Zhang, M. et al. The role of natural IgM in myocardial ischemia-reperfusion injury. J. Mol. Cell. Cardiol. 41, 62-67

The CBR Institute for Biomedical Research, Inc., Harvard Medical School, Boston, MA 02115, and Section of Cardiovascular Sciences, The Methodist Hospital, Houston, TX 77030, USA.
Journal of Molecular and Cellular Cardiology (Impact Factor: 4.66). 08/2006; 41(1):62-7. DOI: 10.1016/j.yjmcc.2006.02.006
Source: PubMed


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.

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Available from: Mark L Entman, Jan 28, 2014
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