PUBLICATION

DDX24 spatiotemporally orchestrates VEGF and Wnt signaling during developmental angiogenesis

Authors
Chen, F., Deng, Z., Wang, X., Liu, Y., Zhao, K., Zhang, Y., He, S., Ran, R., Dong, Y., Guo, S., Zhou, Y., Zhou, B., Pang, P., Ge, W., Liu, C., Shan, H., He, H.
ID
ZDB-PUB-250510-3
Date
2025
Source
Proceedings of the National Academy of Sciences of the United States of America   122: e2417445122e2417445122 (Journal)
Registered Authors
Ge, Wei, He, Huanhuan
Keywords
DEAD-box helicase 24, VEGF, developmental angiogenesis, endothelial cells, spatial transcriptomics
MeSH Terms
  • Zebrafish Proteins*/genetics
  • Zebrafish Proteins*/metabolism
  • DEAD-box RNA Helicases*/genetics
  • DEAD-box RNA Helicases*/metabolism
  • Angiogenesis
  • Neovascularization, Physiologic*/genetics
  • Vascular Endothelial Growth Factor A*/genetics
  • Vascular Endothelial Growth Factor A*/metabolism
  • Vascular Endothelial Growth Factor Receptor-2/genetics
  • Vascular Endothelial Growth Factor Receptor-2/metabolism
  • Animals
  • Gene Expression Regulation, Developmental
  • Zebrafish/embryology
  • Zebrafish/genetics
  • Zebrafish/metabolism
  • Endothelial Cells/metabolism
  • Wnt Signaling Pathway*
PubMed
40339127 Full text @ Proc. Natl. Acad. Sci. USA
Abstract
Vascular development is a precisely controlled process, yet how it is spatiotemporally orchestrated remains enigmatic. We previously identified DEAD-box RNA helicase 24 (DDX24) as a pathogenic gene for multiorgan vascular anomalies. Here, we show that DDX24 is expressed in the endothelium during embryonic angiogenesis in zebrafish. DDX24 deficiency causes intersegmental vessel hyperbranching in the trunk, but inhibits central artery angiogenesis in the brain. Mechanistically, DDX24 deficiency enhances VEGFR2 expression by direct binding to its mRNA in nonbrain endothelial cells (ECs), while suppressing GPR124/RECK-mediated Wnt signaling in brain ECs. Additionally, spatial transcriptome analysis profiles DDX24-mediated crosstalk between ECs and neighboring cells. Finally, pharmacological targeting of these two pathways in a temporal manner can rescue the phenotypes induced by DDX24 deficiency. Overall, our findings highlight an essential role for DDX24 in the spatiotemporal regulation of developmental angiogenesis.
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Human Disease / Model
Sequence Targeting Reagents
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Mapping