PUBLICATION

P130Cas/bcar1 mediates zebrafish caudal vein plexus angiogenesis

Authors
Wisniewski, L., French, V., Lockwood, N., Valdivia, L.E., Frankel, P.
ID
ZDB-PUB-201002-160
Date
2020
Source
Scientific Reports   10: 15589 (Journal)
Registered Authors
Valdivia, Leonardo
Keywords
none
MeSH Terms
  • Animals
  • Animals, Genetically Modified/embryology
  • Animals, Genetically Modified/physiology*
  • Bone Morphogenetic Protein 2/genetics
  • Bone Morphogenetic Protein 2/metabolism
  • Embryo, Nonmammalian/cytology
  • Embryo, Nonmammalian/physiology*
  • Neovascularization, Physiologic*
  • Veins/embryology
  • Veins/physiology*
  • Zebrafish/embryology
  • Zebrafish/physiology*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed
32973180 Full text @ Sci. Rep.
Abstract
P130CAS/BCAR1 belongs to the CAS family of adaptor proteins, with important regulatory roles in cell migration, cell cycle control, and apoptosis. Previously, we and others showed that P130CAS mediates VEGF-A and PDGF signalling in vitro, but its cardiovascular function in vivo remains relatively unexplored. We characterise here a novel deletion model of P130CAS in zebrafish. Using in vivo microscopy and transgenic vascular reporters, we observed that while bcar1-/- zebrafish showed no arterial angiogenic or heart defects during development, they strikingly failed to form the caudal vein plexus (CVP). Endothelial cells (ECs) within the CVP of bcar1-/- embryos produced fewer filopodial structures and did not detach efficiently from neighbouring cells, resulting in a significant reduction in ventral extension and overall CVP area. Mechanistically, we show that P130Cas mediates Bmp2b-induced ectopic angiogenic sprouting of ECs in the developing embryo and provide pharmacological evidence for a role of Src family kinases in CVP development.
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Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping