Activator protein-1 in carotid plaques is related to cerebrovascular symptoms and cholesteryl ester content.
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1511862
- author
- 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
- organization
- publishing date
- 2011
- 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
- pmid:19919900
- ISSN
- 1879-1336
- DOI
- 10.1016/j.carpath.2009.09.003
- 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: Experimental Cardiovascular Research Unit (013242110), Emergency medicine/Medicine/Surgery (013240200)
- 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
- 2016-04-04 07:53:11
- date last changed
- 2022-02-07 11:30:54
@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 (<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}}, doi = {{10.1016/j.carpath.2009.09.003}}, volume = {{20}}, year = {{2011}}, }