Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1997-8-11
pubmed:abstractText
The possibility that Fas/APO 1 is involved in the apoptosis of advanced human coronary atherosclerosis was examined in the present study. Coronary arteries with atherosclerosis were obtained from human hearts with chronic ischemic heart disease at cardiac transplantation. Normal vessels were used as controls. Fas/APO 1 was detected by immunohistochemistry with a monoclonal antibody. Apoptotic cells were stained in situ by terminal deoxynucleotidyl transferase mediated-dUTP nick end labeling (TUNEL) and DNA fragmentation into oligonucleosomes was checked by gel electrophoresis. Bcl-2, an antiapoptotic oncoprotein, was detected by immunohistochemistry and Western blot. Apoptotic cells were present in the neointima in all stages of atherosclerosis, and in intraplaque small vessels. In initial lesions, only a few cells were undergoing apoptosis. By contrast, in advanced lesions, many cells were found to undergo apoptosis. Apoptosis was further confirmed by genomic DNA analysis using gel electrophoresis. Apoptotic cells were either smooth muscle cells or macrophages, but also endothelial and blood borne cells. Fas/APO 1 was present in foam cells. Most of the Fas/APO 1 positive cells were stained for the macrophage marker CD68 and for alpha-smooth muscle actin in serial sections. Several anti-Fas/APO 1 positive foam cells were revealed to undergo apoptosis by double staining. Bcl-2 was detected in Fas/APO 1 expressing plaques. A number of CD3-positive T-lymphocytes were found around foam cells expressing Fas/APO 1. This data suggests that Fas/APO 1 regulated apoptosis is involved in the development of advanced human atherosclerotic lesions and that it probably determines the amount of tissue mass in the diseased vessels.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0021-9150
pubmed:author
pubmed:issnType
Print
pubmed:volume
131
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
177-86
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:9199270-Antibodies, Monoclonal, pubmed-meshheading:9199270-Antigens, CD3, pubmed-meshheading:9199270-Antigens, CD95, pubmed-meshheading:9199270-Apoptosis, pubmed-meshheading:9199270-Biological Markers, pubmed-meshheading:9199270-Blotting, Western, pubmed-meshheading:9199270-Coronary Artery Disease, pubmed-meshheading:9199270-Coronary Vessels, pubmed-meshheading:9199270-DNA, pubmed-meshheading:9199270-DNA Fragmentation, pubmed-meshheading:9199270-Female, pubmed-meshheading:9199270-Genes, bcl-2, pubmed-meshheading:9199270-Heart Transplantation, pubmed-meshheading:9199270-Humans, pubmed-meshheading:9199270-Immunohistochemistry, pubmed-meshheading:9199270-Male, pubmed-meshheading:9199270-Middle Aged, pubmed-meshheading:9199270-Muscle, Smooth, Vascular, pubmed-meshheading:9199270-Spectrophotometry, pubmed-meshheading:9199270-Tunica Intima
pubmed:year
1997
pubmed:articleTitle
The role of Fas/APO 1 and apoptosis in the development of human atherosclerotic lesions.
pubmed:affiliation
Max-Planck-Institute, Department of Experimental Cardiology, Bad Nauheim, Germany.
pubmed:publicationType
Journal Article