Linked Life Data

21375457

Source:http://linkedlifedata.com/resource/pubmed/id/21375457

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2011-4-11
pubmed:abstractText
Neointimal formation in atheromatous blood vessels is associated with both growth factor-induced differentiation of smooth muscle cells and endothelial-to-mesenchymal transition. Transforming growth factor beta (TGF?)-signaling is well known to play a critical role in the regulation of vessel remodeling as well as in atherosclerosis and restenosis. Here, we investigated the role of TGF?1 and N-cadherin on the differentiation and migration of human vascular smooth muscle cells (VSMC). TGF?1-treatment of cultured VSMC reduced their migratory activity as determined in cell migration assays. This reduced migration correlated with increased concentration of N-cadherin on mRNA and protein level. The TGF?1-induced increase of N-cadherin was sensitive against pharmacological inhibition of the ALK5 TGF? receptor and was accompanied by TGF?1-induced expression of the transcription factor snail1. Activation of N-cadherin by using a HAV-containing peptide of N-cadherin also decreased the migration of VSMC. N-cadherin-mediated suppression of VSMC migration was associated with an increased activity of RhoA, which is activated by binding of the HAV peptide to N-cadherin. Our results demonstrate that TGF?1 induces the differentiation of primary VSMC cells by Smad2/3-dependent up-regulation of the transcription factor snail1 and subsequently of N-cadherin, leading to inhibition of VSMC migration by RhoA-dependent modulation of the actin cytoskeleton.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1437-4315
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
392
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
461-74
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
TGF?1 suppresses vascular smooth muscle cell motility by expression of N-cadherin.
pubmed:affiliation
Internal Medicine I, Nephrology, University of Ulm, Albert-Einstein-Allee, Germany.
pubmed:publicationType
Journal Article