Linked Life Data

12187124

Source:http://linkedlifedata.com/resource/pubmed/id/12187124

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2002-8-20
pubmed:abstractText
Proliferation, migration and invasion of smooth muscle cells (SMCs) are essential pathogenic processes in the development of a broad spectrum of cardiovascular disorders, like arteriosclerosis, restenosis after percutaneous transluminal angioplasty and stent implantation as well as transplant vessel disease. As an in vitro model mimicking these processes, the Boyden chamber was employed to characterize the diverging migratory and invasive potentials of proliferating and nonproliferating human arterial SMCs (haSMCs). Using this model, differential gene expression of both phenotypes was analyzed by a cDNA array system (Clontech human cardiovascular array). With these arrays, 558 cardiovascular-associated genes could be compared. Further, gene expression was exactly quantified by real-time RT-PCR. Protein expression was analyzed by ELISA and Western blotting. In total, 47 genes were differentially expressed more than 1.5 times. Most of the differentially regulated genes in this study were associated with the extracellular matrix (ECM) and cell motility. In detail, the respective groups were matrix-organizing proteins, ECM proteins, cell adhesion proteins, extracellular communication and cytoskeleton motility proteins. Genes known to be differentially regulated during haSMC migration and invasion, like TIMP 2, TIMP 3, and MMP 3, were confirmed by the array data. Reduced expression of several cytoskeletal proteins, like vimentin, fibronectin, cytokeratins and beta1 integrin, was shown in the invasive phenotype. Further, angio-associated protein, alpha E-catenin and atrial brain natriuretic peptide receptor were downregulated whereas TFPI 2 was strongly upregulated in invasive haSMCs. In conclusion, several relevant potential candidate genes for the quiescent and the invasive SMC phenotype were identified and genes already known to be differentially regulated by previous analysis were confirmed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1018-1172
pubmed:author
pubmed:copyrightInfo
Copyright 2002 S. Karger AG, Basel
pubmed:issnType
Print
pubmed:volume
39
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
340-52
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12187124-Antigens, CD29, pubmed-meshheading:12187124-Arteriosclerosis, pubmed-meshheading:12187124-Cell Division, pubmed-meshheading:12187124-Cell Movement, pubmed-meshheading:12187124-Cells, Cultured, pubmed-meshheading:12187124-Coronary Restenosis, pubmed-meshheading:12187124-Extracellular Matrix, pubmed-meshheading:12187124-Fibronectins, pubmed-meshheading:12187124-Gene Expression, pubmed-meshheading:12187124-Gene Expression Regulation, pubmed-meshheading:12187124-Humans, pubmed-meshheading:12187124-Keratins, pubmed-meshheading:12187124-Mammary Arteries, pubmed-meshheading:12187124-Matrix Metalloproteinase 3, pubmed-meshheading:12187124-Models, Biological, pubmed-meshheading:12187124-Muscle, Smooth, Vascular, pubmed-meshheading:12187124-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:12187124-Phenotype, pubmed-meshheading:12187124-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:12187124-Tissue Inhibitor of Metalloproteinase-2, pubmed-meshheading:12187124-Tissue Inhibitor of Metalloproteinase-3, pubmed-meshheading:12187124-Vimentin
pubmed:articleTitle
Characterization of differential gene expression in quiescent and invasive human arterial smooth muscle cells.
pubmed:affiliation
Medical Clinic I, University Hospital RWTH Aachen, Aachen, Germany. ruediger.blindt@post.rwth-aachen.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't