Evidence map›Paper›PMID 29474476›Full record

ArticlePloS one2018

RAGE-dependent potentiation of TRPV1 currents in sensory neurons exposed to high glucose.

Doris Lam, Zeinab Momeni, Michael Theaker, Santosh Jagadeeshan, Yasuhiko Yamamoto, Juan P Ianowski, Verónica A Campanucci

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
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  7. Article
  8. Role of TRP Channels in Metabolism-Related Diseases.International journal of molecular sciences · 2024
    Review
  9. Review
  10. Review
  11. The role of protein kinases in diabetic neuropathic pain: an update review.Journal of diabetes and metabolic disorders · 2023
    Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Modulation of Vagal Sensory NeuronsFrontiers in physiology · 2021
    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 2 institutions in 2 countries.

Doris LamDepartment of Physiology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Zeinab MomeniDepartment of Physiology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Michael TheakerDepartment of Physiology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Santosh JagadeeshanDepartment of Physiology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Yasuhiko YamamotoDepartment of Biochemistry and Molecular Vascular Biology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.
Juan P IanowskiDepartment of Physiology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.
Verónica A CampanucciDepartment of Physiology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.ORCID 0000-0003-0924-4733
University of Saskatchewan · CAKanazawa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes mellitus is associated with sensory abnormalities, including exacerbated responses to painful (hyperalgesia) or non-painful (allodynia) stimuli. These abnormalities are symptoms of diabetic peripheral neuropathy (DPN), which is the most common complication that affects approximately 50% of diabetic patients. Yet, the underlying mechanisms linking hyperglycemia and symptoms of DPN remain poorly understood. The transient receptor potential vanilloid 1 (TRPV1) channel plays a central role in such sensory abnormalities and shows elevated expression levels in animal models of diabetes. Here, we investigated the function of TRPV1 channels in sensory neurons cultured from the dorsal root ganglion (DRG) of neonatal mice, under control (5mM) and high glucose (25mM) conditions. After maintaining DRG neurons in high glucose for 1 week, we observed a significant increase in capsaicin (CAP)-evoked currents and CAP-evoked depolarizations, independent of TRPV1 channel expression. These functional changes were largely dependent on the expression of the receptor for Advanced Glycation End-products (RAGE), calcium influx, cytoplasmic ROS accumulation, PKC, and Src kinase activity. Like cultured neurons from neonates, mature neurons from adult mice also displayed a similar potentiation of CAP-evoked currents in the high glucose condition. Taken together, our data demonstrate that under the diabetic condition, DRG neurons are directly affected by elevated levels of glucose, independent of vascular or glial signals, and dependent on RAGE expression. These early cellular and molecular changes to sensory neurons in vitro are potential mechanisms that might contribute to sensory abnormalities that can occur in the very early stages of diabetes.

Indexed as

AnimalsCalcium SignalingCapsaicinDiabetic NeuropathiesEvoked PotentialsGanglia, SpinalGlucoseHumansLong-Term PotentiationMiceMice, KnockoutReactive Oxygen SpeciesReceptor for Advanced Glycation End ProductsSensory Receptor CellsTRPV Cation ChannelsAger protein, mouseCapsaicinGlucoseReactive Oxygen SpeciesReceptor for Advanced Glycation End ProductsTRPV1 protein, mouseTRPV Cation Channels

Identifiers

PMID29474476
PMCPMC5825096
OpenAlexW2792038173

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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.