Chen Tingting, Mi Weidong, Wang Gang, Li Libing, Gao Changqing
Department of Cardiovascular Surgery, General Hospital of Chinese PLA, Beijing 100853, PR China.
Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi. 2010 Oct;24(10):1239-43.
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.
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.
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).
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.
探讨粒细胞集落刺激因子（G-CSF）对心肌梗死（MI）大鼠内皮祖细胞（EPCs）动员的影响，观察MI边缘区新生血管密度及血管内皮生长因子（VEGF）及其受体（Flk-1）的mRNA表达。
36只成年雄性大鼠（体重250~280 g）随机分为对照组、MI组和G-CSF组。MI组和G-CSF组采用冠状动脉左前降支结扎法建立MI模型，分别腹腔注射生理盐水（0.3 mL/d）或G-CSF [30 μg/(kg·d)]，共5天。对照组开胸手术后关胸，不做处理。于第7天检测EPCs水平，测定血浆VEGF和C反应蛋白（CRP）浓度。通过逆转录聚合酶链反应（RT-PCR）检测梗死心肌边缘区VEGF及其受体Flk-1的mRNA表达。
与对照组比较，MI组和G-CSF组循环白细胞（WBC）数量、EPCs水平及血清VEGF和CRP浓度均显著升高（P<0.05）；与MI组比较，G-CSF组循环WBC数量、EPCs水平及血清VEGF浓度升高，CRP浓度降低（P<0.05）。与对照组比较，MI组和G-CSF组梗死心肌边缘区VEGF和Flk-1的mRNA表达及新生血管密度增加，而G-CSF组与MI组比较显著增强（P<0.05）。
在MI大鼠中，G-CSF可促进EPCs动员，增加VEGF和Flk-1的mRNA表达，提高梗死心肌边缘区新生血管密度。
