The role of natural IgM in myocardial ischemia-reperfusion injury.
The role of natural IgM in myocardial ischemia-reperfusion injury.
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DOI：
10.1016/j.yjmcc.2006.02.006
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发表时间：
2006-07
影响因子：
5
通讯作者：
Ming Zhang;L. Michael;S. Grosjean;R. Kelly;M. Carroll;M. Entman
中科院分区：
文献类型：
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作者：
Ming Zhang;L. Michael;S. Grosjean;R. Kelly;M. Carroll;M. Entman
心肌缺血-再灌注损伤是多种因素的综合作用，即对缺血的内在细胞反应和外在急性炎症反应。最近在肠系膜和骨骼肌再灌注模型中的研究将天然IgM鉴定为通过激活补体系统和炎性细胞的病理学的主要引发剂。为了确定心肌组织中是否涉及类似的机制，在冠状动脉缺血的小鼠模型中检查了携带改变的天然IgM库（Cr2-/-）的小鼠。值得注意的是，基于梗死面积减小、心肌细胞凋亡有限和中性粒细胞浸润减少，这些小鼠受到显著保护。保护是IgM依赖性的，因为用野生型IgM重建这些小鼠恢复了心肌再灌注损伤。这些结果支持了一种模型，其中天然IgM在缺血和再灌注后的心肌中引发急性炎症反应。
Myocardial ischemia–reperfusion injury represents a combination of factors, namely the intrinsic cellular response to ischemia and the extrinsic acute inflammatory response. Recent studies in mesenteric and skeletal muscle reperfusion models identified natural IgM as a major initiator of pathology through the activation of the complement system and inflammatory cells. To determine whether a similar mechanism is involved in myocardial tissues, mice bearing an altered natural IgM repertoire (Cr2−/−) were examined in a murine model of coronary artery ischemia. Notably, these mice were significantly protected based on the reduced infarct size, limited apoptosis of cardiomyocytes, and decreased neutrophil infiltration. Protection was IgM-dependent as reconstitution of these mice with wild-type IgM restored myocardial reperfusion injury. These results support a model in which natural IgM initiates the acute inflammatory response in the myocardium following ischemia and reperfusion.