cells (EPCs) in the rats with myocardial infarction (MI), to observe the density of neovascularization and the mRNA expressions of vascular endothelial growth factor (VEGF) and its receptor (Flk-1) in the border area of MI.


METHODS
Thirty-six adult male rats (weighing 250-280 g) were divided randomly into control group, MI group, and G-CSF group. In MI group and G-CSF group, the models of MI were established by left anterior descending coronary artery ligation and were treated with intraperitoneal injection of saline (0.3 mL/d) or G-CSF [30 microg/(kg x d)] for 5 days. In control group, after open chest operation, chest was closed without treatment. The level of EPCs was surveyed and the plasma concentrations of VEGF and C-reaction protein (CRP) were measured at 7 days. The mRNA expressions of VEGF and its receptor Flk-1 in the border area of infarct myocardium were determined through RT-PCR.


RESULTS
Compared with control group, the number of circulating white blood cell (WBC) and EPCs levels, and the serum concentrations of VEGF and CRP were all significantly increased in MI group and G-CSF group (P < 0.05); when compared with MI group, the number of circulating WBC and EPCs levels, and the serum concentrations of VEGF were increased and the concentration of CRP was decreased in G-CSF group (P < 0.05). Compared with control group, the mRNA expressions of VEGF and Flk-1, and the density of neovascularization in the border area of infarct myocardium were increased in MI group and G-CSF group, whereas those in G-CSF group were significantly augmented compared with MI group (P < 0.05).


CONCLUSIONS
In the rats with MI, G-CSF could promote EPCs mobilization, increase the mRNA expressions of VEGF and Flk-1, and augment the density of neovascularization in the border area of infarct myocardium.
Department of Cardiovascular Surgery, General Hospital of Chinese PLA, Beijing 100853, PR China.
Tingting
T
Chen
Weidong
W
Mi
Gang
G
Wang
Libing
L
Li
Changqing
C
Gao
D000818:Animals; D042783:Endothelial Cells / Q000187:drug effects / Q000378:metabolism; D016179:Granulocyte Colony-Stimulating Factor / Q000494:pharmacology*; D008297:Male; D009203:Myocardial Infarction / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism; D018919:Neovascularization, Physiologic / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar; D013234:Stem Cells / Q000187:drug effects / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000378:metabolism; D020257:Ventricular Remodeling / Q000187:drug effects*
D042461:Vascular Endothelial Growth Factor A; C467498:vascular endothelial growth factor A, rat; D016179:Granulocyte Colony-Stimulating Factor; D040301:Vascular Endothelial Growth Factor Receptor-2