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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2001-9-21
pubmed:abstractText
The etiopathogenesis of thoracic aortic aneurysms is currently an issue of debate. The present study investigated ultrastructural, morphometric, and immunohistochemical aspects of smooth muscle cells (SMCs) in chronic aneurysm of the thoracic aorta (aneurysm group), aortic dilatation associated with valvular disease (valvular group), and dissection of the thoracic aorta (dissection group). Fragments of the ascending aorta that had been taken from the patients during coronary bypass surgery were used as controls. No significant difference was observed in the density of SMCs between the 3 pathologic groups put together and the controls. Only separate analysis of SMC density in each of the pathologic groups showed that the valvular group samples had significantly smaller amounts of SMCs in the internal layer of the media than the dissection group samples and controls. Ultrastructural analysis, in situ end labeling, propidium iodide assay, and DNA laddering did not show apoptosis of SMCs in the samples investigated. Ultrastructure of SMCs characteristic of the synthetic phenotype, together with increased expression of osteopontin in the media of pathologic thoracic aortas indicated the transition of SMCs from the contractile to the synthetic phenotype. Immunohistochemical investigation showed that medial SMCs in the samples taken from aortas of all 3 pathologic groups expressed stronger immunoreactivity for matrix metalloproteinase 1, 2, and 9 and tissue inhibitor of metalloproteinase 1 and 2 than the controls. The present study shows that during the formation of aneurysms, dissection of the thoracic aorta, or aortic dilatation associated with valvular disease, loss of SMCs was not of great importance with respect to their transition from the contractile to the synthetic type in leading to increased production of matrix metalloproteinases.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0046-8177
pubmed:author
pubmed:copyrightInfo
Copyright 2001 by W.B. Saunders Company
pubmed:issnType
Print
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1003-11
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11567232-Adult, pubmed-meshheading:11567232-Aged, pubmed-meshheading:11567232-Aneurysm, Dissecting, pubmed-meshheading:11567232-Aorta, Thoracic, pubmed-meshheading:11567232-Aortic Aneurysm, Thoracic, pubmed-meshheading:11567232-Apoptosis, pubmed-meshheading:11567232-DNA Fragmentation, pubmed-meshheading:11567232-Extracellular Matrix, pubmed-meshheading:11567232-Female, pubmed-meshheading:11567232-Heart Valve Diseases, pubmed-meshheading:11567232-Humans, pubmed-meshheading:11567232-Immunohistochemistry, pubmed-meshheading:11567232-In Situ Nick-End Labeling, pubmed-meshheading:11567232-Male, pubmed-meshheading:11567232-Matrix Metalloproteinases, pubmed-meshheading:11567232-Microscopy, Electron, pubmed-meshheading:11567232-Middle Aged, pubmed-meshheading:11567232-Muscle, Smooth, Vascular, pubmed-meshheading:11567232-Osteopontin, pubmed-meshheading:11567232-Sialoglycoproteins, pubmed-meshheading:11567232-Tissue Inhibitor of Metalloproteinases, pubmed-meshheading:11567232-Tunica Media
pubmed:year
2001
pubmed:articleTitle
Smooth muscle cells of the media in the dilatative pathology of ascending thoracic aorta: morphology, immunoreactivity for osteopontin, matrix metalloproteinases, and their inhibitors.
pubmed:affiliation
Institute of Cardiology and Department of Biochemistry, Kaunas University of Medicine, Lithuania.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't