Evidence map›Paper›PMID 24374082›Full record

ArticleNeuroscience2014

Temporal changes in MrgC expression after spinal nerve injury.

S-Q He, L Han, Z Li, Q Xu, V Tiwari, F Yang, X Guan, Y Wang, S N Raja, X Dong and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

13 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Targeting sensory neuron GPCRs for peripheral neuropathic pain.Trends in pharmacological sciences · 2023
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Targeting human Mas-related G protein-coupled receptor X1 to inhibit persistent pain.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. 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

11 authors at 3 institutions in 2 countries.

S-Q HeDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA.
L HanThe Solomon H. Snyder Department of Neuroscience, Center for Sensory Biology, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA.
Z LiThe Solomon H. Snyder Department of Neuroscience, Center for Sensory Biology, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA.
Q XuDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA.
V TiwariDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA.
F YangDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA.
X GuanDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA.
Y WangDepartment of Anesthesiology, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
S N RajaDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA.
X DongThe Solomon H. Snyder Department of Neuroscience, Center for Sensory Biology, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA; Howard Hughes Medical Institute, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA. Electronic address: xdong2@jhmi.edu.
Y GuanDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA. Electronic address: yguan1@jhmi.edu.
Johns Hopkins Medicine · USJohns Hopkins University · USCapital Medical University · CN

Funding

INJURY-INDUCES PAIN-- CHEMICAL MODULATION OF NOCICEPTORSR01NS026363 · NINDS · JOHNS HOPKINS UNIVERSITY · PI RAJA, SRINIVASA N. · 1989 to 2021
$6.8M
Functional analysis of the Mrg receptor family in pain sensationR01NS054791 · NINDS · JOHNS HOPKINS UNIVERSITY · PI DONG, XINZHONG · 2007 to 2020
$5.0M
Mrgs as New Target for the Treatment of Neuropathic PainR01NS070814 · NINDS · JOHNS HOPKINS UNIVERSITY · PI GUAN, YUN · 2011 to 2020
$3.2M
Functional Analysis of Pirt and Pirt2: novel regulators of TRP channelsR01GM087369 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI DONG, XINZHONG · 2010 to 2013
$1.3M
Genetic and Molecular Analysis of sensory nerve innervation in hairy skin and spiR21NS058481 · NINDS · JOHNS HOPKINS UNIVERSITY · PI DONG, XINZHONG · 2007 to 2008
$394k
NIGMS NIH HHS R01 GM087369NINDS NIH HHS NS26363NINDS NIH HHS NS54791NINDS NIH HHS NS70814NINDS NIH HHS R01 NS026363NINDS NIH HHS R01 NS054791NINDS NIH HHS R01 NS070814NINDS NIH HHS R21 NS058481
6 · The paper itself

Abstract

Mas-related G-protein-coupled receptor subtype C (MrgC) may play an important role in pain sensation. However, the distribution of MrgC receptors in different subpopulations of rodent dorsal root ganglion (DRG) neurons has not been clearly demonstrated owing to a lack of MrgC-selective antibody. It is also unclear whether peripheral nerve injury induces different time-dependent changes in MrgC expression in injured and uninjured DRG neurons. Here we showed that MrgC immunoreactivity is distributed in both IB4-positive (non-peptidergic) and calcitonin gene-related peptide-positive (peptidergic) DRG neurons in mice and rats. Importantly, the MrgC mRNA level and MrgC immunoreactivity were both decreased in the injured L5 DRG compared to corresponding levels in the contralateral (uninjured) DRG in rats on days 14 and 30 after an L5 spinal nerve ligation. In contrast, mRNA and protein levels of MrgC were increased in the adjacent uninjured L4 DRG. Thus, nerve injury may induce temporal changes in MrgC expression that differ between injured and uninjured DRG neurons. In animal behavior tests, chronic constriction injury of the sciatic nerve induced mechanical pain hypersensitivity in wild-type mice and Mrg-clusterΔ(-/-) mice (Mrg KO). However, the duration of mechanical hypersensitivity was longer in the Mrg KO mice than in their wild-type littermates, indicating that activation of Mrgs may constitute an endogenous mechanism that inhibits the maintenance of neuropathic pain in mice. These findings extend our knowledge about the distribution of MrgC in rodent DRG neurons and the regulation of its expression by nerve injury.

Indexed as

AnimalsCalcitonin Gene-Related PeptideGanglia, SpinalHyperalgesiaMaleMiceMice, Inbred C57BLMice, KnockoutNeuralgiaNeuronsRatsRats, Sprague-DawleyReceptors, G-Protein-CoupledRNA, MessengerSciatic NeuropathySpinal NervesCalcitonin Gene-Related PeptideMrgC protein, mouseMrgprc protein, ratReceptors, G-Protein-CoupledRNA, Messengerdorsal root ganglionMrgCnerve injuryneuropathic pain

Identifiers

PMID24374082
PMCPMC3945476
OpenAlexW1973185617

What OpenQuestion holds

Textmetadata
LicenceTDM
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.