Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2004-4-16
pubmed:abstractText
The function of cytoskeletal proteins in the modulation of vascular smooth muscle cell (SMC) phenotype during vascular disease is poorly understood. In this report, we used a combination of gene targeting and Cre/lox-mediated cell fate mapping in mice to investigate the role of SM22alpha, an SMC-specific cytoskeletal protein of unknown function, in the development of atherosclerosis. In hypercholesterolemic ApoE-deficient mice, genetic ablation of SM22alpha resulted in increased atherosclerotic lesion area and a higher proportion of proliferating SMC-derived plaque cells. These results identify a role for SM22alpha in the regulation of SMC phenotype during atherogenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1524-4571
pubmed:author
pubmed:issnType
Electronic
pubmed:day
16
pubmed:volume
94
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
863-5
pubmed:dateRevised
2011-11-10
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
SM22alpha modulates vascular smooth muscle cell phenotype during atherogenesis.
pubmed:affiliation
Institut für Pharmakologie und Toxikologie, Technische Universität, Biedersteiner Str. 29, 80802 München, Germany. feil@ipt.med.tu-muenchen.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't