The DOI matches its Crossref record; 31 of the 32 references it cites were found in a registry or an index.
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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Cites
Abnormal blood vessel development and lethality in embryos lacking a single VEGF allele
Carmeliet, P., Ferreira, V., Breier, G., Pollefeyt, S., Kieckens, L., Gertsenstein, M., Fahrig, M., Vandenhoeck, A., Harpal, K., Eberhardt, C., et al. (1996) · Nature · doi:10.1038/380435a0 · Cited by 4,162
Heterozygous embryonic lethality induced by targeted inactivation of the VEGF gene
Ferrara, N., Carver-Moore, K., Chen, H., Dowd, M., Lu, L., O’Shea, K. S., Powell-Braxton, L., Hillan, K. J., & Moore, M. W. (1996) · Nature · doi:10.1038/380439a0 · Cited by 3,661
Angiogenesis in life, disease and medicine
Carmeliet, P. (2005) · Nature · doi:10.1038/nature04478 · Cited by 3,551
The blood–brain barrier: an overview
Ballabh, P., Braun, A., & Nedergaard, M. (2004) · Neurobiology of Disease · doi:10.1016/j.nbd.2003.12.016 · Cited by 2,276
Genes Expressed in Human Tumor Endothelium
Croix, B. S., Rago, C., Velculescu, V. E., Traverso, G., Romans, K. E., Montgomery, E. A., Lal, A., Riggins, G. J., Lengauer, C., Vogelstein, B., et al. (2000) · Science · doi:10.1126/science.289.5482.1197 · Cited by 1,859
Endothelial Cells Stimulate Self-Renewal and Expand Neurogenesis of Neural Stem Cells
Shen, Q., Goderie, S. K., Jin, L., Karanth, N., Sun, Y., Abramova, N. E., Vincent, P. A., Pumiglia, K. M., & Temple, S. (2004) · Science · doi:10.1126/science.1095505 · Cited by 1,574
Phenotypic Heterogeneity of the Endothelium
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Id1 and Id3 are required for neurogenesis, angiogenesis and vascularization of tumour xenografts
Lyden, D. C., Young, A. Z., Zagzag, D., Yan, W. X., Gerald, W. L., O'Reilly, R., Bader, B., Hynes, R. O., Zhuang, Y., Manova, K., et al. (1999) · Nature · doi:10.1038/44334 · Cited by 912
Intraventricular Hemorrhage in Premature Infants: Mechanism of Disease
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Wnt/β-catenin signaling is required for CNS, but not non-CNS, angiogenesis
Daneman, R., Agalliu, D., Zhou, L., Kuhnert, F., Kuo, C. J., & Barres, B. A. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0805165106 · Cited by 753
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Endothelial Cell-Pericyte Crosstalk in the Brain Balances Microvascular Stability and Plasticity
Lee, J. M., Luc, E., & Stratman, A. N. (2026) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.126.323547
Cheerathodi, M., & McCarty, J. H. (2014) · Springer eBooks · doi:10.1007/978-3-7091-1431-5_7
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
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