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The oligodendrocyte-specific G protein–coupled receptor GPR17 is a cell-intrinsic timer of myelination
Open accessAbstract
The basic helix-loop-helix transcription factor Olig1 promotes oligodendrocyte maturation and is required for myelin repair. We characterized an Olig1-regulated G protein-coupled receptor, GPR17, whose function is to oppose the action of Olig1. Gpr17 was restricted to oligodendrocyte lineage cells, but was downregulated during the peak period of myelination and in adulthood. Transgenic mice with sustained Gpr17 expression in oligodendrocytes exhibited stereotypic features of myelinating disorders in the CNS. Gpr17 overexpression inhibited oligodendrocyte differentiation and maturation both in vivo and in vitro. Conversely, Gpr17 knockout mice showed early onset of oligodendrocyte myelination. The opposing action of Gpr17 on oligodendrocyte maturation reflects, at least partially, upregulation and nuclear translocation of the potent oligodendrocyte differentiation inhibitors ID2/4. Collectively, these findings suggest that GPR17 orchestrates the transition between immature and myelinating oligodendrocytes via an ID protein-mediated negative regulation and may serve as a potential therapeutic target for CNS myelin repair.
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“expressed Neu4 and genes involved in keeping oligodendrocytes undifferentiated (Sox6, Bmp4 and Gpr17) (9–11)”
From Oligodendrocyte heterogeneity in the mouse juvenile and adult central nervous system (2016) · cites this paper as [11]
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Metadata
- Authors
- Chen, Y., Wu, H., Wang, S., Koito, H., Li, J., Ye, F., Hoang, J., Escobar, S. S., Gow, A., Arnett, H. A., Trapp, B. D., Karandikar, N. J., Hsieh, J., & Lu, Q. R.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- Texas A&M University (US)
- Wayne State University (US)
- Amgen (United States) (US)
- Cleveland Clinic (US)
- Corresponding author
- Lu, Q Richard
- ORCID
- Venue
- Nature Neuroscience
- Published
- 2009-10-18
- Volume
- 12
- Issue
- 11
- Pages
- 1398-1406
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC2783566
- OpenAlex
- W2061271326
- Cited by
- 346
- References
- 50
- Citations by year
- 2026: 18 · 2025: 19 · 2024: 24 · 2023: 17 · 2022: 28 · 2021: 28 · 2020: 22 · 2019: 19 · 2018: 19 · 2017: 23 · 2016: 16 · 2015: 20 · 2014: 13 · 2013: 25 · 2012: 16
- FWCI
- 5.65
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Multiple Sclerosis Society
- National Institutes of Health (NS060017)
- National Institute of Allergy and Infectious Diseases (K24AI079272)
- National Institute of Neurological Disorders and Stroke (R01NS060017, R01NS050389)
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- GPR17, oligodendrocyte maturation, myelination, Olig1, G protein-coupled receptors, oligodendrocyte differentiation, remyelination, transcriptional regulation, oligodendrocyte lineage
- MeSH terms
- Animals, Brain, Cells, Cultured, Demyelinating Diseases, Disease Models, Animal, Embryo, Mammalian, Encephalomyelitis, Autoimmune, Experimental, Female, Humans, Mice, Inbred C57BL, Mice, Transgenic, Multiple Sclerosis, Nerve Tissue Proteins, Oligodendroglia, Optic Nerve, Rats, Inbred F344, Spinal Cord, Stem Cells, Time Factors, Transfection, Receptors, G-Protein-Coupled, Chromatin Immunoprecipitation, Green Fluorescent Proteins, Mice, Rats
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