|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
4
|
|
pubmed:dateCreated |
2003-10-15
|
|
pubmed:abstractText |
Vascular injury and inflammation are associated with elaboration of a number of cytokines that signal through multiple pathways to act as smooth muscle cell (SMC) mitogens. Activation of the nuclear factor-kappa B (NF-kappaB) transcription factor is essential for SMC proliferation in vitro and is activated by vascular injury in vivo. Activation of NF-kappaB is controlled by several upstream regulators, including the inhibitors of kappa B (IkappaB). These proteins bind to and keep NF-kappaB inactivated. The purpose of this study was to determine whether adenoviral gene transfer of a mutated IkappaBalpha super-repressor (AdIkappaBalphaSR) could inhibit development of intimal hyperplasia in vivo and to investigate how over-expression of this construct influences in vitro SMC proliferation and cell cycle regulatory proteins.
|
|
pubmed:grant |
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cdkn1a protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin-Dependent Kinase Inhibitor...,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclins,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/I-kappa B Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappaB inhibitor alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Proliferating Cell Nuclear Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/beta-Galactosidase
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Oct
|
|
pubmed:issn |
0741-5214
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:volume |
38
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
812-9
|
|
pubmed:dateRevised |
2008-11-21
|
|
pubmed:meshHeading |
pubmed-meshheading:14560235-Adenoviridae,
pubmed-meshheading:14560235-Animals,
pubmed-meshheading:14560235-Aorta,
pubmed-meshheading:14560235-Blotting, Western,
pubmed-meshheading:14560235-Carotid Arteries,
pubmed-meshheading:14560235-Cattle,
pubmed-meshheading:14560235-Cell Division,
pubmed-meshheading:14560235-Cell Survival,
pubmed-meshheading:14560235-Cells, Cultured,
pubmed-meshheading:14560235-Cyclin-Dependent Kinase Inhibitor p21,
pubmed-meshheading:14560235-Cyclins,
pubmed-meshheading:14560235-Enzyme Inhibitors,
pubmed-meshheading:14560235-Fetal Blood,
pubmed-meshheading:14560235-Genetic Vectors,
pubmed-meshheading:14560235-Hyperplasia,
pubmed-meshheading:14560235-I-kappa B Proteins,
pubmed-meshheading:14560235-Immunohistochemistry,
pubmed-meshheading:14560235-Interleukin-1,
pubmed-meshheading:14560235-Interleukin-6,
pubmed-meshheading:14560235-Male,
pubmed-meshheading:14560235-Muscle, Smooth, Vascular,
pubmed-meshheading:14560235-Mutation,
pubmed-meshheading:14560235-NF-kappa B,
pubmed-meshheading:14560235-Proliferating Cell Nuclear Antigen,
pubmed-meshheading:14560235-Rats,
pubmed-meshheading:14560235-Rats, Sprague-Dawley,
pubmed-meshheading:14560235-Signal Transduction,
pubmed-meshheading:14560235-Transcriptional Activation,
pubmed-meshheading:14560235-Transfection,
pubmed-meshheading:14560235-Tumor Necrosis Factor-alpha,
pubmed-meshheading:14560235-Tunica Intima,
pubmed-meshheading:14560235-beta-Galactosidase
|
|
pubmed:year |
2003
|
|
pubmed:articleTitle |
Overexpression of mutated IkappaBalpha inhibits vascular smooth muscle cell proliferation and intimal hyperplasia formation.
|
|
pubmed:affiliation |
Department of Surgery, University of Pittsburgh School of Medicine, 3459 Fifth Avenue, Pittsburgh, PA 15213, USA. zuckerbraun@msx.upmc.edu
|
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|
