Evidence map›Paper›PMID 21290412›Full record

ArticleJournal of neuroscience research2011

Calpeptin attenuated apoptosis and intracellular inflammatory changes in muscle cells.

Kenkichi Nozaki, Arabinda Das, Swapan K Ray, Naren L Banik

Open access · greenAbstract read
In one paragraph

Article in Journal of neuroscience research, 2011. 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
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

13 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Neutral sphingomyelinase 2 is required for cytokine-induced skeletal muscle calpain activation.American journal of physiology. Lung cellular and molecular physiology · 2015
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Novel approaches in the treatment of myositis and myopathies.Therapeutic advances in musculoskeletal disease · 2012
    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

4 authors at 2 institutions in 1 country.

Kenkichi NozakiDivision of Neurology, Department of Neurosciences, Medical University of South Carolina, Charleston, South Carolina 29425, USA.
Arabinda Das
Swapan K Ray
Naren L Banik
Medical University of South Carolina · USUniversity of South Carolina · US

Funding

ROLE OF PROTEINASE IN SPINAL CORD INJURYR01NS031622 · NINDS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BANIK, NAREN L · 1994 to 2011
$3.4M
CALPAIN ACTIVATION OF T CELLS IN DEMYELINATING DISEASER01NS041088 · NINDS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BANIK, NAREN L · 2001 to 2009
$2.9M
CALPAIN IN THE PATHOPHYSIOLOGY OF DEMYELINATING DISEASER01NS038146 · NINDS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BANIK, NAREN L · 1999 to 2003
$918k
NINDS NIH HHS NS-31622NINDS NIH HHS NS-38146NINDS NIH HHS NS-41088NINDS NIH HHS R01 NS031622NINDS NIH HHS R01 NS038146NINDS NIH HHS R01 NS041088
6 · The paper itself

Abstract

In idiopathic inflammatory myopathies (IIMs), extracellular inflammatory stimulation is considered to induce secondary intracellular inflammatory changes including expression of major histocompatibility complex class-I (MHC-I) and to produce a self-sustaining loop of inflammation. We hypothesize that activation of calpain, a Ca(2+) -sensitive protease, bridges between these extracellular inflammatory stress and intracellular secondary inflammatory changes in muscle cells. In this study, we demonstrated that treatment of rat L6 myoblast cells with interferon-γ (IFN-γ) caused expression of MHC-I and inflammation-related transcription factors (phosphorylated-extracellular signal-regulated kinase 1/2 and nuclear factor-κB). We also demonstrated that treatment with tumor necrosis factor-α (TNF-α) induced apoptotic changes and activation of calpain and cyclooxygenase-2. Furthermore, we found that posttreatment with calpeptin attenuated the intracellular changes induced by IFN-γ or TNF-α. Our results indicate that calpain inhibition attenuates apoptosis and secondary inflammatory changes induced by extracellular inflammatory stimulation in the muscle cells. These results suggest calpain as a potential therapeutic target for treatment of IIMs.

Indexed as

AnimalsApoptosisBlotting, WesternCalpainCell LineCyclooxygenase 2Cysteine Proteinase InhibitorsDipeptidesHistocompatibility Antigens Class IInflammationInterferon-gammaMyoblastsMyositisNF-kappa BRatsSignal TransductionCalpaincalpeptinCyclooxygenase 2Cysteine Proteinase InhibitorsDipeptidesHistocompatibility Antigens Class IInterferon-gammaNF-kappa BTumor Necrosis Factor-alpha

Identifiers

PMID21290412
PMCPMC3076617
OpenAlexW2056394000

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.