ArticleFrontiers in cell and developmental biology2023
Endothelin-1-Endothelin receptor B complex contributes to oligodendrocyte differentiation and myelin deficits during preterm white matter injury.
Article in Frontiers in cell and developmental biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 10 citations in OpenAlex.
- Endothelial Netrin-4 regulates oligodendrocyte precursor cell proliferation and differentiation via ET-1 signaling in preterm white matter injury.Brain pathology (Zurich, Switzerland) · 2026Article
- Prenatal valproic acid on the basis of gestational diabetes also induces autistic behavior and disrupts myelination and oligodendroglial maturation slightly in offspring.Translational psychiatry · 2025Article
- Enhancing myelinogenesis through LIN28A rescues impaired cognition in PWMI mice.Stem cell research & therapy · 2025Article
- Korean Red Ginseng and Rb1 restore altered social interaction, gene expressions in the medial prefrontal cortex, and gut metabolites under post-weaning social isolation in mice.Journal of ginseng research · 2024Article
- GSDMD gene knockout alleviates hyperoxia-induced hippocampal brain injury in neonatal mice.Research square · 2023Article
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7 authors at 3 institutions in 1 country.
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Abstract
Preterm cerebral white matter injury (WMI), a major form of prenatal brain injury, may potentially be treated by oligodendrocyte (OL) precursor cell (OPC) transplantation. However, the defective differentiation of OPCs during WMI seriously hampers the clinical application of OPC transplantation. Thus, improving the ability of transplanted OPCs to differentiate is critical to OPC transplantation therapy for WMI. We established a hypoxia-ischemia-induced preterm WMI model in mice and screened the molecules affected by WMI using single-cell RNA sequencing. We revealed that endothelin (ET)-1 and endothelin receptor B (ETB) are a pair of signaling molecules responsible for the interaction between neurons and OPCs and that preterm WMI led to an increase in the number of ETB-positive OPCs and premyelinating OLs. Furthermore, the maturation of OLs was reduced by knocking out ETB but promoted by stimulating ET-1/ETB signaling. Our research reveals a new signaling module for neuron-OPC interaction and provides new insight for therapy targeting preterm WMI.
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