Activation of calpain-1 in human carotid artery atherosclerotic lesions
Autor: | José Fernandes e Fernandes, Isabel Gonçalves, Luís Mendes Pedro, Mikko P.S. Ares, Nuno Dias, Isabella Pörn-Ares, Mihaela Nitulescu, Takaomi C. Saido |
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Rok vydání: | 2008 |
Předmět: |
Male
lcsh:Diseases of the circulatory (Cardiovascular) system Pathology medicine.medical_specialty Programmed cell death medicine.medical_treatment Apoptosis 030204 cardiovascular system & hematology Asymptomatic 03 medical and health sciences 0302 clinical medicine Internal medicine medicine Humans Carotid Stenosis 030304 developmental biology Endarterectomy Aged 0303 health sciences TUNEL assay biology business.industry Calpain Middle Aged 3. Good health Blot Enzyme Activation Carotid Arteries lcsh:RC666-701 biology.protein Cardiology Immunohistochemistry Female medicine.symptom Cardiology and Cardiovascular Medicine business Research Article |
Zdroj: | BMC Cardiovascular Disorders BMC Cardiovascular Disorders, Vol 9, Iss 1, p 26 (2009) |
ISSN: | 1471-2261 |
Popis: | Background 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. Methods 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 α-fodrin was used on western blots. Results 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. Conclusion 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. |
Databáze: | OpenAIRE |
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