ArticleDevelopmental biology2007
FoxH1 negatively modulates flk1 gene expression and vascular formation in zebrafish.
Article in Developmental biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.
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Who cites it
117 citing papers in PubMed, 223 citations in OpenAlex.
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- In vivo profiling of the endothelium using 'AngioTag' zebrafish.Angiogenesis · 2025Article
- Microinjection of angiotensin II into zebrafish embryos induces transient dilation and elastin disruption of the dorsal aorta.Physiological reports · 2025Article
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- Distribution and developmental timing of zebrafish liver innervation.Biology letters · 2024Article
- Endocardium gives rise to blood cells in zebrafish embryos.Cell reports · 2024Article
- Single-cell analysis reveals distinct fibroblast plasticity during tenocyte regeneration in zebrafish.Science advances · 2023Article
- Defining the cellular complexity of the zebrafish bipotential gonad.Biology of reproduction · 2023Article
- Review
57 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Flk1 is the major receptor for VEGF on endothelial cells. During embryogenesis, flk1 is required for both vasculogenesis and angiogenesis and abnormally elevated flk1 expression is often associated with pathological conditions in adults. While the biological function of flk1 has been studied extensively, very little is known about how the flk1 gene is regulated at the transcriptional level. Our transgenic study led to the identification of a flk1 endothelial enhancer positioned approximately 5 kb upstream of the flk1 translation initiation site. Binding sites for FoxH1, scl, ets and gata factors are found in the zebrafish flk1 endothelial enhancer, as well as in upstream sequences of mouse flk1 and human kdr genes, suggesting that the regulatory machinery for flk1/kdr is conserved from fish to mammals. The roles of scl, ets and gata factors in hemangioblasts have been well defined, but the significance of FoxH1 in vessel formation has not been explored previously. Here we show that FoxH1 binds to the flk1 endothelial enhancer in vitro and functions as a repressor for flk1 transcription in cultured cells. Consistent with these findings, the expression level of flk1 is elevated in embryos lacking both maternal and zygotic FoxH1. We further show that overexpression of FoxH1 has a negative effect on vascular formation that can be counteracted by the down-regulation of smad2 activity in zebrafish embryos. Taken together, our data provide the first evidence that flk1 is a direct target of FoxH1 and that FoxH1 is involved in vessel formation in zebrafish.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.