Evidence map›Paper›PMID 20698758›Full record

ArticleJournal of neurotrauma2010

Vascular endothelial growth factor and spinal cord injury pain.

Olivera Nesic, Laura M Sundberg, Juan J Herrera, Venkata U L Mokkapati, Julieann Lee, Ponnada A Narayana

Open access · greenAbstract read
In one paragraph

Article in Journal of neurotrauma, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

22 citing papers in PubMed, 40 citations in OpenAlex.

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  16. Targeting VEGF and Its Receptors for the Treatment of Osteoarthritis and Associated Pain.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2016
    Review
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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

6 authors at 2 institutions in 1 country.

Olivera NesicDepartment of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas 77555-1072, USA. olnesic@utmb.edu
Laura M Sundberg
Juan J Herrera
Venkata U L Mokkapati
Julieann Lee
Ponnada A Narayana
The University of Texas Health Science Center at Houston · USThe University of Texas Medical Branch at Galveston · US

Funding

MRI of Angiogenesis in Spinal Cord InjuryR01NS045624 · NINDS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI NARAYANA, PONNADA A · 2005 to 2009
$2.8M
High Field MRI Scanner for Animal StudiesS10RR017205 · NCRR · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI NARAYANA, PONNADA A · 2003 to 2003
$1.6M
Aquaporins and Neuropathic Pain after Spinal Cord InjuryR21NS058417 · NINDS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI NESIC-TAYLOR, OLIVERA · 2008 to 2009
$483k
NCRR NIH HHS S10 RR17205-01NINDS NIH HHS NS045624NINDS NIH HHS NS058417
6 · The paper itself

Abstract

Vascular endothelial growth factor (VEGF)-A mRNA was previously identified as one of the significantly upregulated transcripts in spinal cord injured tissue from adult rats that developed allodynia. To characterize the role of VEGF-A in the development of pain in spinal cord injury (SCI), we analyzed mechanical allodynia in SCI rats that were treated with either vehicle, VEGF-A isoform 165 (VEGF(165)), or neutralizing VEGF(165)-specific antibody. We have observed that exogenous administration of VEGF(165) increased both the number of SCI rats that develop persistent mechanical allodynia, and the level of hypersensitivity to mechanical stimuli. Our analysis identified excessive and aberrant growth of myelinated axons in dorsal horns and dorsal columns of chronically injured spinal cords as possible mechanisms for both SCI pain and VEGF(165)-induced amplification of SCI pain, suggesting that elevated endogenous VEGF(165) may have a role in the development of allodynia after SCI. However, the neutralizing VEGF(165) antibody showed no effect on allodynia or axonal sprouting after SCI. It is possible that another endogenous VEGF isoform activates the same signaling pathway as the exogenously-administered 165 isoform and contributes to SCI pain. Our transcriptional analysis revealed that endogenous VEGF(188) is likely to be the isoform involved in the development of allodynia after SCI. To the best of our knowledge, this is the first study to suggest a possible link between VEGF, nonspecific sprouting of myelinated axons, and mechanical allodynia following SCI.

Indexed as

AnimalsAntibodies, NeutralizingHyperalgesiaImmunohistochemistryMaleMotor ActivityOligonucleotide Array Sequence AnalysisPain ThresholdPhysical StimulationRandom AllocationRatsRats, Sprague-DawleySpinal Cord InjuriesStatistics, NonparametricVascular Endothelial Growth Factor AAntibodies, NeutralizingVascular Endothelial Growth Factor A

Identifiers

PMID20698758
PMCPMC2953928
OpenAlexW2053750076

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.