Document Detail


Expression of Fas ligand in arteries of hypercholesterolemic rabbits accelerates atherosclerotic lesion formation.
MedLine Citation:
PMID:  10669624     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Fas ligand (FasL) is expressed by cells of the arterial wall and is present in human atherosclerotic lesions. However, the role of FasL in modifying the initiation and progression of atherosclerosis is unclear. To investigate the role of arterial FasL expression in the development of atherosclerosis, we first established a model of primary lesion formation in rabbit carotid arteries. In this model, infusion of adenoviral vectors into surgically isolated, nondenuded arteries of hypercholesterolemic rabbits leads to the formation of human-like early atherosclerotic lesions. Expression of FasL in arterial endothelium in this model decreased T-cell infiltration and expression of vascular cell adhesion molecule-1 but did not affect expression of intercellular adhesion molecule-1. Intimal lesions grew more rapidly in FasL-transduced arteries than in arteries transduced with a control adenovirus that did not express a transgene. Total intimal macrophage accumulation was increased in FasL-transduced arteries; however, the proportion of lesion area occupied by macrophages was not elevated. The accelerated lesion growth was primarily due to the accumulation of intimal smooth muscle cells with a synthetic proliferative phenotype. There was no significant apoptosis in FasL-transduced or control arteries and no granulocytic infiltrates. Thus, the net result of elevated FasL expression is to accelerate atherosclerotic lesion growth by increasing lesion cellularity. Vascular expression of FasL may contribute to the progression of atherosclerosis.
Authors:
D B Schneider; G Vassalli; S Wen; R M Driscoll; A B Sassani; M B DeYoung; R Linnemann; R Virmani; D A Dichek
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Arteriosclerosis, thrombosis, and vascular biology     Volume:  20     ISSN:  1079-5642     ISO Abbreviation:  Arterioscler. Thromb. Vasc. Biol.     Publication Date:  2000 Feb 
Date Detail:
Created Date:  2000-03-03     Completed Date:  2000-03-03     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  9505803     Medline TA:  Arterioscler Thromb Vasc Biol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  298-308     Citation Subset:  IM    
Affiliation:
Gladstone Institute of Cardiovascular Disease, University of California, San Francisco 94141-9100, USA.
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MeSH Terms
Descriptor/Qualifier:
Adenoviridae / physiology
Animals
Apoptosis / physiology
Arteries / metabolism*
Arteriosclerosis / etiology*,  metabolism,  pathology
Cell Division / drug effects
Endothelium, Vascular / metabolism
Fas Ligand Protein
Gene Expression
Hypercholesterolemia / complications*,  metabolism*
Macrophages / pathology
Membrane Glycoproteins / genetics,  metabolism*,  pharmacology
Muscle, Smooth, Vascular / cytology,  drug effects,  physiology
Rabbits
T-Lymphocytes / physiology
Transgenes / genetics
Vascular Cell Adhesion Molecule-1 / metabolism
Grant Support
ID/Acronym/Agency:
HL-59963/HL/NHLBI NIH HHS; HL-60504/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/FASLG protein, human; 0/Fas Ligand Protein; 0/Membrane Glycoproteins; 0/Vascular Cell Adhesion Molecule-1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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