Evidence map›Paper›PMID 22530047›Full record

ArticlePloS one2012

Identification of protein networks involved in the disease course of experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis.

Annelies Vanheel, Ruth Daniels, Stéphane Plaisance, Kurt Baeten, Jerome J A Hendriks, Pierre Leprince, Debora Dumont, Johan Robben, Bert Brône, Piet Stinissen and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-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

17 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. 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

12 authors at 3 institutions in 1 country.

Annelies VanheelBiomedical Research Institute, Hasselt University and Transnationale Universiteit Limburg, School of Life Sciences, Hasselt, Belgium.
Ruth Daniels
Stéphane Plaisance
Kurt Baeten
Jerome J A Hendriks
Pierre Leprince
Debora Dumont
Johan Robben
Bert Brône
Piet Stinissen
Jean-Paul Noben
Niels Hellings
Hasselt University · BEKU Leuven · BEUniversity of Liège · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A more detailed insight into disease mechanisms of multiple sclerosis (MS) is crucial for the development of new and more effective therapies. MS is a chronic inflammatory autoimmune disease of the central nervous system. The aim of this study is to identify novel disease associated proteins involved in the development of inflammatory brain lesions, to help unravel underlying disease processes. Brainstem proteins were obtained from rats with MBP induced acute experimental autoimmune encephalomyelitis (EAE), a well characterized disease model of MS. Samples were collected at different time points: just before onset of symptoms, at the top of the disease and following recovery. To analyze changes in the brainstem proteome during the disease course, a quantitative proteomics study was performed using two-dimensional difference in-gel electrophoresis (2D-DIGE) followed by mass spectrometry. We identified 75 unique proteins in 92 spots with a significant abundance difference between the experimental groups. To find disease-related networks, these regulated proteins were mapped to existing biological networks by Ingenuity Pathway Analysis (IPA). The analysis revealed that 70% of these proteins have been described to take part in neurological disease. Furthermore, some focus networks were created by IPA. These networks suggest an integrated regulation of the identified proteins with the addition of some putative regulators. Post-synaptic density protein 95 (DLG4), a key player in neuronal signalling and calcium-activated potassium channel alpha 1 (KCNMA1), involved in neurotransmitter release, are 2 putative regulators connecting 64% of the identified proteins. Functional blocking of the KCNMA1 in macrophages was able to alter myelin phagocytosis, a disease mechanism highly involved in EAE and MS pathology. Quantitative analysis of differentially expressed brainstem proteins in an animal model of MS is a first step to identify disease-associated proteins and networks that warrant further research to study their actual contribution to disease pathology.

Indexed as

Protein Interaction MappingProteomeAnimalsBrainDisease Models, AnimalDisks Large Homolog 4 ProteinEncephalomyelitis, Autoimmune, ExperimentalFemaleIntracellular Signaling Peptides and ProteinsLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsMembrane ProteinsMultiple SclerosisPrincipal Component AnalysisProtein Interaction MapsProteomicsRatsDisks Large Homolog 4 ProteinDlg4 protein, ratIntracellular Signaling Peptides and ProteinsKcnma1 protein, ratLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsMembrane ProteinsProteome

Identifiers

PMID22530047
PMCPMC3328452
OpenAlexW2084849712

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.