Ras/MAPK Signaling Modulates VEGFR-3 Expression through Ets-Mediated p300 Recruitment and Histone Acetylation on the Vegfr3 Gene in Lymphatic Endothelial Cells
Identifieur interne : 005483 ( Ncbi/Checkpoint ); précédent : 005482; suivant : 005484Ras/MAPK Signaling Modulates VEGFR-3 Expression through Ets-Mediated p300 Recruitment and Histone Acetylation on the Vegfr3 Gene in Lymphatic Endothelial Cells
Auteurs : Taeko Ichise ; Nobuaki Yoshida ; Hirotake IchiseSource :
- PLoS ONE [ 1932-6203 ] ; 2012.
Abstract
Modulation of VEGFR-3 expression is important for altering lymphatic endothelial cell (LEC) characteristics during the lymphangiogenic processes that occur under developmental, physiological, and pathological conditions. However, the mechanisms underlying the modulation of
Url:
DOI: 10.1371/journal.pone.0051639
PubMed: 23284731
PubMed Central: 3524184
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Ras/MAPK Signaling Modulates VEGFR-3 Expression through Ets-Mediated p300 Recruitment and Histone Acetylation on the <italic>Vegfr3</italic>
Gene in Lymphatic Endothelial Cells</title>
<author><name sortKey="Ichise, Taeko" sort="Ichise, Taeko" uniqKey="Ichise T" first="Taeko" last="Ichise">Taeko Ichise</name>
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<author><name sortKey="Yoshida, Nobuaki" sort="Yoshida, Nobuaki" uniqKey="Yoshida N" first="Nobuaki" last="Yoshida">Nobuaki Yoshida</name>
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<author><name sortKey="Ichise, Hirotake" sort="Ichise, Hirotake" uniqKey="Ichise H" first="Hirotake" last="Ichise">Hirotake Ichise</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Ras/MAPK Signaling Modulates VEGFR-3 Expression through Ets-Mediated p300 Recruitment and Histone Acetylation on the <italic>Vegfr3</italic>
Gene in Lymphatic Endothelial Cells</title>
<author><name sortKey="Ichise, Taeko" sort="Ichise, Taeko" uniqKey="Ichise T" first="Taeko" last="Ichise">Taeko Ichise</name>
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<author><name sortKey="Yoshida, Nobuaki" sort="Yoshida, Nobuaki" uniqKey="Yoshida N" first="Nobuaki" last="Yoshida">Nobuaki Yoshida</name>
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<author><name sortKey="Ichise, Hirotake" sort="Ichise, Hirotake" uniqKey="Ichise H" first="Hirotake" last="Ichise">Hirotake Ichise</name>
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<series><title level="j">PLoS ONE</title>
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<front><div type="abstract" xml:lang="en"><p>Modulation of VEGFR-3 expression is important for altering lymphatic endothelial cell (LEC) characteristics during the lymphangiogenic processes that occur under developmental, physiological, and pathological conditions. However, the mechanisms underlying the modulation of <italic>Vegfr3</italic>
gene expression remain largely unknown. Using genetically engineered mice and LECs, we demonstrated previously that Ras signaling is involved not only in VEGFR-3-induced signal transduction but also in <italic>Vegfr3</italic>
gene expression. Here, we investigated the roles of the transcription factor Ets and the histone acetyltransferase p300 in LECs in Ras-mediated transcriptional regulation of <italic>Vegfr3</italic>
. Ras activates Ets proteins via MAPK-induced phosphorylation. Ets knockdown, similar to Ras knockdown, resulted in a decrease in both <italic>Vegfr3</italic>
transcript levels and acetylated histone H3 on the <italic>Vegfr3</italic>
gene. <italic>Vegfr3</italic>
knockdown results in altered LEC phenotypes, such as aberrant cell proliferation and network formation, and Ets knockdown led to milder but similar phenotypic changes. We identified evolutionarily conserved, non-coding regulatory elements within the <italic>Vegfr3</italic>
gene that harbor Ets-binding motifs and have enhancer activities in LECs. Chromatin immunoprecipitation (ChIP) assays revealed that acetylated histone H3 on the regulatory elements of the <italic>Vegfr3</italic>
gene was decreased following Ras and Ets knockdown, and that activated Ets proteins, together with p300, were associated with these regulatory elements, consistent with a reduction in <italic>Vegfr3</italic>
gene expression in p300-knockdown LECs. Our findings demonstrate a link between Ras signaling and Ets- and p300-mediated transcriptional regulation of <italic>Vegfr3</italic>
, and provide a potential mechanism by which VEGFR-3 expression levels may be modulated during lymphangiogenesis.</p>
</div>
</front>
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<tree><noCountry><name sortKey="Ichise, Hirotake" sort="Ichise, Hirotake" uniqKey="Ichise H" first="Hirotake" last="Ichise">Hirotake Ichise</name>
<name sortKey="Ichise, Taeko" sort="Ichise, Taeko" uniqKey="Ichise T" first="Taeko" last="Ichise">Taeko Ichise</name>
<name sortKey="Yoshida, Nobuaki" sort="Yoshida, Nobuaki" uniqKey="Yoshida N" first="Nobuaki" last="Yoshida">Nobuaki Yoshida</name>
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