miR-150 controls developmental angiogenesis via ribosome biogenesis-dependent regulation of Notch signaling.

Authors

Haotian Kong, Kang Ai, Jinghe Zhang, Ziting Liu, Yue Wu, Li Zhang, Huixin Zhang, Xiuli Chen, Linglu Li, Yuanyuan Fu, Xiaojing Wang, Lei Li

Published in

Angiogenesis. Volume 29. Issue 3. Jun 15, 2026. Epub Jun 15, 2026.

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.

PMID:
42295545
Bibliographic data and abstract were imported from PubMed on 15 Jun 2026.

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