The role of natural IgM in myocardial ischemia-reperfusion injury

J Mol Cell Cardiol. 2006 Jul;41(1):62-7. doi: 10.1016/j.yjmcc.2006.02.006. Epub 2006 Jun 16.


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.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Apoptosis
  • Disease Models, Animal
  • Homeodomain Proteins / genetics
  • Homeodomain Proteins / metabolism
  • Immunoglobulin M / physiology*
  • Mice
  • Mice, Mutant Strains
  • Myocardial Ischemia / immunology*
  • Myocardial Reperfusion Injury / immunology*
  • Myocardial Reperfusion Injury / pathology*
  • Necrosis
  • Neutrophils / pathology
  • Receptors, Complement / genetics


  • Homeodomain Proteins
  • Immunoglobulin M
  • Receptors, Complement
  • RAG-1 protein