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Essential Regulation of CNS Angiogenesis by the Orphan G Protein–Coupled Receptor GPR124
Open accessAbstract
The orphan G protein-coupled receptor (GPCR) GPR124/tumor endothelial marker 5 is highly expressed in central nervous system (CNS) endothelium. Here, we show that complete null or endothelial-specific GPR124 deletion resulted in embryonic lethality from CNS-specific angiogenesis arrest in forebrain and neural tube. Conversely, GPR124 overexpression throughout all adult vascular beds produced CNS-specific hyperproliferative vascular malformations. In vivo, GPR124 functioned cell-autonomously in endothelium to regulate sprouting, migration, and developmental expression of the blood-brain barrier marker Glut1, whereas in vitro, GPR124 mediated Cdc42-dependent directional migration to forebrain-derived, vascular endothelial growth factor-independent cues. Our results demonstrate CNS-specific angiogenesis regulation by an endothelial receptor and illuminate functions of the poorly understood adhesion GPCR subfamily. Further, the functional tropism of GPR124 marks this receptor as a therapeutic target for CNS-related vascular pathologies.
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“Wnt signaling pathway including Wnt ligands, Norrins, Frizzled receptors, Lrp5/6 coreceptors, Gpr124 and Reck cofactors, and 𝛃 -catenin are critical for both vascular development and barriergenesis (138, 332, 558, 636, 682, 689);”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [332]
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Metadata
- Authors
- Kuhnert, F., Mancuso, M. R., Shamloo, A., Wang, H.-T., Choksi, V., Florek, M., Su, H., Fruttiger, M., Young, W. L., Heilshorn, S. C., & Kuo, C. J.
- Affiliations
- Stanford Medicine (US)
- Stanford University (US)
- University of California, San Francisco (US)
- University College London (GB)
- Corresponding author
- Kuo, Calvin J.
- ORCID
- Venue
- Science
- Published
- 2010-11-12
- Volume
- 330
- Issue
- 6006
- Pages
- 985-989
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC3099479
- OpenAlex
- W2115716038
- Cited by
- 301
- References
- 32
- Citations by year
- 2026: 11 · 2025: 16 · 2024: 17 · 2023: 16 · 2022: 29 · 2021: 23 · 2020: 17 · 2019: 21 · 2018: 18 · 2017: 20 · 2016: 20 · 2015: 19 · 2014: 22 · 2013: 16 · 2012: 20
- FWCI
- 6.78
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- National Institutes of Health (5r21ns058600-02, 1dp2od006477-01)
- National Heart, Lung, and Blood Institute (R01HL074267)
- National Cancer Institute (R01CA095654, T32CA009302)
- National Institute of General Medical Sciences (T32GM007365, GM 07365)
- National Institute of Neurological Disorders and Stroke (1R21 NS058600, P01NS044155, R01NS027713, R01NS052830, P01 NS 44155, R01NS064517, R01-NS 27713, R21 NS058600, R21NS070153)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- GPR124, orphan G protein-coupled receptor, adhesion GPCRs, endothelial cells, embryonic lethality, neural tube, forebrain, vascular malformations, Cdc42, endothelial cell migration, sprouting angiogenesis, blood-brain barrier, GLUT1
- MeSH terms
- Animals, Blood Vessels, Blood-Brain Barrier, Cell Movement, Endothelium, Vascular, Mesencephalon, Mice, Transgenic, Rhombencephalon, Telencephalon, Prosencephalon, Gene Deletion, Mice, Knockout, Neovascularization, Physiologic, Endothelial Cells, Receptors, G-Protein-Coupled, Embryonic Development, Glucose Transporter Type 1, Mice, Neural Tube
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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