Evidence map›Paper›PMID 27038931›Full record

ArticleNeurochemical research2016

Stromal Cell-Derived Factor 1 Increases Tetrodotoxin-Resistant Sodium Currents Nav1.8 and Nav1.9 in Rat Dorsal Root Ganglion Neurons via Different Mechanisms.

Fang Qiu, Yang Li, Qiang Fu, Yong-Yan Fan, Chao Zhu, Yan-Hong Liu, Wei-Dong Mi

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. CXCL13/CXCR5: a new target for pain treatment.International journal of surgery (London, England) · 2025
    Review
  2. Article
  3. NaJournal of neurophysiology · 2022
    Article
  4. Review
  5. Article
  6. Article
  7. Transcriptional Regulation of Voltage-Gated Sodium Channels Contributes to GM-CSF-Induced Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  8. Article
  9. Article
  10. Inhibitory GMolecular pain
    Review
  11. 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 1 institution in 1 country.

Fang QiuAnesthesia and Operation Center, Chinese PLA General Hospital, Fuxing Road 28, Beijing, 100853, China.
Yang LiInstitute of Geriatric Cardiology, Chinese PLA General Hospital, Fuxing Road 28, Beijing, China.
Qiang FuAnesthesia and Operation Center, Chinese PLA General Hospital, Fuxing Road 28, Beijing, 100853, China.
Yong-Yan FanInstitute of Geriatric Cardiology, Chinese PLA General Hospital, Fuxing Road 28, Beijing, China.
Chao ZhuInstitute of Geriatric Cardiology, Chinese PLA General Hospital, Fuxing Road 28, Beijing, China.
Yan-Hong LiuAnesthesia and Operation Center, Chinese PLA General Hospital, Fuxing Road 28, Beijing, 100853, China. yliu919@gmail.com.ORCID http://orcid.org/0000-0001-9315-9245
Wei-Dong MiAnesthesia and Operation Center, Chinese PLA General Hospital, Fuxing Road 28, Beijing, 100853, China. wdmi1962@163.com.
Chinese PLA General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stromal cell-derived factor 1 (SDF-1)/chemokine CXC motif ligand 12 (CXCL12), a chemokine that is upregulated in dorsal root ganglion (DRG) during chronic pain models, has recently been found to play a central role in pain hypersensitivity. The purpose of present study is to investigate the functional impact of SDF-1 and its receptor, chemokine CXC motif receptor 4 (CXCR4), on two TTXR sodium channels in rat DRG using electrophysiological techniques. Preincubation with SDF-1 caused a concentration-dependent increase of Nav1.8 and Nav1.9 currents amplitudes in acutely isolated small diameter DRG neurons in short-term culture. As to Nav1.9, changes in current density and kinetic properties of Nav1.9 current evoked by SDF-1(50 ng/ml) was eliminated by CXCR4 antagonist AMD3100 and phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002. The increase in Nav1.9 current was also blocked by pertussis toxin (PTX) but not cholera toxin (CTX), showing involvement of Gi/o but not Gs subunits. As to Nav1.8, inhibitors (AMD3100, PTX, CTX, LY294002) used in present study didn't inhibit the increased amplitude of Nav1.8 current and shifted activation curve of Nav1.8 in a hyperpolarizing direction in the presence of SDF-1 (50 ng/ml). In conclusion, our data demonstrated that SDF-1 may excite primary nociceptive sensory neurons by acting on the biophysical properties of Nav1.8 and Nav1.9 currents but via different mechanisms.

Indexed as

Action PotentialsAnimalsCells, CulturedChemokine CXCL12Dose-Response Relationship, DrugGanglia, SpinalNAV1.8 Voltage-Gated Sodium ChannelNAV1.9 Voltage-Gated Sodium ChannelRatsRats, Sprague-DawleySodium Channel BlockersTetrodotoxinChemokine CXCL12CXCL12 protein, ratNAV1.8 Voltage-Gated Sodium ChannelNAV1.9 Voltage-Gated Sodium ChannelScn10a protein, ratScn11a protein, ratSodium Channel BlockersTetrodotoxinDorsal root ganglionG-protein coupled receptorsNociceptionStromal cell-derived factor 1Tetrodotoxin-resistant sodium channel

Identifiers

PMID27038931
OpenAlexW2332111725

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.