Evidence map›Paper›PMID 32519268›Full record

ArticleInflammation2020

Lysophosphatidylinositol, an Endogenous Ligand for G Protein-Coupled Receptor 55, Has Anti-inflammatory Effects in Cultured Microglia.

Tomoki Minamihata, Katsura Takano, Mitsuaki Moriyama, Yoichi Nakamura

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Targeting the LPI/GPR55 Axis in MAFLD and MASH: Novel Insights, Therapeutic Strategies and Future Directions.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Review
  4. Article
  5. Ageing, Neurodegeneration and the Endocannabinoid System.Current topics in behavioral neurosciences · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
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  15. Article
  16. Article
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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

4 authors at 1 institution in 1 country.

Tomoki MinamihataLaboratory of Integrative Physiology in Veterinary Sciences, Osaka Prefecture University, 1-58 Rinku Ourai Kita, Izumisano, Osaka, 598-8531, Japan.
Katsura TakanoLaboratory of Integrative Physiology in Veterinary Sciences, Osaka Prefecture University, 1-58 Rinku Ourai Kita, Izumisano, Osaka, 598-8531, Japan.
Mitsuaki MoriyamaLaboratory of Integrative Physiology in Veterinary Sciences, Osaka Prefecture University, 1-58 Rinku Ourai Kita, Izumisano, Osaka, 598-8531, Japan. moriyama@vet.osakafu-u.ac.jp.ORCID https://orcid.org/0000-0001-8123-8835
Yoichi NakamuraLaboratory of Integrative Physiology in Veterinary Sciences, Osaka Prefecture University, 1-58 Rinku Ourai Kita, Izumisano, Osaka, 598-8531, Japan.
Osaka Prefecture University · JP

Funding

JSPS KAKENHI JP17K08127JSPS KAKENHI JP17K15390JSPS KAKENHI JP18K05999
6 · The paper itself

Abstract

Lysophosphatidylinositol (LysoPI), an endogenous ligand for G protein-coupled receptor (GPR) 55, has been known to show various functions in several tissues and cells; however, its roles in the central nervous system (CNS) are not well known. In particular, the detailed effects of LysoPI on microglial inflammatory responses remain unknown. Microglia is the immune cell that has important functions in maintaining immune homeostasis of the CNS. In this study, we explored the effects of LysoPI on inflammatory responses using the mouse microglial cell line BV-2, which was stimulated with lipopolysaccharide (LPS), and some results were confirmed also in rat primary microglia. LysoPI was found to reduce LPS-induced nitric oxide (NO) production and inducible NO synthase protein expression without affecting cell viability in BV-2 cells. LysoPI also suppressed intracellular generation of reactive oxygen species both in BV-2 cells and primary microglia and cytokine release in BV-2 cells. In addition, LysoPI treatment decreased phagocytic activity of LPS-stimulated BV-2 cells and primary microglia. The GPR55 antagonist CID16020046 completely inhibited LysoPI-induced downregulation of phagocytosis in BV-2 microglia, but did not affect the LysoPI-induced decrease in NO production. Our results suggest that LysoPI suppresses microglial phagocytosis via a GPR55-dependent pathway and NO production via a GPR55-independent pathway. LysoPI may contribute to neuroprotection in pathological conditions such as brain injury or neurodegenerative diseases, through its suppressive role in the microglial inflammatory response.

Indexed as

AnimalsAnimals, NewbornAnti-Inflammatory AgentsCell LineCells, CulturedCell SurvivalDose-Response Relationship, DrugLysophospholipidsMiceMicrogliaRatsRats, WistarReceptors, CannabinoidReceptors, G-Protein-CoupledAnti-Inflammatory AgentsGPR55 protein, ratlysophosphatidylinositolLysophospholipidsReceptors, CannabinoidReceptors, G-Protein-CoupledGPR55lysophosphatidylinositolmicroglianeuroinflammationphagocytosis

Identifiers

PMID32519268
OpenAlexW3033039299

What OpenQuestion holds

Textmetadata
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.