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Publication
The VEGF receptor Flt-1 spatially modulates Flk-1 signaling and blood vessel
branching.
Authors
Kappas NC, Zeng G, Chappell JC, Kearney JB, Hazarika S, Kallianos KG, Patterson
C, Annex BH, Bautch VL
Submitted By
Thomas Coffman on 8/11/2010
Status
Published
Journal
The Journal of cell biology
Year
2008
Date Published
6/2/2008
Volume : Pages
181 : 847 - 858
PubMed Reference
18504303
Abstract
Blood vessel formation requires the integrated regulation of endothelial cell
proliferation and branching morphogenesis, but how this coordinated regulation
is achieved is not well understood. Flt-1 (vascular endothelial growth factor
[VEGF] receptor 1) is a high affinity VEGF-A receptor whose loss leads to vessel
overgrowth and dysmorphogenesis. We examined the ability of Flt-1 isoform
transgenes to rescue the vascular development of embryonic stem cell-derived
flt-1-/- mutant vessels. Endothelial proliferation was equivalently rescued by
both soluble (sFlt-1) and membrane-tethered (mFlt-1) isoforms, but only sFlt-1
rescued vessel branching. Flk-1 Tyr-1173 phosphorylation was increased in
flt-1-/- mutant vessels and partially rescued by the Flt-1 isoform transgenes.
sFlt-1-rescued vessels exhibited more heterogeneous levels of pFlk than did
mFlt-1-rescued vessels, and reporter gene expression from the flt-1 locus was
also heterogeneous in developing vessels. Our data support a model whereby
sFlt-1 protein is more efficient than mFlt-1 at amplifying initial expression
differences, and these amplified differences set up local discontinuities in
VEGF-A ligand availability that are important for proper vessel branching.
Investigators with authorship
Name
Institution
Thomas Coffman
Duke University Medical Center
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(DiaComp) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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