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J Mol Cell Cardiol. 2006 Jul;41(1):62-7. Epub 2006 Jun 16.

The role of natural IgM in myocardial ischemia-reperfusion injury.

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1
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.

Abstract

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.

PMID:
16781728
DOI:
10.1016/j.yjmcc.2006.02.006
[Indexed for MEDLINE]
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