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Activator protein-1 in carotid plaques is related to cerebrovascular symptoms and cholesteryl ester content.

Goncalves, Isabel LU ; Stollenwerk, Maria LU ; Lindholm, Marie LU ; Dias, Nuno LU ; Pedro, Luís M; Fernandes, José Fernandes E; Moses, Jonatan; Nordin Fredrikson, Gunilla LU ; Nilsson, Jan LU and Ares, Mikko LU (2011) In Cardiovascular Pathology 20. p.36-43
Abstract
INTRODUCTION: Transcription factor activator protein-1 regulates genes involved in inflammation and repair. The aim of this study was to determine whether transcription factor activator protein-1 activity in carotid plaques is related to symptoms, lipid accumulation, or extracellular matrix composition. METHODS: Twenty-eight atherosclerotic carotid plaques were removed by endarterectomy and divided into two groups based on the presence or absence of ipsilateral symptoms (<1 month ago). Activator protein-1 DNA binding activity was assessed, and subunit (c-Jun, JunD, JunB, c-Fos, FosB, Fra-1, Fra-2) protein levels analyzed by immunoblotting. Distribution of c-Jun in plaques was analyzed by immunohistochemistry. RESULTS: Plaques associated... (More)
INTRODUCTION: Transcription factor activator protein-1 regulates genes involved in inflammation and repair. The aim of this study was to determine whether transcription factor activator protein-1 activity in carotid plaques is related to symptoms, lipid accumulation, or extracellular matrix composition. METHODS: Twenty-eight atherosclerotic carotid plaques were removed by endarterectomy and divided into two groups based on the presence or absence of ipsilateral symptoms (<1 month ago). Activator protein-1 DNA binding activity was assessed, and subunit (c-Jun, JunD, JunB, c-Fos, FosB, Fra-1, Fra-2) protein levels analyzed by immunoblotting. Distribution of c-Jun in plaques was analyzed by immunohistochemistry. RESULTS: Plaques associated with symptoms had increased activator protein-1 activity and increased expression of c-Jun and JunD, as compared to asymptomatic plaques. Fra-1 and Fra-2 were present in equal amounts in both groups, whereas JunB, FosB, and c-Fos were undetectable. Activator protein-1 activity correlated with cholesteryl ester and elastin in plaques and decreased with age. Activator protein-1 activity did not correlate with collagen, calcified tissue, or proteoglycan content. CONCLUSIONS: Activator protein-1 is increased in plaques associated with symptoms. The correlation between activator protein-1 and cholesteryl esters suggests that high activator protein-1 is a marker of plaque vulnerability. Activator protein-1 expression can also reflect the activation of repair processes. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Cardiovascular Pathology
volume
20
pages
36 - 43
publisher
Elsevier
external identifiers
  • wos:000285902700007
  • pmid:19919900
  • scopus:78650420195
ISSN
1879-1336
DOI
10.1016/j.carpath.2009.09.003
language
English
LU publication?
yes
id
245e8f93-332d-4742-8bc6-3a1c63a0dc24 (old id 1511862)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/19919900?dopt=Abstract
date added to LUP
2009-12-03 14:56:26
date last changed
2017-01-01 07:33:45
@article{245e8f93-332d-4742-8bc6-3a1c63a0dc24,
  abstract     = {INTRODUCTION: Transcription factor activator protein-1 regulates genes involved in inflammation and repair. The aim of this study was to determine whether transcription factor activator protein-1 activity in carotid plaques is related to symptoms, lipid accumulation, or extracellular matrix composition. METHODS: Twenty-eight atherosclerotic carotid plaques were removed by endarterectomy and divided into two groups based on the presence or absence of ipsilateral symptoms (&lt;1 month ago). Activator protein-1 DNA binding activity was assessed, and subunit (c-Jun, JunD, JunB, c-Fos, FosB, Fra-1, Fra-2) protein levels analyzed by immunoblotting. Distribution of c-Jun in plaques was analyzed by immunohistochemistry. RESULTS: Plaques associated with symptoms had increased activator protein-1 activity and increased expression of c-Jun and JunD, as compared to asymptomatic plaques. Fra-1 and Fra-2 were present in equal amounts in both groups, whereas JunB, FosB, and c-Fos were undetectable. Activator protein-1 activity correlated with cholesteryl ester and elastin in plaques and decreased with age. Activator protein-1 activity did not correlate with collagen, calcified tissue, or proteoglycan content. CONCLUSIONS: Activator protein-1 is increased in plaques associated with symptoms. The correlation between activator protein-1 and cholesteryl esters suggests that high activator protein-1 is a marker of plaque vulnerability. Activator protein-1 expression can also reflect the activation of repair processes.},
  author       = {Goncalves, Isabel and Stollenwerk, Maria and Lindholm, Marie and Dias, Nuno and Pedro, Luís M and Fernandes, José Fernandes E and Moses, Jonatan and Nordin Fredrikson, Gunilla and Nilsson, Jan and Ares, Mikko},
  issn         = {1879-1336},
  language     = {eng},
  pages        = {36--43},
  publisher    = {Elsevier},
  series       = {Cardiovascular Pathology},
  title        = {Activator protein-1 in carotid plaques is related to cerebrovascular symptoms and cholesteryl ester content.},
  url          = {http://dx.doi.org/10.1016/j.carpath.2009.09.003},
  volume       = {20},
  year         = {2011},
}