ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Endothelial PD-1 Regulates Vascular Homeostasis and Oligodendrogenesis during Brain Development.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Endothelial cell, but not neutrophil, programmed cell death receptor-ligand 1 loss has a morbid impact on experimental murine shock/sepsis-induced lung injury.Frontiers in immunology · 2026Article
- Emerging pathological mechanisms of Alzheimer's disease pathogenesis: from neuroimmune interactions to intercellular communication.Frontiers in aging neuroscience · 2026Review
- Differential Effects of Endothelial Cell- as opposed to Neutrophil-Lineage Restricted PD-L1 Gene Expression on Experimental Murine Shock/ Sepsis-Induced Lung Injury.Research square · 2025Article
- Endothelial PD-1 Regulates Vascular Homeostasis and Oligodendrogenesis during Brain Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Appropriate vascular and neural development is essential for central nervous system (CNS). Although programmed cell death receptor 1 (PD-1) mediates neurogenesis, its role in cerebrovascular development remains poorly understood. Here, a correlation between cerebral vessels and oligodendrocyte precursor cells (OPCs) is revealed during brain development. The ablation of endothelial PD-1 triggers cortical hypervascularization through excessive angiogenic sprouting, concomitantly driving OPC differentiation. These alterations disrupt blood brain barrier (BBB) maturation, induce dysmyelination, and ultimately result in abnormal behavior in mice. Mechanistically, the loss of endothelial PD-1 suppresses the activity of the Wnt/β-catenin signaling pathway, thereby disrupting normal angiogenesis. Concurrently, it activates the MEK1/2-ERK1/2-GLI1 pathway, leading to increased GREMLIN1 (GREM1) expression. Elevated GREM1 secretion inhibits the BMP/SMAD1/5/SMAD4 signaling cascade in OPCs, which inhibits oligodendrogenesis and myelination. These findings indicate the importance of endothelial cell-intrinsic PD-1 in regulating the oligovascular niche, and suggest potential therapeutic implications for neurological disorders associated with disrupted vascular development.
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Registered trials
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