Interleukin-8 is associated with circulating CD133+progenitor cells in acute myocardial infarction
Interleukin-8 is associated with circulating CD133+progenitor cells in acute myocardial infarction
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DOI：
10.1093/eurheartj/ehi761
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发表时间：
2006-05-01
影响因子：
39.3
通讯作者：
Ott, I
中科院分区：
文献类型：
--
作者：
Schömig, K;Busch, G;Ott, I
目的在炎症条件下观察到祖细胞的释放，并有助于新血管形成。因此，我们试图研究急性心肌梗死（AMI）患者循环祖细胞和白细胞介素（IL）-8的关系。方法和结果从稳定型心绞痛和AMI患者，连续静脉血样本。通过流式细胞术分析循环CD 133 + CD 45-祖细胞、内皮祖细胞（EPC）和循环内皮P1 H12 + CD 45-细胞的数量。AMI患者支架植入后，血浆IL-8和血管内皮生长因子（VEGF）浓度升高，而稳定型心绞痛患者仅极轻微升高。仅在AMI患者中，这随后是循环CD 133 + CD 45-祖细胞的增加。相比之下，循环内皮细胞P1 H12 + CD 45-细胞和E-选择素RNA表达在外周血中仅在AMI早期升高，表明活化的内皮细胞脱落。多因素分析显示，IL-8与AMI患者外周血CD 133 + CD 45-祖细胞的表达存在相关性，同时与他汀类药物治疗和危险因素有关。除了IL-8和VEGF的促血管生成功能外，该机制可能有助于新血管生成，从而改善心肌功能。
Aims Release of progenitor cells is observed during inflammatory conditions and contributes to neovascularization. We, therefore, sought to investigate the relationship of circulating progenitor cells and interleukin (IL)-8 in acute myocardial infarction (AMI).Methods and results From patients with stable angina and AMI, serial venous blood samples were obtained. The number of circulating CD133+CD45- progenitor cells, endothelial progenitor cells (EPCs), and circulating endothelial P1H12+CD45- cells was analyzed by flow cytometry. After stenting in patients with AMI, an increase in plasma IL-8 and vascular endothelial growth factor (VEGF) concentrations was observed, which was only minimal in patients with stable angina. Only in patients with AMI, this was followed by an increase in circulating CD133+CD45- progenitor cells. In contrast, circulating endothelial P1H12+CD45- cells and E-selectin RNA expression in peripheral blood were only elevated early in AMI, indicating shedding of activated endothelial cells. Multivariable analysis revealed an association of IL-8 and circulating CD133+CD45- progenitor cells in AMI, in addition to statin therapy and risk factor profile.Conclusion In AMI, IL-8 is associated with circulating progenitor cells. In addition to the pro-angiogenic functions of IL-8 and VEGF, this mechanism may contribute to new vessel generation and, thereby, improve myocardial function.