PUBLICATION
miR-150 controls developmental angiogenesis via ribosome biogenesis-dependent regulation of Notch signaling
- Authors
- Kong, H., Ai, K., Zhang, J., Liu, Z., Wu, Y., Zhang, L., Zhang, H., Chen, X., Li, L., Fu, Y., Wang, X., Li, L.
- ID
- ZDB-PUB-260616-20
- Date
- 2026
- Source
- Angiogenesis 29: 45 (Journal)
- Registered Authors
- Li, Lei
- Keywords
- Angiogenesis, Notch, Ribosome biogenesis, Zebrafish, microRNA
- MeSH Terms
- none
- PubMed
- 42295545 Full text @ Angiogenesis
Citation
Kong, H., Ai, K., Zhang, J., Liu, Z., Wu, Y., Zhang, L., Zhang, H., Chen, X., Li, L., Fu, Y., Wang, X., Li, L. (2026) miR-150 controls developmental angiogenesis via ribosome biogenesis-dependent regulation of Notch signaling. Angiogenesis. 29:45.
Abstract
The development of a functional vasculature is controlled by the coordination of various mechanisms. Key molecules and signaling pathways regulating vascular development remain far from understood. Here, we demonstrate that miR-150 is highly enriched in zebrafish vascular endothelial cells (ECs), and plays a key role in regulating developmental angiogenesis during embryogenesis. Depletion of miR-150 impairs intersegmental vessel (ISV) sprouting, whereas EC-overexpression of miR-150 induces ectopic vascular sprouting. Mechanistically, miR-150 binds to the 3'UTR of zebrafish wdr75 to modulate ribosome biogenesis. Loss of miR-150 led to upregulated ribosome biogenesis, which enhanced Notch signaling activity and inhibited developmental angiogenesis. Pharmacological inhibition of ribosome biogenesis or Notch signaling effectively rescued the angiogenic defects in miR-150-deficient embryos. These findings establish miR-150 as a key regulator of developmental angiogenesis through modulation of ribosome biogenesis and downstream Notch signaling during zebrafish embryogenesis.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping