Evidence map›Paper›PMID 29540737›Full record

ArticleScientific reports2018

G-Protein-Coupled Receptor Gpr17 Regulates Oligodendrocyte Differentiation in Response to Lysolecithin-Induced Demyelination.

Changqing Lu, Lihua Dong, Hui Zhou, Qianmei Li, Guojiao Huang, Shu Jun Bai, Linchuan Liao

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.7field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Advances in Therapeutics Research for Demyelinating Diseases.Pharmaceuticals (Basel, Switzerland) · 2025
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. eNeuro · 2023
    Article
  15. Article
  16. Remyelination in Multiple Sclerosis: Findings in the Cuprizone Model.International journal of molecular sciences · 2022
    Review
  17. Article
  18. Review
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Changqing LuDepartment of Forensic Analytical Toxicology, West China School of Basic Medical and Forensic Medicine, Sichuan University, Chengdu, 610041, Sichuan, China. changing_lu@126.com.
Lihua DongDepartment of Anatomy, West China School of Basic Medical and Forensic Medicine, Sichuan University, Chengdu, 610041, Sichuan, China.
Hui ZhouDepartment of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, Sichuan Province, China.
Qianmei LiDepartment of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, Sichuan Province, China.
Guojiao HuangDepartment of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, Sichuan Province, China.
Shu Jun BaiDepartment of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, Sichuan Province, China.
Linchuan LiaoDepartment of Forensic Analytical Toxicology, West China School of Basic Medical and Forensic Medicine, Sichuan University, Chengdu, 610041, Sichuan, China. linchuanliao@scu.edu.cn.
West China Medical Center of Sichuan University · CNWest China Second University Hospital of Sichuan University · CNSichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oligodendrocytes are the myelin-producing cells of the central nervous system (CNS). A variety of brain disorders from "classical" demyelinating diseases, such as multiple sclerosis, stroke, schizophrenia, depression, Down syndrome and autism, are shown myelination defects. Oligodendrocyte myelination is regulated by a complex interplay of intrinsic, epigenetic and extrinsic factors. Gpr17 (G protein-coupled receptor 17) is a G protein-coupled receptor, and has been identified to be a regulator for oligodendrocyte development. Here, we demonstrate that the absence of Gpr17 enhances remyelination in vivo with a toxin-induced model whereby focal demyelinated lesions are generated in spinal cord white matter of adult mice by localized injection of LPC(L-a-lysophosphatidylcholine). The increased expression of the activated form of Erk1/2 (phospho-Erk1/2) in lesion areas suggested the potential role of Erk1/2 activity on the Gpr17-dependent modulation of myelination. The absence of Gpr17 enhances remyelination is correlate with the activated Erk1/2 (phospho-Erk1/2).Being a membrane receptor, Gpr17 represents an ideal druggable target to be exploited for innovative regenerative approaches to acute and chronic CNS diseases.

Indexed as

Cell DifferentiationAnimalsBiomarkersDemyelinating DiseasesDisease Models, AnimalExtracellular Signal-Regulated MAP KinasesFluorescent Antibody TechniqueGene ExpressionLysophosphatidylcholinesMiceMice, KnockoutMyelin SheathNerve Tissue ProteinsOligodendrogliaPhosphorylationReceptors, G-Protein-CoupledBiomarkersExtracellular Signal-Regulated MAP KinasesGPR17 protein, mouseLysophosphatidylcholinesNerve Tissue ProteinsReceptors, G-Protein-Coupled

Identifiers

PMID29540737
PMCPMC5852120
OpenAlexW2791016949

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.