Comparison of Myocardial Remodeling between Cryoinfarction and Reperfused Infarction in Mice
Comparison of Myocardial Remodeling between Cryoinfarction and Reperfused Infarction in Mice
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DOI：
10.1155/2011/961298
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发表时间：
2011-01-01
影响因子：
--
通讯作者：
Dewald, Oliver
中科院分区：
文献类型：
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作者：
Duerr, Georg D.;Elhafi, Naziha;Dewald, Oliver
心肌梗死与导致组织重塑的炎症反应有关。我们比较了冷冻心肌梗死(CMI)和再灌流性心肌梗死(MI)之间的组织重构，以便更好地了解我们应用细胞疗法的局部环境。C57/BL6-小鼠采用开胸1h缺血再灌注MI和CMI模型。再灌注组7d后肉芽组织快速生长，瘢痕致密。相反，CMI心脏在7天后显示持续的心肌细胞碎片和细胞浸润，14天后部分致密的瘢痕形成伴随持续的巨噬细胞和肌成纤维细胞。心肌梗死后一过性诱导促炎介质基因表达，心肌梗死后持续上调。Tenascin C和Osteopontin-1对CMI有延迟诱导作用。总而言之，与再灌注心肌梗死相比，深低温心肌梗死与炎症延长和活跃的心肌重塑有关。这些重塑方面的显著差异可能会影响细胞的植入，在细胞治疗研究中应予以考虑。
Myocardial infarction is associated with inflammatory reaction leading to tissue remodeling. We compared tissue remodeling between cryoinfarction (cMI) and reperfused myocardial infarction (MI) in order to better understand the local environment where we apply cell therapies. Models of closed-chest one-hour ischemia/reperfusion MI and cMI were used in C57/Bl6-mice. The reperfused MI showed rapid development of granulation tissue and compacted scar formation after 7 days. In contrast, cMI hearts showed persistent cardiomyocyte debris and cellular infiltration after 7 days and partially compacted scar formation accompanied by persistent macrophages and myofibroblasts after 14 days. The mRNA of proinflammatory mediators was transiently induced in MI and persistently upregulated in cMI. Tenascin C and osteopontin-1 showed delayed induction in cMI. In conclusion, the cryoinfarction was associated with prolonged inflammation and active myocardial remodeling when compared to the reperfused MI. These substantial differences in remodeling may influence cellular engraftment and should be considered in cell therapy studies.