Cytokine therapy prevents left ventricular remodeling and dysfunction after myocardial infarction through neovascularization
Cytokine therapy prevents left ventricular remodeling and dysfunction after myocardial infarction through neovascularization
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DOI：
10.1096/fj.03-0637fje
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发表时间：
2004-03-01
期刊：
影响因子：
4.8
通讯作者：
Komuro, I
中科院分区：
文献类型：
--
作者：
Ohtsuka, M;Takano, H;Komuro, I
据报道，粒细胞集落刺激因子 (G-CSF) 和干细胞因子 (SCF) 联合预处理可减轻急性心肌梗死 (MI) 后的左心室 (LV) 重塑。我们在这里检查了心肌梗死后开始的细胞因子治疗是否也有有益的作用。前部心肌梗死是在受体小鼠中产生的，这些小鼠的骨髓已被表达增强型绿色荧光蛋白（GFP）的转基因小鼠的骨髓所取代。我们根据以下处理将小鼠分为五组：1）盐水； 2)从MI前5天到MI后3天施用G-CSF和SCF； 3) MI后给予G-CSF和SCF 5天； 4) MI后单独施用G-CSF 5天； 5) MI后单独施用SCF 5天。所有三个 G-CSF 治疗组均显示出较少的左室重构，并改善了 MI 后的心功能和存活率。在所有G-CSF处理组的边缘区域，表达GFP的毛细血管数量增加，凋亡细胞数量减少。即使在心肌梗死后开始细胞因子治疗，它也可以通过增加新血管形成和减少边缘区域的细胞凋亡来预防心肌梗死后的左室重塑和功能障碍。
Pretreatment with a combination of granulocyte colony-stimulating factor (G-CSF) and stem cell factor (SCF) has been reported to attenuate left ventricular (LV) remodeling after acute myocardial infarction (MI). We here examined whether the cytokine treatment started after MI has also beneficial effects. Anterior MI was created in the recipient mice whose bone marrow had been replaced with that of transgenic mice expressing enhanced green fluorescent protein (GFP). We categorized mice into five groups according to the following treatment: 1) saline; 2) administration of G-CSF and SCF from 5 days before MI through 3 days after; 3) administration of G-CSF and SCF for 5 days after MI; 4) administration of G-CSF alone for 5 days after MI; 5) administration of SCF alone for 5 days after MI. All the three treatment groups with G-CSF showed less LV remodeling and improved cardiac function and survival rate after MI. The number of capillaries, which express GFP, was increased and the number of apoptotic cells was decreased in the border area of all the treatment groups with G-CSF. Even if the cytokine treatment is started after MI, it could prevent LV remodeling and dysfunction after MI-at least in part-through an increase in neovascularization and a decrease in apoptosis in the border area.