Evidence map›Paper›PMID 32276265›Full record

ArticleAging2020

NO up-regulates migraine-related CGRP via activation of an Akt/GSK-3β/NF-κB signaling cascade in trigeminal ganglion neurons.

Gang Yao, Yu-Hong Man, An-Ran Li, Yu Guo, Yun Dai, Ping Wang, Yi-Fa Zhou

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Animal Models of Chronic Migraine: From the Bench to Therapy.Current pain and headache reports · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Pharmacological evaluation of carvacrol anti-migraine potential.Naunyn-Schmiedeberg's archives of pharmacology · 2023
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  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 4 institutions in 1 country.

Gang YaoDepartment of Neurology, The Second Hospital of Jilin University, Changchun, Jilin, China.
Yu-Hong ManDepartment of Neurology, The Second Hospital of Jilin University, Changchun, Jilin, China.
An-Ran LiDepartment of Neurology, The Second Hospital of Jilin University, Changchun, Jilin, China.
Yu GuoDepartment of Neurology, The Second Hospital of Jilin University, Changchun, Jilin, China.
Yun DaiLaboratory of Cancer Precision Medicine, The First Hospital of Jilin University, Changchun, Jilin, China.
Ping WangDepartment of Otolaryngology - Head and Neck Surgery, The First Hospital of Jilin University, Changchun, Jilin, China.
Yi-Fa ZhouSchool of Life Sciences, Northeast Normal University, Changchun, Jilin, China.
Second Affiliated Hospital of Jilin University · CNNortheast Normal University · CNFirst Hospital of Jilin University · CNJilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The release of the neuropeptide CGRP from the trigeminal ganglion neurons (TGNs) plays a central role in migraine. Whereas CGRP can activate NO release from ganglionic glial cells, NO in turn enhances CGRP release. However, it remains unclear how NO promotes CGRP release. Here, we report that the NO donor SNAP triggered CGRP release from cultured primary TGNs. This event was associated with GSK-3β activation and Akt inactivation. Immunofluorescent staining revealed that GSK-3β primarily located in neurons. Furthermore, GSK-3β inhibition resulted in a marked reduction in expression of CGRP as well as other migraine-related factors, including substance P, cholecystokinin, and prostaglandin E2. Last, exposure to SNAP also activated NF-κB, while NF-κB inhibition prevented the induction of CGRP by SNAP. Interestingly, this event was blocked by GSK-3β inhibition, in association with inhibition of NF-κB/p65 expression and nuclear translocation. Together, these findings argue that NO could stimulate TGNs to release of CGRP as well as other migraine-related factors, likely by activating GSK-3β, providing a novel mechanism underlying a potential feed-forward loop between NO and CGRP in migraine. They also raise a possibility that GSK-3β might act to trigger migraine through activation of NF-κB, suggesting a link between neuroinflammation and migraine.

Indexed as

Calcitonin Gene-Related PeptideCells, CulturedGlycogen Synthase Kinase 3 betaHumansMigraine DisordersNitric OxideNitric Oxide DonorsProto-Oncogene Proteins c-aktSignal TransductionS-Nitroso-N-AcetylpenicillamineTranscription Factor RelATrigeminal GanglionCalcitonin Gene-Related PeptideGlycogen Synthase Kinase 3 betaNitric OxideNitric Oxide DonorsProto-Oncogene Proteins c-aktS-Nitroso-N-AcetylpenicillamineTranscription Factor RelAcalcitonin gene-related peptideglycogen synthase kinase 3βNF-κBnitric oxidetrigeminal ganglion neuron

Identifiers

PMID32276265
PMCPMC7185139
OpenAlexW3015208939

What OpenQuestion holds

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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.