Linked Life Data

14970264

Source:http://linkedlifedata.com/resource/pubmed/id/14970264

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
Pt 7
pubmed:dateCreated
2004-3-3
pubmed:abstractText
The basic helix-loop-helix tal-1 gene (or scl), known for its fundamental role in embryonic and adult hematopoiesis in vertebrates, is also required for embryonic vascular remodeling. In adults, TAL-1 protein is undetectable in quiescent endothelium but it is present in newly formed vessels including tumoral vasculature, indicating its involvement in angiogenesis. Here, we demonstrate that TAL-1 expression is tightly regulated during in vitro angiogenesis: it is low during the initial step of migration and is upregulated during formation of capillary-like structures. We investigated whether ectopic expression of either wild-type TAL-1 or a dominant-negative mutant lacking the DNA-binding domain (Delta-bas) modulates the activity of human primary endothelial cells in the angiogenic processes of migration, proliferation and cell morphogenesis. Overexpression of either wild-type or Delta-bas TAL-1 affected chemotactic migration of primary endothelial cells without modifying their proliferative properties. Ectopic expression of wild-type TAL-1 accelerated the formation of capillary-like structures in vitro and, in vivo, enhanced vascularisation in mice (Matrigel implants) associated with a general enlargement of capillary lumens. Importantly, transduction of the mutant Delta-bas completely impaired in vitro angiogenesis and strongly inhibited vascularisation in mice. Taken together, our data show that TAL-1 modulates the angiogenic response of endothelial cells by stimulating cell morphogenesis and by influencing their behavior in migration. This study highlights the importance of TAL-1 regulation in postnatal vascular remodeling and provides the first physiological evidence that links TAL-1 activity to endothelial cell morphogenic processes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0021-9533
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
117
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1161-71
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:14970264-Animals, pubmed-meshheading:14970264-Base Sequence, pubmed-meshheading:14970264-Basic Helix-Loop-Helix Transcription Factors, pubmed-meshheading:14970264-Cell Division, pubmed-meshheading:14970264-Cell Movement, pubmed-meshheading:14970264-Cells, Cultured, pubmed-meshheading:14970264-DNA-Binding Proteins, pubmed-meshheading:14970264-Endothelium, Vascular, pubmed-meshheading:14970264-Gene Expression Regulation, Developmental, pubmed-meshheading:14970264-Helix-Loop-Helix Motifs, pubmed-meshheading:14970264-Humans, pubmed-meshheading:14970264-Male, pubmed-meshheading:14970264-Mice, pubmed-meshheading:14970264-Mice, SCID, pubmed-meshheading:14970264-Neovascularization, Physiologic, pubmed-meshheading:14970264-Proto-Oncogene Proteins, pubmed-meshheading:14970264-RNA, Small Interfering, pubmed-meshheading:14970264-RNA Interference, pubmed-meshheading:14970264-Sequence Deletion, pubmed-meshheading:14970264-Transcription Factors
pubmed:year
2004
pubmed:articleTitle
The bHLH TAL-1/SCL regulates endothelial cell migration and morphogenesis.
pubmed:affiliation
UMR 5535, Institut de Génétique Moléculaire, IFR122, 1919 Route de Mende, Montpellier, France.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't