C4b-binding protein is present in affected areas of myocardial infarction during the acute inflammatory phase and covers a larger area than C3.
Trouw, Leendert LU ; Okroj, Marcin LU ; Kupreishvili, Koba ; Landberg, Göran LU ; Johansson, Bengt ; Niessen, Hans W M and Blom, Anna LU
(2008)
In PLoS ONE
3(8).
- Abstract
- 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... (More)
- 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. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1223440
- author
- Trouw, Leendert
LU
; Okroj, Marcin
LU
; Kupreishvili, Koba
; Landberg, Göran
LU
; Johansson, Bengt
; Niessen, Hans W M
and Blom, Anna
LU
- organization
- publishing date
- 2008
- type
- Contribution to journal
- publication status
- published
- subject
- in
- PLoS ONE
- volume
- 3
- issue
- 8
- article number
- e2886
- publisher
- Public Library of Science (PLoS)
- external identifiers
-
- wos:000264366600042
- pmid:18682851
- scopus:51449108790
- ISSN
- 1932-6203
- DOI
- 10.1371/journal.pone.0002886
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Protein Chemistry (013017510), Pathology, (Lund) (013030000), Clinical Chemistry, Malmö (013016000), Department of Translational Medicine (013017500)
- id
- 7414c759-bf65-4c06-9f84-96178205c2f7 (old id 1223440)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/18682851?dopt=Abstract
- date added to LUP
- 2016-04-04 09:05:27
- date last changed
- 2022-01-29 08:12:03
@article{7414c759-bf65-4c06-9f84-96178205c2f7,
abstract = {{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.}},
author = {{Trouw, Leendert and Okroj, Marcin and Kupreishvili, Koba and Landberg, Göran and Johansson, Bengt and Niessen, Hans W M and Blom, Anna}},
issn = {{1932-6203}},
language = {{eng}},
number = {{8}},
publisher = {{Public Library of Science (PLoS)}},
series = {{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.}},
url = {{https://lup.lub.lu.se/search/files/5228910/1259670.pdf}},
doi = {{10.1371/journal.pone.0002886}},
volume = {{3}},
year = {{2008}},
}