Evidence map›Paper›PMID 22872320›Full record

ArticleCellular and molecular neurobiology2013

Secretion of matrix metalloproteinase-9 from astrocytes by inhibition of tonic P2Y14-receptor-mediated signal(s).

Manao Kinoshita, Kaoru Nasu-Tada, Kayoko Fujishita, Kaoru Sato, Schuichi Koizumi

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2013. 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
1.4field-weighted citation impact, top 20% 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, 35 citations in OpenAlex.

  1. Review
  2. Frontiers in cell and developmental biology · 2026
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  3. Design, Synthesis and Anti-Inflammation Evaluation ofDrug design, development and therapy · 2025
    Article
  4. Review
  5. Review
  6. Article
  7. Chemogenetic stimulation of the GPharmacology research & perspectives · 2021
    Article
  8. Structure-Activity Relationship of Heterocyclic P2YJournal of medicinal chemistry · 2021
    Article
  9. Article
  10. Role of UDP-Sugar Receptor P2YInternational journal of molecular sciences · 2020
    Article
  11. Article
  12. Article
  13. Review
  14. P2Y receptors in Alzheimer's disease.Biology of the cell · 2015
    Review
  15. Review
  16. Review
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

5 authors at 2 institutions in 1 country.

Manao KinoshitaDepartment of Neuropharmacology, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, 1110 Shimokato, Chuo, Yamanashi, 409-3898, Japan.
Kaoru Nasu-Tada
Kayoko Fujishita
Kaoru Sato
Schuichi Koizumi
University of Yamanashi · JPNational Institute of Health Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glial cells have various important roles in regulation of brain functions. For such events, extracellular nucleotides/P2 receptors have central roles. Although there have been huge amount of literature about activation of P2 receptors and glial functions, little is known about what happens in glia or the brain if glial P2 receptor is inhibited. Here we show that the inhibition of P2 receptors in astrocytes, the most abundant glial cells and cause a constitutive release of nucleotides, resulted in secretion of metalloproteinase-9 (MMP-9), a metal-dependent endopeptidase that degrades extracellular matrix molecules and is important in regulation of brain remodeling. When cultured astrocytes were treated with apyrase (ecto-nucleotidase), reactive blue 2 (P2 receptor antagonist), and pertussis toxin, they secreted MMP-9, suggesting that Gi-coupled P2Y receptor-mediated signals constitutively suppress the production of MMP-9. Among Gi-coupled P2Y receptors, we found that an inhibition of P2Y(14) receptor, a receptor for nucleotide-sugars such as UDP-glucose, is responsible for the production of MMP-9 by pharmacological and molecular biochemical analysis. As for the mechanisms, the inhibition of P2Y(14) receptors resulted in the release of tumor necrosis factor (TNF)-α which then acted on astrocytes to induce MMP-9. Taken together, our results suggest that the constitutive releases of nucleotide-sugars in astrocytes should play an important role in maintaining the normal status of the cell, through Gi-coupled P2Y(14) receptors, and when the signal is removed, the cells start to release TNF-α, which then acts on astrocytes in a feedback fashion to boost MMP-9 synthesis and secretion.

Indexed as

AnimalsAnimals, NewbornApyraseAstrocytesCells, CulturedMatrix Metalloproteinase 9Neural InhibitionRatsRats, WistarReceptors, Purinergic P2Receptors, Purinergic P2YSignal TransductionSuraminTriazinesTumor Necrosis Factor-alphaApyraseCibacron Blue F 3GAMatrix Metalloproteinase 9P2Y14 receptor, ratReceptors, Purinergic P2Receptors, Purinergic P2YSuraminTriazinesTumor Necrosis Factor-alpha

Identifiers

PMID22872320
PMCPMC11497964
OpenAlexW2074171476

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.