Linked Life Data

11779403

Source:http://linkedlifedata.com/resource/pubmed/id/11779403

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
18
pubmed:dateCreated
2002-1-7
pubmed:abstractText
Adenovirus-mediated gene transfer of Fas ligand (FasL) inhibits neointimal formation in balloon-injured rat carotid arteries. Vascular smooth muscle (VSM) cells coexpressing murine FasL and p35, a baculovirus gene that inhibits caspase activity, are not susceptible to FasL-mediated apoptosis in vitro but are capable of inducing apoptosis of VSM cells that do not express p35. We reasoned that coexpression of p35 in FasL-transduced VSM cells in vivo would promote their survival, enhance FasL-induced apoptosis of adjacent VSM cells, and thereby facilitate a greater inhibition of neointimal formation. In balloon-injured rabbit femoral arteries, either Ad2/FasL/p35 or Ad2/FasL was infused into the injured site and withdrawn 20 min later. Both vectors induced a dose-dependent reduction (p < 0.05) of the neointima-to-media ratio when assessed 14 days later. However, Ad2/FasL/p35 exhibited a significantly greater inhibition of neointimal formation than Ad2/FasL. In a more clinically relevant model of restenosis, rabbit iliac arteries were injured with an angioplasty catheter under fluoroscopic guidance. Adenoviral vectors were delivered locally to the injured site over a period of 2 min, using a porous infusion balloon catheter. Twenty-eight days after gene transfer angiographic and histologic assessments indicated a significant (p < 0.05) inhibition of iliac artery lumen stenosis and neointimal formation by Ad2/FasL/p35 (5 x 10(11) particles per artery). The extent of inhibition was comparable to that achieved with Ad2/TK, an adenoviral vector encoding thymidine kinase (5 x 10(11) particles per artery) and coadministration of ganciclovir for 7 days. These data suggest that coexpression of p35 in FasL-transduced VSM cells is more potent at inhibiting neointimal formation and as such represents an improved gene therapy approach for restenosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1043-0342
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2191-202
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11779403-Adenoviruses, Human, pubmed-meshheading:11779403-Animals, pubmed-meshheading:11779403-Apoptosis, pubmed-meshheading:11779403-Balloon Occlusion, pubmed-meshheading:11779403-Coronary Restenosis, pubmed-meshheading:11779403-Cysteine Proteinase Inhibitors, pubmed-meshheading:11779403-Fas Ligand Protein, pubmed-meshheading:11779403-Femoral Artery, pubmed-meshheading:11779403-Gene Expression, pubmed-meshheading:11779403-Gene Transfer Techniques, pubmed-meshheading:11779403-Genetic Vectors, pubmed-meshheading:11779403-Humans, pubmed-meshheading:11779403-Iliac Artery, pubmed-meshheading:11779403-Inhibitor of Apoptosis Proteins, pubmed-meshheading:11779403-Male, pubmed-meshheading:11779403-Membrane Glycoproteins, pubmed-meshheading:11779403-Rabbits, pubmed-meshheading:11779403-Thymidine Kinase, pubmed-meshheading:11779403-Tunica Intima, pubmed-meshheading:11779403-Viral Proteins
pubmed:year
2001
pubmed:articleTitle
Enhancement of Fas ligand-induced inhibition of neointimal formation in rabbit femoral and iliac arteries by coexpression of p35.
pubmed:affiliation
Genzyme Corporation, 31 New York Avenue, Framingham, MA 01701, USA.
pubmed:publicationType
Journal Article