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<p>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 <i>miR-150</i> is highly enriched in zebrafish vascular endothelial cells (ECs), and plays a key role in regulating developmental angiogenesis during embryogenesis. Depletion of <i>miR-150</i> impairs intersegmental vessel (ISV) sprouting, whereas EC-overexpression of <i>miR-150</i> induces ectopic vascular sprouting. Mechanistically, <i>miR-150</i> binds to the 3’UTR of zebrafish <i>wdr75</i> to modulate ribosome biogenesis. Loss of <i>miR-150</i> 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 <i>miR-150-</i>deficient embryos. These findings establish <i>miR-150</i> as a key regulator of developmental angiogenesis through modulation of ribosome biogenesis and downstream Notch signaling during zebrafish embryogenesis.</p>

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

  • 期刊论文

  • 发表日期：

    2026年6月15日

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

摘要

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.