The role of natural IgM in myocardial ischemia-reperfusion injury
- PMID: 16781728
- DOI: 10.1016/j.yjmcc.2006.02.006
The role of natural IgM in myocardial ischemia-reperfusion injury
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.
Similar articles
-
Involvement of neutrophils in the pathogenesis of lethal myocardial reperfusion injury.Cardiovasc Res. 2004 Feb 15;61(3):481-97. doi: 10.1016/j.cardiores.2003.10.011. Cardiovasc Res. 2004. PMID: 14962479 Review.
-
Opposing effects mediated by the chemokine receptor CXCR2 on myocardial ischemia-reperfusion injury: recruitment of potentially damaging neutrophils and direct myocardial protection.Circulation. 2003 Nov 11;108(19):2387-92. doi: 10.1161/01.CIR.0000093192.72099.9A. Epub 2003 Oct 20. Circulation. 2003. PMID: 14568904
-
Myocardial expression of a dominant-negative form of Daxx decreases infarct size and attenuates apoptosis in an in vivo mouse model of ischemia/reperfusion injury.Circulation. 2007 Dec 4;116(23):2709-17. doi: 10.1161/CIRCULATIONAHA.107.694844. Epub 2007 Nov 19. Circulation. 2007. PMID: 18025529
-
Murine hindlimb reperfusion injury can be initiated by a self-reactive monoclonal IgM.Surgery. 2004 Aug;136(2):401-6. doi: 10.1016/j.surg.2004.05.016. Surgery. 2004. PMID: 15300207
-
Natural antibody mediated innate autoimmune response.Mol Immunol. 2007 Jan;44(1-3):103-10. doi: 10.1016/j.molimm.2006.06.022. Epub 2006 Jul 28. Mol Immunol. 2007. PMID: 16876247 Review.
Cited by
-
Humoral innate immune response and disease.Clin Immunol. 2012 Aug;144(2):142-58. doi: 10.1016/j.clim.2012.06.002. Epub 2012 Jun 18. Clin Immunol. 2012. PMID: 22771788 Free PMC article. Review.
-
The immunology of B-1 cells: from development to aging.Immun Ageing. 2024 Aug 2;21(1):54. doi: 10.1186/s12979-024-00455-y. Immun Ageing. 2024. PMID: 39095816 Free PMC article. Review.
-
The role of complement C3 in the outcome of regional myocardial infarction.Biochem Biophys Rep. 2023 Jan 26;33:101434. doi: 10.1016/j.bbrep.2023.101434. eCollection 2023 Mar. Biochem Biophys Rep. 2023. PMID: 36748063 Free PMC article.
-
The Fifth Domain of Beta 2 Glycoprotein I Protects from Natural IgM Mediated Cardiac Ischaemia Reperfusion Injury.PLoS One. 2016 Mar 31;11(3):e0152681. doi: 10.1371/journal.pone.0152681. eCollection 2016. PLoS One. 2016. PMID: 27031114 Free PMC article.
-
The Expression of Non B Cell-Derived Immunoglobulins.Adv Exp Med Biol. 2024;1445:11-36. doi: 10.1007/978-981-97-0511-5_2. Adv Exp Med Biol. 2024. PMID: 38967747 Review.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources
Molecular Biology Databases