Evidence map›Paper›PMID 24902717›Full record

ArticleBritish journal of pharmacology2014

Controlling the activation of the Bv8/prokineticin system reduces neuroinflammation and abolishes thermal and tactile hyperalgesia in neuropathic animals.

D Maftei, V Marconi, F Florenzano, L A Giancotti, M Castelli, S Moretti, E Borsani, L F Rodella, G Balboni, L Luongo and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 55 citations in OpenAlex.

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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

14 authors at 6 institutions in 1 country.

D MafteiDepartment of Physiology and Pharmacology 'Vittorio Erspamer', University of Rome, Rome, Italy.
V Marconi
F Florenzano
L A Giancotti
M Castelli
S Moretti
E Borsani
L F Rodella
G Balboni
L Luongo
S Maione
P Sacerdote
L Negri
R Lattanzi
American University of Rome · ITUniversity of Milan · ITUniversity of Brescia · ITUniversity of Campania "Luigi Vanvitelli" · ITEuropean Brain Research Institute · ITUniversity of Cagliari · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeChemokines are involved in neuroinflammation and contribute to chronic pain processing. The new chemokine prokineticin 2 (PROK2) and its receptors (PKR1 and PKR2 ) have a role in inflammatory pain and immunomodulation. In the present study, we investigated the involvement of PROK2 and its receptors in neuropathic pain. EXPERIMENTAL APPROACH: Effects of single, intrathecal, perineural and s.c. injections of the PKR antagonist PC1, or of 1 week s.c. treatment, on thermal hyperalgesia and tactile allodynia was evaluated in mice with chronic constriction of the sciatic nerve (CCI). Expression and localization of PROK2 and of its receptors at peripheral and central level was evaluated 10 days after CCI, following treatment for 1 week with saline or PC1. IL-1β and IL-10 levels, along with glia activation, were evaluated. KEY

resultsSubcutaneous, intrathecal and perineural PC1 acutely abolished the CCI-induced hyperalgesia and allodynia. At 10 days after CCI, PROK2 and its receptor PKR2 were up-regulated in nociceptors, in Schwann cells and in activated astrocytes of the spinal cord. Therapeutic treatment with PC1 (s.c., 1 week) alleviated established thermal hyperalgesia and allodynia, reduced the injury-induced overexpression of PROK2, significantly blunted nerve injury-induced microgliosis and astrocyte activation in the spinal cord and restored the physiological levels of proinflammatory and anti-inflammatory cytokines in periphery and in spinal cord. CONCLUSION AND IMPLICATIONS: The prokineticin system contributes to pain modulation via neuron-glia interaction. Sustained inhibition of the prokineticin system, at peripheral or central levels, blocked both pain symptoms and some events underlying disease progression.

Indexed as

AnimalsGanglia, SpinalGastrointestinal HormonesHyperalgesiaInterleukin-10Interleukin-1betaMaleMiceNeuralgiaNeurogliaNeuropeptidesReceptors, G-Protein-CoupledRNA, MessengerSciatic NerveSpinal CordGastrointestinal HormonesIL10 protein, mouseIL1B protein, mouseInterleukin-10Interleukin-1betaNeuropeptidesPKR1 protein, mousePKR2 protein, mouseProk2 protein, mouseReceptors, G-Protein-CoupledRNA, Messenger

Identifiers

PMID24902717
PMCPMC4294109
OpenAlexW1495922595

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.