Evidence map›Paper›PMID 25982557›Full record

ArticleNeuroscience2015

Differential expression of CaMKII isoforms and overall kinase activity in rat dorsal root ganglia after injury.

M L Y Bangaru, J Meng, D J Kaiser, H Yu, G Fischer, Q H Hogan, A Hudmon

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
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  8. CaMKIIα Mediates the Effect of IL-17 To Promote Ongoing Spontaneous and Evoked Pain in Multiple Sclerosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
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  9. Review
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  16. CaMKII Controls Whether Touch Is Painful.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    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

7 authors at 3 institutions in 1 country.

M L Y BangaruDepartment of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI 53226, United States.
J MengDepartment of Biochemistry and Molecular Biology, Stark Neuroscience Research Institute, Indiana University School of Medicine, Indianapolis, IN 46202, United States.
D J KaiserDepartment of Biochemistry and Molecular Biology, Stark Neuroscience Research Institute, Indiana University School of Medicine, Indianapolis, IN 46202, United States.
H YuDepartment of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI 53226, United States.
G FischerDepartment of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI 53226, United States.
Q H HoganDepartment of Anesthesiology, Medical College of Wisconsin, Milwaukee, WI 53226, United States; Milwaukee Veterans Affairs Medical Center, Milwaukee, WI, United States.
A HudmonDepartment of Biochemistry and Molecular Biology, Stark Neuroscience Research Institute, Indiana University School of Medicine, Indianapolis, IN 46202, United States.
Medical College of Wisconsin · USIndiana University – Purdue University Indianapolis · USIndiana University School of Medicine

Funding

TRAUMATIC PAINFUL NEUROPATHY AND CALCIUM SIGNALINGR01NS042150 · NINDS · MEDICAL COLLEGE OF WISCONSIN · PI HOGAN, QUINN H · 2001 to 2011
$2.8M
CaMKII in neuronal signaling and degenerationR01NS078171 · NINDS · INDIANA UNIVERSITY INDIANAPOLIS · PI CUMMINS, THEODORE R, HUDMON, ANDY · 2012 to 2015
$1.3M
NINDS NIH HHS NS078171NINDS NIH HHS NS42150NINDS NIH HHS R01 NS042150NINDS NIH HHS R01 NS078171
6 · The paper itself

Abstract

Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) decodes neuronal activity by translating cytoplasmic Ca(2+) signals into kinase activity that regulates neuronal functions including excitability, gene expression, and synaptic transmission. Four genes lead to developmental and differential expression of CaMKII isoforms (α, β, γ, δ). We determined mRNA levels of these isoforms in the dorsal root ganglia (DRG) of adult rats with and without nerve injury in order to determine if differential expression of CaMKII isoforms may contribute to functional differences that follow injury. DRG neurons express mRNA for all four isoforms, and the relative abundance of CaMKII isoforms was γ>α>β=δ, based on the CT values. Following ligation of the 5th lumbar (L5) spinal nerve (SNL), the β isoform did not change, but mRNA levels of both the γ and α isoforms were reduced in the directly injured L5 neurons, and the α isoform was reduced in L4 neurons, compared to their contemporary controls. In contrast, expression of the δ isoform mRNA increased in L5 neurons. CaMKII protein decreased following nerve injury in both L4 and L5 populations. Total CaMKII activity measured under saturating Ca(2+)/CaM conditions was decreased in both L4 and L5 populations, while autonomous CaMKII activity determined in the absence of Ca(2+) was selectively reduced in axotomized L5 neurons 21days after injury. Thus, loss of CaMKII signaling in sensory neurons after peripheral nerve injury may contribute to neuronal dysfunction and pain.

Indexed as

AnimalsAxotomyCalcium-Calmodulin-Dependent Protein Kinase Type 2CatalysisDisease Models, AnimalGanglia, SpinalGene ExpressionHEK293 CellsHumansHyperalgesiaIsoenzymesLumbar VertebraeMaleRats, Sprague-DawleyRNA, MessengerSensory Receptor CellsCalcium-Calmodulin-Dependent Protein Kinase Type 2IsoenzymesRNA, MessengerCa(2+) signalingCaMKIInerve injuryneuropathic painsensory neuron

Identifiers

PMID25982557
PMCPMC4485599
OpenAlexW257920779

What OpenQuestion holds

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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.