The Foxc2 Transcription Factor Regulates Angiogenesis via Induction of Integrin β3 Expression*S⃞
Identifieur interne : 006916 ( Main/Exploration ); précédent : 006915; suivant : 006917The Foxc2 Transcription Factor Regulates Angiogenesis via Induction of Integrin β3 Expression*S⃞
Auteurs : Hisaki Hayashi ; Hideto Sano ; Seungwoon Seo ; Tsutomu KumeSource :
- The Journal of Biological Chemistry [ 0021-9258 ] ; 2008.
Abstract
Forkhead transcription factor Foxc2 is an essential regulator of the
cardiovascular system in development and disease. However, the cellular and
molecular functions of Foxc2 in vascular endothelial cells are still not fully
understood. Here, through gene expression profiling in endothelial cells, we
identified molecules associated with cell-extracellular matrix interactions,
integrin β3 (Itgb3), integrin β5 (Itgb5), and fibronectin, as
downstream targets of Foxc2. We found that
Url:
DOI: 10.1074/jbc.M800190200
PubMed: 18579532
PubMed Central: 2527100
Affiliations:
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<front><div type="abstract" xml:lang="en"><p>Forkhead transcription factor Foxc2 is an essential regulator of the
cardiovascular system in development and disease. However, the cellular and
molecular functions of Foxc2 in vascular endothelial cells are still not fully
understood. Here, through gene expression profiling in endothelial cells, we
identified molecules associated with cell-extracellular matrix interactions,
integrin β3 (Itgb3), integrin β5 (Itgb5), and fibronectin, as
downstream targets of Foxc2. We found that <italic>Itgb3</italic>
expression is
directly regulated by Foxc2 through multiple Forkhead-binding elements within
two high homology regions in the <italic>Itgb3</italic>
promoter. Because Itgb3 is
known to regulate angiogenesis, we further tested whether Foxc2 is directly
involved in angiogenesis by regulating Itgb3 expression by <italic>in vitro</italic>
experiments. Overexpression of <italic>Foxc2</italic>
significantly enhanced
endothelial cell migration and adhesion, whereas this effect was strongly
inhibited by Itgb3 neutralization antibody. In accordance with these results,
pulmonary microvascular endothelial cells isolated from <italic>Foxc2</italic>
heterozygous mutant mice showed a marked reduction in <italic>Itgb3</italic>
expression and cell migration. Finally, <italic>ex vivo</italic>
aortic ring assay to
test the sprouting and microvessel formation revealed enhanced microvessel
outgrowth by <italic>Foxc2</italic>
overexpression. Conversely, microvessel outgrowth
from aortas of <italic>Foxc2</italic>
heterozygous mutant mice was reduced. Taken
together, these results suggest that Foxc2 directly induces <italic>Itgb3</italic>
expression and regulates angiogenesis by Itgb3-mediated endothelial cell
adhesion and migration.</p>
</div>
</front>
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<tree><noCountry><name sortKey="Hayashi, Hisaki" sort="Hayashi, Hisaki" uniqKey="Hayashi H" first="Hisaki" last="Hayashi">Hisaki Hayashi</name>
<name sortKey="Kume, Tsutomu" sort="Kume, Tsutomu" uniqKey="Kume T" first="Tsutomu" last="Kume">Tsutomu Kume</name>
<name sortKey="Sano, Hideto" sort="Sano, Hideto" uniqKey="Sano H" first="Hideto" last="Sano">Hideto Sano</name>
<name sortKey="Seo, Seungwoon" sort="Seo, Seungwoon" uniqKey="Seo S" first="Seungwoon" last="Seo">Seungwoon Seo</name>
</noCountry>
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