C4b-binding protein is present in affected areas of myocardial infarction during the acute inflammatory phase and covers a larger area than C3.

BACKGROUND: During myocardial infarction reduced blood flow in the heart muscle results in cell death. These dying/dead cells have been reported to bind several plasma proteins such as IgM and C-reactive protein (CRP). In the present study we investigated whether fluid-phase complement inhibitor C4b...

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Main Authors: Leendert A Trouw, Marcin Okroj, Koba Kupreishvili, Göran Landberg, Bengt Johansson, Hans W M Niessen, Anna M Blom
Format: Article
Sprog:English
Udgivet: Public Library of Science (PLoS) 2008-01-01
Serier:PLoS ONE
Online adgang:http://europepmc.org/articles/PMC2483938?pdf=render
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author Leendert A Trouw
Marcin Okroj
Koba Kupreishvili
Göran Landberg
Bengt Johansson
Hans W M Niessen
Anna M Blom
author_facet Leendert A Trouw
Marcin Okroj
Koba Kupreishvili
Göran Landberg
Bengt Johansson
Hans W M Niessen
Anna M Blom
author_sort Leendert A Trouw
collection DOAJ
description BACKGROUND: During myocardial infarction reduced blood flow in the heart muscle results in cell death. These dying/dead cells have been reported to bind several plasma proteins such as IgM and C-reactive protein (CRP). In the present study we investigated whether fluid-phase complement inhibitor C4b-binding protein (C4BP) would also bind to the infarcted heart tissue. METHODS AND FINDINGS: Initial studies using immunohistochemistry on tissue arrays for several cardiovascular disorders indicated that C4BP can be found in heart tissue in several cardiac diseases but that it is most abundantly found in acute myocardial infarction (AMI). This condition was studied in more detail by analyzing the time window and extent of C4BP positivity. The binding of C4BP correlates to the same locations as C3b, a marker known to correlate to the patterns of IgM and CRP staining. Based on criteria that describe the time after infarction we were able to pinpoint that C4BP binding is a relatively early marker of tissue damage in myocardial infarction with a peak of binding between 12 hours and 5 days subsequent to AMI, the phase in which infiltration of neutrophilic granulocytes in the heart is the most extensive. CONCLUSIONS: C4BP, an important fluid-phase inhibitor of the classical and lectin pathway of complement activation binds to jeopardized cardiomyocytes early after AMI and co-localizes to other well known markers such as C3b.
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spelling doaj.art-1de85213c7f44522bcb87264a68f59de2022-12-22T01:46:15ZengPublic Library of Science (PLoS)PLoS ONE1932-62032008-01-0138e288610.1371/journal.pone.0002886C4b-binding protein is present in affected areas of myocardial infarction during the acute inflammatory phase and covers a larger area than C3.Leendert A TrouwMarcin OkrojKoba KupreishviliGöran LandbergBengt JohanssonHans W M NiessenAnna M BlomBACKGROUND: During myocardial infarction reduced blood flow in the heart muscle results in cell death. These dying/dead cells have been reported to bind several plasma proteins such as IgM and C-reactive protein (CRP). In the present study we investigated whether fluid-phase complement inhibitor C4b-binding protein (C4BP) would also bind to the infarcted heart tissue. METHODS AND FINDINGS: Initial studies using immunohistochemistry on tissue arrays for several cardiovascular disorders indicated that C4BP can be found in heart tissue in several cardiac diseases but that it is most abundantly found in acute myocardial infarction (AMI). This condition was studied in more detail by analyzing the time window and extent of C4BP positivity. The binding of C4BP correlates to the same locations as C3b, a marker known to correlate to the patterns of IgM and CRP staining. Based on criteria that describe the time after infarction we were able to pinpoint that C4BP binding is a relatively early marker of tissue damage in myocardial infarction with a peak of binding between 12 hours and 5 days subsequent to AMI, the phase in which infiltration of neutrophilic granulocytes in the heart is the most extensive. CONCLUSIONS: C4BP, an important fluid-phase inhibitor of the classical and lectin pathway of complement activation binds to jeopardized cardiomyocytes early after AMI and co-localizes to other well known markers such as C3b.http://europepmc.org/articles/PMC2483938?pdf=render
spellingShingle Leendert A Trouw
Marcin Okroj
Koba Kupreishvili
Göran Landberg
Bengt Johansson
Hans W M Niessen
Anna M Blom
C4b-binding protein is present in affected areas of myocardial infarction during the acute inflammatory phase and covers a larger area than C3.
PLoS ONE
title C4b-binding protein is present in affected areas of myocardial infarction during the acute inflammatory phase and covers a larger area than C3.
title_full C4b-binding protein is present in affected areas of myocardial infarction during the acute inflammatory phase and covers a larger area than C3.
title_fullStr C4b-binding protein is present in affected areas of myocardial infarction during the acute inflammatory phase and covers a larger area than C3.
title_full_unstemmed C4b-binding protein is present in affected areas of myocardial infarction during the acute inflammatory phase and covers a larger area than C3.
title_short C4b-binding protein is present in affected areas of myocardial infarction during the acute inflammatory phase and covers a larger area than C3.
title_sort c4b binding protein is present in affected areas of myocardial infarction during the acute inflammatory phase and covers a larger area than c3
url http://europepmc.org/articles/PMC2483938?pdf=render
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