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Oct, 2015;25 (10): 1093-107.

G protein-coupled receptor 183 facilitates endothelial-to-hematopoietic transition via Notch1 inhibition.

Panpan Zhang, Qiuping He, Dongbo Chen, Weixiao Liu, Lu Wang, Chunxia Zhang, Dongyuan Ma, Wei Li, Bing Liu, Feng Liu
Author Information
  1. Panpan Zhang: State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China.
  2. Qiuping He: State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China.
  3. Dongbo Chen: 307-Ivy Translational Medicine Center, Laboratory of Oncology, Affiliated Hospital of Academy of Military Medical Sciences, Beijing 100071, China.
  4. Weixiao Liu: State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China.
  5. Lu Wang: State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China.
  6. Chunxia Zhang: State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China.
  7. Dongyuan Ma: State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China.
  8. Wei Li: State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China.
  9. Bing Liu: 307-Ivy Translational Medicine Center, Laboratory of Oncology, Affiliated Hospital of Academy of Military Medical Sciences, Beijing 100071, China.
  10. Feng Liu: State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China.
PMID: 26358189 DOI: 10.1038/cr.2015.109

Abstract

In vertebrates, embryonic hematopoietic stem and progenitor cells (HSPCs) are derived from a subset of endothelial cells, the hemogenic endothelium (HE), through the endothelial-to-hematopoietic transition (EHT). Notch signaling is essential for HSPC development during embryogenesis across vertebrates. However, whether and how it regulates EHT remains unclear. Here, we show that G protein-coupled receptor 183 (Gpr183) signaling serves as an indispensable switch for HSPC emergence by repressing Notch signaling before the onset of EHT. Inhibition of Gpr183 significantly upregulates Notch signaling and abolishes HSPC emergence. Upon activation by its ligand 7α-25-OHC, Gpr183 recruits β-arrestin1 and the E3 ligase Nedd4 to degrade Notch1 in specified HE cells and then facilitates the subsequent EHT. Importantly, 7α-25-OHC stimulation promotes HSPC emergence in vivo and in vitro, providing an attractive strategy for enhancing the in vitro generation of functional HSPCs.

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MeSH Term

Animals
Arrestins
Endosomal Sorting Complexes Required for Transport
Hemangioblasts
Hematopoiesis
Hematopoietic Stem Cells
Nedd4 Ubiquitin Protein Ligases
Receptor, Notch1
Receptors, G-Protein-Coupled
Signal Transduction
Ubiquitin-Protein Ligases
Ubiquitination
Zebrafish
Zebrafish Proteins
beta-Arrestins

Chemicals

Arrestins
Endosomal Sorting Complexes Required for Transport
Receptor, Notch1
Receptors, G-Protein-Coupled
Zebrafish Proteins
beta-Arrestins
gpr183a protein, zebrafish
Nedd4 Ubiquitin Protein Ligases
Ubiquitin-Protein Ligases
Journal Article Research Support, Non-U.S. Gov't

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