Evidence map›Paper›PMID 24152582›Full record

ArticleGene therapy2014

Sustained relief of neuropathic pain by AAV-targeted expression of CBD3 peptide in rat dorsal root ganglion.

G Fischer, B Pan, D Vilceanu, Q H Hogan, H Yu

Open access · hybridAbstract read
In one paragraph

Article in Gene therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 80 citations in OpenAlex.

  1. Article
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  3. Review
  4. Article
  5. Article
  6. Review
  7. Precision spinal gene delivery-induced functional switch in nociceptive neurons reverses neuropathic pain.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  8. Article
  9. Article
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  11. Article
  12. Article
  13. AAV-encoded CaGene therapy · 2019
    Article
  14. Article
  15. Article
  16. Review
  17. Article
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  20. 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 1 institution in 1 country.

G FischerDepartment of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA.
B PanDepartment of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA.
D VilceanuDepartment of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA.
Q H Hogan1] Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA [2] Department of Anesthesiology, Medical College of Wisconsin, Zablocki VA Medical Center, Milwaukee, WI, USA.
H YuDepartment of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI, USA.
Medical College of Wisconsin · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Ca(2+) channel-binding domain 3 (CBD3) peptide, derived from the collapsin response mediator protein 2 (CRMP-2), is a recently discovered voltage-gated Ca(2+) channel (VGCC) blocker with a preference for CaV2.2. Rodent administration of CBD3 conjugated to cell penetrating motif TAT (TAT-CBD3) has been shown to reduce pain behavior in inflammatory and neuropathic pain models. However, TAT-CBD3 analgesia has limitations, including short half-life, lack of cellular specificity and undesired potential off-site effects. We hypothesized that these issues could be addressed by expressing CBD3 encoded by high-expression vectors in primary sensory neurons. We constructed an adeno-associated viral (AAV) vector expressing recombinant fluorescent CBD3 peptide and injected it into lumbar dorsal root ganglia (DRGs) of rats before spared nerve injury (SNI). We show that selective expression of enhanced green fluorescent protein (EGFP)-CBD3 in lumbar 4 (L4) and L5 DRG neurons and their axonal projections results in effective attenuation of nerve injury-induced neuropathic pain in the SNI model. We conclude that AAV-encoded CBD3 delivered to peripheral sensory neurons through DRG injection may be a valuable approach for exploring the role of presynaptic VGCCs and long-term modulation of neurotransmission, and may also be considered for development as a gene therapy strategy to treat chronic neuropathic pain.

Indexed as

Genetic VectorsAnalgesicsAnimalsAptamers, PeptideCalcium Channels, N-TypeDependovirusDisease Models, AnimalGanglia, SpinalHEK293 CellsHumansIntercellular Signaling Peptides and ProteinsLumbar VertebraeMaleNerve Tissue ProteinsNeuralgiaPeptide FragmentsAnalgesicsAptamers, PeptideCalcium Channels, N-TypeCBD3 peptidecollapsin response mediator protein-2Intercellular Signaling Peptides and ProteinsNerve Tissue ProteinsPeptide Fragments

Identifiers

PMID24152582
PMCPMC3881029
OpenAlexW2142844399

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.