Evidence map›Paper›PMID 30226562›Full record

ArticleInternational journal of molecular medicine2018

GPR17 mediates ischemia-like neuronal injury via microglial activation.

Bing Zhao, Hao Wang, Cai-Xia Li, Sheng-Wen Song, San-Hua Fang, Er-Qing Wei, Qiao-Juan Shi

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Trial
  2. GPR17 modulates anxiety-like behaviorsActa pharmaceutica Sinica. B · 2024
    Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Involvement of GPR17 in Neuronal Fibre Outgrowth.International journal of molecular sciences · 2021
    Article
  9. Review
  10. The Roles of Orphan G Protein-Coupled Receptors in Autoimmune Diseases.Clinical reviews in allergy & immunology · 2021
    Review
  11. Review
  12. Article
  13. [Mechanisms underlying remyelination with special focus on demyelination models of multiple sclerosis].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2020
    Review
  14. Article
  15. Review
  16. 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.

Bing ZhaoDepartment of Anesthesiology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.
Hao WangDepartment of Neurology, Tongde Hospital of Zhejiang Province, Hangzhou, Zhejiang 310012, P.R. China.
Cai-Xia LiDepartment of Anesthesiology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.
Sheng-Wen SongDepartment of Anesthesiology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.
San-Hua FangDepartment of Pharmacology, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310058, P.R. China.
Er-Qing WeiDepartment of Pharmacology, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310058, P.R. China.
Qiao-Juan ShiExperimental Animal Center, Zhejiang Academy of Medical Sciences, Hangzhou, Zhejiang 310013, P.R. China.
Zhejiang University · CNTongde Hospital of Zhejiang Province · CNZhejiang Academy of Medical Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

GPR17 is a G (i)-coupled dual receptor, linked to P2Y and CysLT receptors stimulated by uracil nucleotides and cysteinyl leukotrienes, respectively. Recent evidence has demonstrated that GPR17 inhibition ameliorates the progression of cerebral ischemic injury by regulating neuronal death and microglial activation. The present study aimed to assess the detailed regulatory roles of this receptor in oxygen‑glucose deprivation/recovery (OGD/R)‑induced ischemia‑like injury in vitro and explore the underlying mechanism. The results demonstrated that OGD/R induced ischemic neuronal injury and microglial activation, including enhanced phagocytosis and increased inflammatory cytokine release in neuron‑glial mixed cultures of cortical cells. GPR17 upregulation during OGD/R was spatially and temporally correlated with neuronal injury and microglial activation. In addition, GPR17 knockdown inhibited OGD/R‑induced responses in neuron‑glial mixed cultures. GPR17 knockdown also attenuated cell injury induced by the agonist leukotriene D4 (LTD4) or uridine 5'‑diphosphate (UDP) in neuron‑glial mixed cultures. However, GPR17 knockdown did not affect OGD/R‑induced ischemic neuronal injury in primary cultures of neurons. In primary astrocyte cultures, neither GPR17 nor OGD/R induced injury. By contrast, GPR17 knockdown ameliorated OGD/R‑induced microglial activation, boosting phagocytosis and inflammatory cytokine release in primary microglia cultures. Finally, the results demonstrated that the conditioned medium of microglia pretreated with OGD/R induced neuronal death, and the neuronal injury was significantly inhibited by GPR17 knockdown. These findings suggested that GPR17 may mediate ischemia‑like neuronal injury and microglial activation in vitro; however, the protective effects on ischemic neuronal injury might depend upon microglial activation. Whether GPR17 regulates neuronal injury mediated by oligodendrocyte linkage remains to be investigated.

Indexed as

AnimalsAstrocytesBrain IschemiaCell DeathCells, CulturedCytokinesMicrogliaNeuronsPhagocytosisRats, Sprague-DawleyReceptors, G-Protein-CoupledReperfusion InjuryRNA InterferenceUp-RegulationCytokinesGPR17 protein, ratReceptors, G-Protein-Coupled

Identifiers

PMID30226562
PMCPMC6192776
OpenAlexW2889278392

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.