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Journal of Clinical Pathology 2003;56:194-199; doi:10.1136/jcp.56.3.194
Copyright © 2003 by the BMJ Publishing Group Ltd & Association of Clinical Pathologists.
Journal of Clinical Pathology 2003;56:194-199
© 2003 BMJ Publishing Group & Association of Clinical Pathologists

ORIGINAL ARTICLE

Increased Nox2 expression in human cardiomyocytes after acute myocardial infarction

P A J Krijnen1, C Meischl4, C E Hack3, C J L M Meijer1, C A Visser2, D Roos4, H W M Niessen1

1 Department of Pathology, VU Medical Center, De Boelelaan 1117, PO Box 7057, 1007 MB Amsterdam, The Netherlands
2 Department of Cardiology, VU Medical Center
3 Department of Clinical Chemistry, VU Medical Center
4 Sanquin Research at CLB, and Landsteiner Laboratory of the Academic Medical Center, University of Amsterdam, 1066 CX, Amsterdam, The Netherlands

Correspondence to:
Correspondence to:
Dr P A J Krijnen, VU University Medical Center, Department of Pathology, Room number 0E16, De Boelelaan 1117, PO Box 7057, 1007 MB Amsterdam, The Netherlands;
paj.krijnen{at}vumc.nl

Background/Aims: Recent studies indicate the presence of reactive oxygen species (ROS) producing homologues of the enzymatic subunit (Nox2) of phagocytic NADPH oxidase in non-phagocytic cells. Interestingly, in these cells, ROS produced by the Nox2 homologue(s) was shown to play a role in various regulatory processes, including cell death, proliferation, and aging. The purpose of this study was to investigate whether human cardiomyocytes express Nox2.

Methods: The expression of Nox2 was studied in human cardiomyocytes using western blot and immunohistochemical analysis. To analyse the putative expression of Nox2 in human heart disease, cardiac samples from patients who had died subsequent to acute myocardial infarction (AMI) were studied.

Results: Both in western blot and immunohistochemical studies, Nox2 expression was found in normal human cardiomyocytes. In patients with AMI, a significant increase in Nox2 expression was found both in viable and in jeopardised cardiomyocytes in the infarcted area. In addition, in the "remote from infarction" area, Nox2 expression was present in cardiomyocytes, but was not increased.

Conclusions: Nox2 or its homologue(s) is expressed in normal and jeopardised human cardiomyocytes. This expression is increased in patients with AMI, suggesting a role for this ROS producing Nox2 homologue(s) in the human heart after AMI.

Keywords: acute myocardial infarction; Nox2; cardiomyocytes; immunohistochemistry; protein expression

Abbreviations: AMI, acute myocardial infarction; BSA, bovine serum albumin; HPF, high power field; LD, lactate dehydrogenase; PBS, phosphate buffered saline; RaM-HRP, horseradish peroxidase conjugated rabbit antimouse immunoglobulin; ROS, reactive oxygen species; SDS, sodium dodecyl sulfate


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