Register for email alerts and news feeds:
This journal | BMJ Group
rss
Journal of Clinical Pathology 2005;58:382-388; doi:10.1136/jcp.2004.022988
Copyright © 2005 by the BMJ Publishing Group Ltd & Association of Clinical Pathologists.
Journal of Clinical Pathology 2005;58:382-388
© 2005 BMJ Publishing Group Ltd & Association of Clinical Pathologists

ORIGINAL ARTICLE

IgM colocalises with complement and C reactive protein in infarcted human myocardium

P A J Krijnen1, C Ciurana4, T Cramer3, T Hazes3, C J L M Meijer1, C A Visser2, H W M Niessen1, C E Hack4

1 Department of Pathology, VU Medical Centre, Amsterdam, De Boelelaan 1117, 1007 MB The Netherlands
2 Department of Cardiology, VU Medical Center
3 ICaR-VU, 1007 MB Amsterdam, The Netherlands
4 Sanquin Research at CLB, Department of Immunopathology and Laboratory of Experimental and Clinical Immunology, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands

Correspondence to:
Correspondence to:
Dr P A J Krijnen
VU Medical Centre, Department of Pathology, Room 0E16, De Boelelaan 1117, 1007 MB Amsterdam, The Netherlands; paj.krijnen{at}vumc.nl

Aims: Reperfusion of ischaemic myocardium after acute myocardial infarction (AMI) can induce ischaemia/reperfusion (I/R) injury, as a result of local activation of the complement system. C reactive protein (CRP) is involved in this activation. This study analysed the potential role of IgM in complement activation in the infarcted human myocardium.

Methods: Immunochemical analysis was carried out on heart specimens from 59 patients who died from AMI. Serial slides of frozen tissue from the infarction site were stained for IgM, complement factors C3d and C5b–9 (membrane attack complex), and CRP.

Results: IgM deposits were found on the plasma membrane, cross striations, and in the cytoplasm of jeopardised cardiomyocytes in infarcts of one to five days duration. IgM depositions were remarkably similar to those of CRP and both complement factors. The relative staining intensities of IgM and CRP varied greatly among patients.

Conclusions: Similar to CRP, IgM targets complement locally to jeopardised cardiomyocytes in the human heart after AMI. Localisation patterns and relative staining intensities suggest that IgM and CRP recognise similar epitopes in the ischaemic heart, but that the relative contribution of each protein to complement activation in the ischaemic myocardium differs among patients.

Abbreviations: AMI, acute myocardial infarction; BSA, bovine serum albumin; CRP, Creactive protein; I/R, ischaemia/reperfusion; mAb, monoclonal antibody; PBS, phosphate buffered saline; PLA2, phospholipase A2; PMN, polymorphonuclear leucocyte

Keywords: IgM; immunology; inflammation; myocardial infarction


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?

This article has been cited by other articles:

  • Krijnen, P. A. J., Cillessen, S. A. G. M., Manoe, R., Muller, A., Visser, C. A., Meijer, C. J. L. M., Musters, R. J. P., Hack, C. E., Aarden, L. A., Niessen, H. W. M. (2005). Clusterin: a protective mediator for ischemic cardiomyocytes?. Am. J. Physiol. Heart Circ. Physiol. 289: H2193-H2202 [Abstract] [Full Text]  

This Article

Services
Citing Articles
Google Scholar
PubMed
Topic Collections
Bookmark with

Register for free content

The full back archive is now available for all BMJ Journals. Institutional subscribers may access the entire archive as part of their subscription. Personal subscribers will also have access to all content when logged in. Non-subscribers who register have free access to all articles published before 2006 right back to volume 1 issue 1. Register here to access the free archive of all BMJ Journals.

Don't forget to sign up for content alerts so you keep up to date with all the articles as they are published.

Pathology jobs

Pathology jobs