G-CSF administration after myocardial infarction in mice attenuates late ischemic cardiomyopathy by enhanced arteriogenesis

被引:128
作者
Deindl, Elisabeth
Zaruba, Marc-Michael
Brunner, Stefan
Huber, Bruno
Mehl, Ursula
Assmann, Gerald
Hoefer, Imo E.
Mueller-Hoecker, Josef
Franz, Wolfgang-Michael
机构
[1] Univ Munich, Klinikum Grosshadern, Dept Med 1, D-81377 Munich, Germany
[2] Univ Munich, Inst Pathol, D-8000 Munich, Germany
[3] UMC, Dept Expt Cardiol, Utrecht, Netherlands
关键词
granulocyte-colony stimulating factor; bone marrow derived cells; intercellular adhesion molecule-1;
D O I
10.1096/fj.05-4763fje
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Granulocyte-colony stimulating factor (G-CSF) has been shown to improve cardiac function after myocardial infarction (MI) by bone marrow cell mobilization and by protecting cardiomyocytes from apoptotic cell death. However, its role in collateral artery growth (arteriogenesis) has not been elucidated. Here, we investigated the effect of G-CSF on arteriolar growth and cardiac function in a murine MI model. Mice were treated with G-CSF (100 mu g/kg/day) directly after MI for 5 consecutive days. G-CSF application resulted in a significant increase of circulating mononuclear cells expressing stem cell markers. Arterioles in the border zone of infarcted myocardium showed an increased expression of ICAM-1 accompanied by an accumulation of bone marrow derived cells and a pronounced proliferation of endothelial and smooth muscle cells. Histology of G-CSF treated mice revealed a lower amount of granulation tissue (67.8 vs. 84.4%) associated with a subsequent reduction in free LV wall thinning and scar extension (23.1 vs. 30.8% of LV). Furthermore, G-CSF treated animals showed a significant improvement of post-MI survival (68.8 vs. 46.2%). Pressure-volume relations revealed a partially restored myocardial function at day 30 (EF: 32.5 vs. 17.2%). Our results demonstrate that G-CSF administration after MI stimulates arteriogenesis and attenuates ischemic cardiomyopathy after MI.
引用
收藏
页码:956 / +
页数:10
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