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Endothelial beta-Catenin Signaling Supports Postnatal Brain and Retinal Angiogenesis by Promoting Sprouting, Tip Cell Formation, and VEGFR (Vascular Endothelial Growth Factor Receptor) 2 Expression

Martowicz, Agnieszka (author)
Karolinska Inst, Dept Med Biochem & Biophys, Div Vasc Biol, Biomedicum 6D, S-17165 Stockholm, Sweden
Trusohamn, Marta (author)
Karolinska Inst, Dept Med Biochem & Biophys, Div Vasc Biol, Biomedicum 6D, S-17165 Stockholm, Sweden
Jensen, Nina (author)
Karolinska Inst, Dept Med Biochem & Biophys, Div Vasc Biol, Biomedicum 6D, S-17165 Stockholm, Sweden
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Wisniewska-Kruk, Joanna (author)
Karolinska Inst, Dept Med Biochem & Biophys, Div Vasc Biol, Biomedicum 6D, S-17165 Stockholm, Sweden
Corada, Monica (author)
FIRC Inst Mol Oncol, IFOM, Milan, Italy
Ning, Frank Chenfei (author)
Karolinska Institutet
Kele, Julianna (author)
Karolinska Institutet
Dejana, Elisabetta (author)
Uppsala universitet,Vaskulärbiologi,FIRC Inst Mol Oncol, IFOM, Milan, Italy
Nyqvist, Daniel (author)
Karolinska Institutet
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 (creator_code:org_t)
LIPPINCOTT WILLIAMS & WILKINS, 2019
2019
English.
In: Arteriosclerosis, Thrombosis and Vascular Biology. - : LIPPINCOTT WILLIAMS & WILKINS. - 1079-5642 .- 1524-4636. ; 39:11, s. 2273-2288
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • Objective: Activation of endothelial beta-catenin signaling by neural cell-derived Norrin or Wnt ligands is vital for the vascularization of the retina and brain. Mutations in members of the Norrin/beta-catenin pathway contribute to inherited blinding disorders because of defective vascular development and dysfunctional blood-retina barrier. Despite a vital role for endothelial beta-catenin signaling in central nervous system health and disease, its contribution to central nervous system angiogenesis and its interactions with downstream signaling cascades remains incompletely understood.Approach and Results: Here, using genetically modified mouse models, we show that impaired endothelial beta-catenin signaling caused hypovascularization of the postnatal retina and brain because of deficient endothelial cell proliferation and sprouting. Mosaic genetic analysis demonstrated that endothelial beta-catenin promotes but is not required for tip cell formation. In addition, pharmacological treatment revealed that angiogenesis under conditions of inhibited Notch signaling depends upon endothelial beta-catenin. Importantly, impaired endothelial beta-catenin signaling abrogated the expression of the VEGFR (vascular endothelial growth factor receptor)-2 and VEGFR3 in brain microvessels but not in the lung endothelium.Conclusions: Our study identifies molecular crosstalk between the Wnt/beta-catenin and the Notch and VEGF-A signaling pathways and strongly suggest that endothelial beta-catenin signaling supports central nervous system angiogenesis by promoting endothelial cell sprouting, tip cell formation, and VEGF-A/VEGFR2 signaling.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Cell- och molekylärbiologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Cell and Molecular Biology (hsv//eng)

Keyword

beta catenin
blood-brain barrier
central nervous system
endothelial cell
vegf

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