Evidence map›Paper›PMID 20623621›Full record

ArticleJournal of neuroscience research2010

Calpeptin attenuated inflammation, cell death, and axonal damage in animal model of multiple sclerosis.

M Kelly Guyton, Arabinda Das, Supriti Samantaray, Gerald C Wallace, Jonathan T Butler, Swapan K Ray, Naren L Banik

Open access · greenAbstract read
In one paragraph

Article in Journal of neuroscience research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

37 citing papers in PubMed, 46 citations in OpenAlex.

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  12. Calpain in the cleavage of alpha-synuclein and the pathogenesis of Parkinson's disease.Progress in molecular biology and translational science · 2019
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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

7 authors at 2 institutions in 1 country.

M Kelly GuytonDepartment of Neurosciences, Medical University of South Carolina, Charleston, South Carolina 29425, USA.
Arabinda Das
Supriti Samantaray
Gerald C Wallace
Jonathan T Butler
Swapan K Ray
Naren L Banik
Medical University of South Carolina · USUniversity of South Carolina · US

Funding

CALPAIN ACTIVATION OF T CELLS IN DEMYELINATING DISEASER01NS041088 · NINDS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BANIK, NAREN L · 2001 to 2009
$2.9M
MUSC FACIL EXPANSION &RENOV: SLE C06RR015455 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RAYMOND, JOHN R · 2002 to 2002
$2.0M
Attenuation of Axonal Damage and Neuronal Death in EAER01NS056176 · NINDS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BANIK, NAREN L · 2006 to 2010
$1.6M
Inflammation and Degeneration of Optic Nerve in EAER01NS065456 · NINDS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BANIK, NAREN L · 2009 to 2013
$1.6M
DIFFERENTIATION AND APOPTOSIS IN MALIGNANT NEUROBLASTOMAR01NS057811 · NINDS · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI RAY, SWAPAN K. · 2006 to 2009
$1.3M
PROTEOLYTIC CONTROL OF GLIOBLASTOMAR01CA091460 · NCI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI RAY, SWAPAN K · 2003 to 2007
$1.1M
CALPAIN IN THE PATHOPHYSIOLOGY OF DEMYELINATING DISEASER01NS038146 · NINDS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BANIK, NAREN L · 1999 to 2003
$918k
NCI NIH HHS CA-91460NCI NIH HHS R01 CA091460NCRR NIH HHS C06 RR015455NCRR NIH HHS C06RR-015455NINDS NIH HHS NS-38146NINDS NIH HHS NS-41088NINDS NIH HHS NS-56176NINDS NIH HHS NS-57811NINDS NIH HHS R01 NS038146NINDS NIH HHS R01 NS041088NINDS NIH HHS R01 NS056176NINDS NIH HHS R01 NS057811NINDS NIH HHS R01 NS065456
6 · The paper itself

Abstract

Experimental autoimmune encephalomyelitis (EAE) is an animal model for studying multiple sclerosis (MS). Calpain has been implicated in many inflammatory and neurodegenerative events that lead to disability in EAE and MS. Thus, treating EAE animals with calpain inhibitors may block these events and ameliorate disability. To test this hypothesis, acute EAE Lewis rats were treated dose dependently with the calpain inhibitor calpeptin (50-250 microg/kg). Calpain activity, gliosis, loss of myelin, and axonal damage were attenuated by calpeptin therapy, leading to improved clinical scores. Neuronal and oligodendrocyte death were also decreased, with down-regulation of proapoptotic proteins, suggesting that decreases in cell death were due to decreases in the expression or activity of proapoptotic proteins. These results indicate that calpain inhibition may offer a novel therapeutic avenue for treating EAE and MS.

Indexed as

AnimalsAxonsBlotting, WesternCalpainCell DeathCysteine Proteinase InhibitorsDipeptidesDown-RegulationEncephalomyelitis, Autoimmune, ExperimentalFluorescent Antibody TechniqueGliosisInflammationIn Situ Nick-End LabelingMaleMultiple SclerosisNerve Tissue ProteinsCalpaincalpeptinCysteine Proteinase InhibitorsDipeptidesNerve Tissue Proteins

Identifiers

PMID20623621
PMCPMC3164817
OpenAlexW2104987800

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.