Linked Life Data

18816823

Source:http://linkedlifedata.com/resource/pubmed/id/18816823

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2008-10-2
pubmed:abstractText
The nuclear factor-kappaB (NF-kappaB) signaling pathway regulates cellular growth, survival, differentiation and development. In this study, the functions of IkappaB kinase (IKK)beta in angiogenesis during mouse development were examined. Conditional disruption of the Ikkbeta locus in endothelial cells using the well-characterized Tie2-Cre transgene resulted in embryonic lethality between embryonic day (E) 13.5 and E15.5. Examination of the mutant embryos revealed that while deletion of Ikkbeta occurred in endothelial cells throughout the embryo, only the vascular network in the fetal liver was affected. Disruption of the fetal liver vasculature was accompanied by decreased cell proliferation and increased apoptosis of hepatocytes, but hematopoiesis was not affected. Increased apoptosis was not observed outside of fetal liver in the mutant embryos. These results indicate that the IKKbeta/NF-kappaB pathway plays a previously unappreciated role in development of the sinusoidal vasculature in the fetal liver and additionally that this pathway is critical in the crosstalk between endothelial cells and hepatocytes during mouse development.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1058-8388
pubmed:author
pubmed:copyrightInfo
Copyright (c) 2008 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
237
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2926-35
pubmed:dateRevised
2011-5-27
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Analysis of the IKKbeta/NF-kappaB signaling pathway during embryonic angiogenesis.
pubmed:affiliation
Department of Molecular and Cellular Biochemistry and Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio 43210, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural