The Foxc2 Transcription Factor Regulates Angiogenesis via Induction of Integrin β3 Expression*S⃞
Identifieur interne : 002D93 ( Ncbi/Merge ); précédent : 002D92; suivant : 002D94The 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
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Integrin β3
Expression<xref ref-type="fn" rid="fn1">*</xref>
<xref ref-type="fn" rid="fn2">S⃞</xref>
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<author><name sortKey="Hayashi, Hisaki" sort="Hayashi, Hisaki" uniqKey="Hayashi H" first="Hisaki" last="Hayashi">Hisaki Hayashi</name>
</author>
<author><name sortKey="Sano, Hideto" sort="Sano, Hideto" uniqKey="Sano H" first="Hideto" last="Sano">Hideto Sano</name>
</author>
<author><name sortKey="Seo, Seungwoon" sort="Seo, Seungwoon" uniqKey="Seo S" first="Seungwoon" last="Seo">Seungwoon Seo</name>
</author>
<author><name sortKey="Kume, Tsutomu" sort="Kume, Tsutomu" uniqKey="Kume T" first="Tsutomu" last="Kume">Tsutomu Kume</name>
</author>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">The Foxc2 Transcription Factor Regulates Angiogenesis via Induction of
Integrin β3
Expression<xref ref-type="fn" rid="fn1">*</xref>
<xref ref-type="fn" rid="fn2">S⃞</xref>
</title>
<author><name sortKey="Hayashi, Hisaki" sort="Hayashi, Hisaki" uniqKey="Hayashi H" first="Hisaki" last="Hayashi">Hisaki Hayashi</name>
</author>
<author><name sortKey="Sano, Hideto" sort="Sano, Hideto" uniqKey="Sano H" first="Hideto" last="Sano">Hideto Sano</name>
</author>
<author><name sortKey="Seo, Seungwoon" sort="Seo, Seungwoon" uniqKey="Seo S" first="Seungwoon" last="Seo">Seungwoon Seo</name>
</author>
<author><name sortKey="Kume, Tsutomu" sort="Kume, Tsutomu" uniqKey="Kume T" first="Tsutomu" last="Kume">Tsutomu Kume</name>
</author>
</analytic>
<series><title level="j">The Journal of Biological Chemistry</title>
<idno type="ISSN">0021-9258</idno>
<idno type="eISSN">1083-351X</idno>
<imprint><date when="2008">2008</date>
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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>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Biol Chem</journal-id>
<journal-id journal-id-type="publisher-id">jbc</journal-id>
<journal-title-group><journal-title>The Journal of Biological Chemistry</journal-title>
</journal-title-group>
<issn pub-type="ppub">0021-9258</issn>
<issn pub-type="epub">1083-351X</issn>
<publisher><publisher-name>American Society for Biochemistry and Molecular Biology</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">18579532</article-id>
<article-id pub-id-type="pmc">2527100</article-id>
<article-id pub-id-type="publisher-id">23791</article-id>
<article-id pub-id-type="doi">10.1074/jbc.M800190200</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Molecular Basis of Cell and Developmental Biology</subject>
</subj-group>
</article-categories>
<title-group><article-title>The Foxc2 Transcription Factor Regulates Angiogenesis via Induction of
Integrin β3
Expression<xref ref-type="fn" rid="fn1">*</xref>
<xref ref-type="fn" rid="fn2">S⃞</xref>
</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Hayashi</surname>
<given-names>Hisaki</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Sano</surname>
<given-names>Hideto</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Seo</surname>
<given-names>Seungwoon</given-names>
</name>
</contrib>
<contrib contrib-type="author"><name><surname>Kume</surname>
<given-names>Tsutomu</given-names>
</name>
<xref ref-type="corresp" rid="cor1">1</xref>
</contrib>
</contrib-group>
<aff id="d31e50">Division of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee 37232-6300</aff>
<author-notes><corresp id="cor1"><label>1</label>
To whom correspondence should be addressed: Div. of Cardiovascular Medicine,
Dept. of Medicine, Vanderbilt University Medical Center, 2220 Pierce Ave.,
Nashville, TN 37232-6300. Tel.: 615-936-2884; Fax: 615-936-1872; E-mail:
<email>tsutomu.kume@vanderbilt.edu</email>
.
</corresp>
</author-notes>
<pub-date pub-type="ppub"><day>29</day>
<month>8</month>
<year>2008</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>29</day>
<month>8</month>
<year>2009</year>
</pub-date>
<pmc-comment> PMC Release delay is 12 months and 0 days and was based on the copyright element. </pmc-comment>
<volume>283</volume>
<issue>35</issue>
<fpage>23791</fpage>
<lpage>23800</lpage>
<history><date date-type="received"><day>9</day>
<month>1</month>
<year>2008</year>
</date>
<date date-type="rev-recd"><day>9</day>
<month>6</month>
<year>2008</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2008, The American Society for Biochemistry and
Molecular Biology, Inc.</copyright-statement>
<copyright-year>2008</copyright-year>
</permissions>
<self-uri xlink:title="pdf" xlink:href="zbc03508023791.pdf"></self-uri>
<abstract><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>
</abstract>
</article-meta>
<notes><fn-group><fn id="fn1"><label>*</label>
<p>This work was supported, in whole or in part, by <funding-source>National
Institutes of Health</funding-source>
Grants
<award-id>HL067105</award-id>
, <award-id>DK068547</award-id>
, and
<award-id>HL074121</award-id>
(to T. K.). The costs of publication of this
article were defrayed in part by the payment of page charges. This article
must therefore be hereby marked “<italic>advertisement</italic>
” in
accordance with 18 U.S.C. Section 1734 solely to indicate this fact.</p>
</fn>
<fn id="fn2"><label></label>
<p>The on-line version of this article (available at
<ext-link ext-link-type="uri" xlink:href="http://www.jbc.org">http://www.jbc.org</ext-link>
)
contains supplemental “Materials and Methods,” Figs. 1–4,
Table 1, and an additional reference.</p>
</fn>
</fn-group>
</notes>
</front>
</pmc>
<affiliations><list></list>
<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>
</tree>
</affiliations>
</record>
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