The endothelial transcription factor erg promotes vascular stability and growth through Wnt/β-catenin signaling

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Abstract

Blood vessel stability is essential for embryonic development; in the adult, many diseases are associated with loss of vascular integrity. The ETS transcription factor ERG drives expression of VE-cadherinand controls junctional integrity. We show that constitutive endothelial deletion of ERG (ErgcEC-KO) in mice causes embryonic lethality with vascular defects. Inducible endothelial deletion of ERG (ErgiEC-KO) results in defective physiological and pathological angiogenesis in the postnatal retina and tumors, with decreased vascular stability. ERG controls the Wnt/β-catenin pathway by promoting β-catenin stability, through signals mediated by VE-cadherin and the Wnt receptor Frizzled-4. Wnt signaling is decreased in ERG-deficient endothelial cells; activation of Wnt signaling with lithium chloride, which stabilizes β-catenin levels, corrects vascular defects in ErgcEC-KO embryos. Finally, overexpression of ERG invivo reduces permeability and increases stability of VEGF-induced blood vessels. These data demonstrate that ERG is an essential regulator of angiogenesis and vascular stability through Wnt signaling.

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Birdsey, G. M., Shah, A. V., Dufton, N., Reynolds, L. E., Almagro, L. O., Yang, Y., … Randi, A. M. (2015). The endothelial transcription factor erg promotes vascular stability and growth through Wnt/β-catenin signaling. Developmental Cell, 32(1), 82–96. https://doi.org/10.1016/j.devcel.2014.11.016

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