Evidence map›Paper›PMID 24155322›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

Spinal mitogen-activated protein kinase phosphatase-3 (MKP-3) is necessary for the normal resolution of mechanical allodynia in a mouse model of acute postoperative pain.

Madhurima Saha, Sladjana Skopelja, Elena Martinez, Daniel L Alvarez, Brenna S Liponis, E Alfonso Romero-Sandoval

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Myeloid-specific tristetraprolin mitigates postsurgical incisional pain by suppressing proinflammatory responses.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  2. Article
  3. Dual-Specificity Phosphatase Regulation in Neurons and Glial Cells.International journal of molecular sciences · 2019
    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 1 institution in 1 country.

Madhurima SahaDepartment of Anesthesiology and Department of Pharmacology/Toxicology, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire 03755, and Department of Pharmaceutical and Administrative Sciences, Presbyterian College School of Pharmacy, Clinton, South Carolina 29325.
Sladjana Skopelja
Elena Martinez
Daniel L Alvarez
Brenna S Liponis
E Alfonso Romero-Sandoval
Dartmouth College · US

Funding

Cannabinoids and Neuroimmune InteractionsR01DA025211 · NIDA · DARTMOUTH COLLEGE · PI ROMERO-SANDOVAL, E. ALFONSO · 2009 to 2010
$711k
NIDA NIH HHS R01 DA025211
6 · The paper itself

Abstract

The mechanisms that drive the normal resolution of acute postoperative pain are not completely understood. We hypothesize a pivotal role of a major spinal mitogen-activated protein kinase (MAPKs) regulator, MAPK phosphatase (MKP)-3, in the resolution of postoperative pain. We used wild-type and MKP-3 knock-out (KO) mice, a paw incision model of acute postoperative pain, and behavioral and molecular biology experiments. We observed persistent mechanical allodynia in mice lacking MKP-3 (postoperative day 21), concurrently with persistent phosphorylation of spinal p38 and extracellular signal-regulated kinases (ERK)-1/2 on postoperative day 12, while both MAPK phosphorylation and allodynia resolved on postoperative day 7 in wild-type mice. Spinal p-ERK was expressed mainly in neurons and microglia, while spinal p-p38 was expressed mostly in microglia in MKP-3 KO mice, and their selective pharmacological inhibition reduced the persistent allodynia observed in these mice. Our findings strongly suggest that dysregulation of MKP-3 prevents spontaneous resolution of acute postoperative pain and drives its transition to persistent pain via persistent neuronal and microglial MAPK phosphorylation in the spinal cord.

Indexed as

Acute PainAnimalsDisease Models, AnimalDual Specificity Phosphatase 6HyperalgesiaMAP Kinase Signaling SystemMiceMicrogliaMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Neuronsp38 Mitogen-Activated Protein KinasesPhosphorylationPostoperative PainSpinal CordDual Specificity Phosphatase 6Dusp6 protein, mouseMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3p38 Mitogen-Activated Protein Kinases

Identifiers

PMID24155322
PMCPMC6618446
OpenAlexW1968198979

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.