Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2011-8-12
pubmed:abstractText
Low birth weight (LBW) is associated with increased risk of cardiovascular diseases at adulthood. Nevertheless, the impact of LBW on the endothelium is not clearly established. We investigate whether LBW alters the angiogenic properties of cord blood endothelial colony forming cells (LBW-ECFCs) in 25 preterm neonates compared with 25 term neonates (CT-ECFCs). We observed that LBW decreased the number of colonies formed by ECFCs and delayed the time of appearance of their clonal progeny. LBW dramatically reduced LBW-ECFC capacity to form sprouts and tubes, to migrate and to proliferate in vitro. The angiogenic defect of LBW-ECFCs was confirmed in vivo by their inability to form robust capillary networks in Matrigel plugs injected in nu/nu mice. Gene profile analysis of LBW-ECFCs demonstrated an increased expression of antiangiogenic genes. Among them, thrombospondin 1 (THBS1) was highly expressed at RNA and protein levels in LBW-ECFCs. Silencing THBS1 restored the angiogenic properties of LBW-ECFCs by increasing AKT phosphorylation. The imbalance toward an angiostatic state provide a mechanistic link between LBW and the impaired angiogenic properties of ECFCs and allows the identification of THBS1 as a novel player in LBW-ECFC defect, opening new perspectives for novel deprogramming agents.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1528-0020
pubmed:author
pubmed:issnType
Electronic
pubmed:day
11
pubmed:volume
118
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1699-709
pubmed:meshHeading
pubmed-meshheading:21659549-Animals, pubmed-meshheading:21659549-Blood Vessels, pubmed-meshheading:21659549-Blotting, Western, pubmed-meshheading:21659549-Cell Proliferation, pubmed-meshheading:21659549-Cells, Cultured, pubmed-meshheading:21659549-Endothelial Cells, pubmed-meshheading:21659549-Female, pubmed-meshheading:21659549-Fetal Blood, pubmed-meshheading:21659549-Gene Expression Profiling, pubmed-meshheading:21659549-Humans, pubmed-meshheading:21659549-Infant, Low Birth Weight, pubmed-meshheading:21659549-Infant, Newborn, pubmed-meshheading:21659549-Infant, Premature, pubmed-meshheading:21659549-Male, pubmed-meshheading:21659549-Mice, pubmed-meshheading:21659549-Mice, Inbred Strains, pubmed-meshheading:21659549-Mice, Nude, pubmed-meshheading:21659549-Neovascularization, Physiologic, pubmed-meshheading:21659549-Phosphorylation, pubmed-meshheading:21659549-Proto-Oncogene Proteins c-akt, pubmed-meshheading:21659549-RNA Interference, pubmed-meshheading:21659549-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:21659549-Stem Cell Transplantation, pubmed-meshheading:21659549-Stem Cells, pubmed-meshheading:21659549-Thrombospondin 1
pubmed:year
2011
pubmed:articleTitle
A switch toward angiostatic gene expression impairs the angiogenic properties of endothelial progenitor cells in low birth weight preterm infants.
pubmed:affiliation
Inserm, Unité Mixte de Recherche 608, Physiopathologie de l'Endothélium Marseille, Marseille, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't