Evidence map›Paper›PMID 23626716›Full record

ArticlePloS one2013

Role of tachykinin 1 and 4 gene-derived neuropeptides and the neurokinin 1 receptor in adjuvant-induced chronic arthritis of the mouse.

Eva Borbély, Zsófia Hajna, Katalin Sándor, László Kereskai, István Tóth, Erika Pintér, Péter Nagy, János Szolcsányi, John Quinn, Andreas Zimmer and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  10. Hemokinin-1 as a Mediator ofFrontiers in pharmacology · 2020
    Article
  11. Human Dorsal Root Ganglia.Frontiers in cellular neuroscience · 2019
    Review
  12. Article
  13. Article
  14. Role of capsaicin-sensitive nerves and tachykinins in mast cell tryptase-induced inflammation of murine knees.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016
    Article
  15. Article
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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 5 institutions in 4 countries.

Eva BorbélyDepartment of Pharmacology and Pharmacotherapy, Faculty of Medicine, University of Pécs, Pécs, Hungary.
Zsófia Hajna
Katalin Sándor
László Kereskai
István Tóth
Erika Pintér
Péter Nagy
János Szolcsányi
John Quinn
Andreas Zimmer
James Stewart
Christopher Paige
Alexandra Berger
Zsuzsanna Helyes
University of Pecs · HUUniversity of Liverpool · GBOntario Institute for Cancer Research · CAUniversity of Bonn · DEUniversity of Toronto · CA

Funding

Canadian Institutes of Health Research 9862
6 · The paper itself

Abstract

objectiveSubstance P, encoded by the Tac1 gene, is involved in neurogenic inflammation and hyperalgesia via neurokinin 1 (NK1) receptor activation. Its non-neuronal counterpart, hemokinin-1, which is derived from the Tac4 gene, is also a potent NK1 agonist. Although hemokinin-1 has been described as a tachykinin of distinct origin and function compared to SP, its role in inflammatory and pain processes has not yet been elucidated in such detail. In this study, we analysed the involvement of tachykinins derived from the Tac1 and Tac4 genes, as well as the NK1 receptor in chronic arthritis of the mouse.

methodsComplete Freund's Adjuvant was injected intraplantarly and into the tail of Tac1(-/-), Tac4(-/-), Tacr1(-/-) (NK1 receptor deficient) and Tac1(-/-/)Tac4(-/-) mice. Paw volume was measured by plethysmometry and mechanosensitivity using dynamic plantar aesthesiometry over a time period of 21 days. Semiquantitative histopathological scoring and ELISA measurement of IL-1β concentrations of the tibiotarsal joints were performed.

resultsMechanical hyperalgesia was significantly reduced from day 11 in Tac4(-/-) and Tacr1(-/-) animals, while paw swelling was not altered in any strain. Inflammatory histopathological alterations (synovial swelling, leukocyte infiltration, cartilage destruction, bone damage) and IL-1β concentration in the joint homogenates were significantly smaller in Tac4(-/-) and Tac1(-/-/)Tac4(-/-) mice.

conclusionsHemokinin-1, but not substance P increases inflammation and hyperalgesia in the late phase of adjuvant-induced arthritis. While NK1 receptors mediate its antihyperalgesic actions, the involvement of another receptor in histopathological changes and IL-1β production is suggested.

Indexed as

AnimalsArthritis, ExperimentalEdemaFreund's AdjuvantGene Expression RegulationHyperalgesiaInflammationInterleukin-1betaJointsMaleMiceMice, Inbred C57BLMice, KnockoutPlethysmographyProtein PrecursorsReceptors, Neurokinin-1Freund's AdjuvantInterleukin-1betaProtein PrecursorsReceptors, Neurokinin-1Substance PTac4 protein, mouseTachykinins

Identifiers

PMID23626716
PMCPMC3634005
OpenAlexW2081512390

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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.