Activation of calpain-1 in human carotid artery atherosclerotic lesions

In a previous study, we observed that oxidized low-density lipoprotein-induced death of endothelial cells was calpain-1-dependent. The purpose of the present paper was to study the possible activation of calpain in human carotid plaques, and to compare calpain activity in the plaques from symptomati...

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Bibliographic Details
Published in:BMC cardiovascular disorders 2009-06, Vol.9 (26), p.26-26, Article 26
Main Authors: Gonçalves, Isabel, Nitulescu, Mihaela, Saido, Takaomi C, Dias, Nuno, Pedro, Luis M, E Fernandes, José Fernandes, Ares, Mikko P S, Pörn-Ares, Isabella
Format: Article
Language:English
Subjects:
Aged
Apoptosis
Atherosclerotic plaque
Calpain
Calpain - metabolism
Cardiac and Cardiovascular Systems
Carotid Arteries - enzymology
Carotid Arteries - pathology
Carotid Stenosis - enzymology
Carotid Stenosis - pathology
Clinical Medicine
Development and progression
Enzyme Activation - physiology
Female
Humans
Kardiologi
Klinisk medicin
Male
Medical and Health Sciences
Medicin och hälsovetenskap
Middle Aged
Physiological aspects
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Summary:In a previous study, we observed that oxidized low-density lipoprotein-induced death of endothelial cells was calpain-1-dependent. The purpose of the present paper was to study the possible activation of calpain in human carotid plaques, and to compare calpain activity in the plaques from symptomatic patients with those obtained from patients without symptoms. Human atherosclerotic carotid plaques (n = 29, 12 associated with symptoms) were removed by endarterectomy. Calpain activity and apoptosis were detected by performing immunohistochemical analysis and TUNEL assay on human carotid plaque sections. An antibody specific for calpain-proteolyzed alpha-fodrin was used on western blots. We found that calpain was activated in all the plaques and calpain activity colocalized with apoptotic cell death. Our observation of autoproteolytic cleavage of the 80 kDa subunit of calpain-1 provided further evidence for enzyme activity in the plaque samples. When calpain activity was quantified, we found that plaques from symptomatic patients displayed significantly lower calpain activity compared with asymptomatic plaques. These novel results suggest that calpain-1 is commonly active in carotid artery atherosclerotic plaques, and that calpain activity is colocalized with cell death and inversely associated with symptoms.
ISSN:1471-2261
1471-2261
DOI:10.1186/1471-2261-9-26