Evidence map›Paper›PMID 25149422›Full record

ArticleActa neuropathologica communications2014

Discrepancy in CCL2 and CCR2 expression in white versus grey matter hippocampal lesions of Multiple Sclerosis patients.

Marloes Prins, Ranjan Dutta, Bart Baselmans, John J P Brevé, John G J M Bol, Sadie A Deckard, Paul van der Valk, Sandra Amor, Bruce D Trapp, Helga E de Vries and 2 more

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

  1. Engineered immunological niche directs therapeutic development in models of progressive multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Functional immune cell-astrocyte interactions.The Journal of experimental medicine · 2021
    Review
  9. Article
  10. Review
  11. Review
  12. Investigating the Causal Effect of Brain Expression ofFrontiers in bioengineering and biotechnology · 2020
    Article
  13. Review
  14. Dual CCR5/CCR2 targeting: opportunities for the cure of complex disorders.Cellular and molecular life sciences : CMLS · 2019
    Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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 4 institutions in 3 countries.

Marloes Prins
Ranjan Dutta
Bart Baselmans
John J P Brevé
John G J M Bol
Sadie A Deckard
Paul van der Valk
Sandra Amor
Bruce D Trapp
Helga E de Vries
Benjamin Drukarch
Anne-Marie van Dam
Amsterdam UMC Location VUmc · NLAmsterdam Neuroscience · NLUniversity Medical Center · USCleveland Clinic Lerner College of Medicine · US

Funding

PATHOGENESIS OF DEMYELINATION IN MS BRAINSR01NS035058 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI TRAPP, BRUCE D · 1996 to 2011
$3.0M
NINDS NIH HHS NS35058NINDS NIH HHS R01 NS035058PHS HHS 38667
6 · The paper itself

Abstract

A remarkable pathological difference between grey matter lesions (GML) and white matter lesions (WML) in Multiple Sclerosis (MS) patients is the paucity of infiltrating leukocytes in GML. To better understand these pathological differences, we hypothesize that the chemokine monocyte chemotactic protein-1 (MCP-1 or CCL2), of importance for leukocyte migration, and its receptor CCR2 are more abundantly expressed in WML than in GML of MS patients. To this end, we analyzed CCL2 and CCR2 expression in the hippocampus, comprising WML and GML,of post-mortem MS patients, and of control subjects. CCL2 and CCR2 mRNA were significantly increased in demyelinated MS hippocampus. Semi-quantification of CCL2 and CCR2 immunoreactivity showed that CCL2 is present in astrocytes only in active WML. CCR2 is upregulated in monocytes/macrophages or amoeboid microglia in active WML, and in ramified microglia in active GML, although to a lesser extent. As a follow-up, we observed a significantly increased CCL2 production by WM-, but not GM-derived astrocytes upon stimulation with bz-ATP in vitro. Finally, upon CCL2 stimulation, GM-derived microglia significantly increased their proliferation rate. We conclude that within hippocampal lesions, CCL2 expression is mainly restricted to WML, whereas the receptor CCR2 is upregulated in both WML and GML. The relative absence of CCL2 in GML may explain the lack of infiltrating immune cells in this type of lesions. We propose that the divergent expression of CCL2 and CCR2 in WML and GML explains or contributes to the differences in WML and GML formation in MS.

Indexed as

Adenosine TriphosphateAdultAgedAnimalsAnimals, NewbornBromodeoxyuridineCell ProliferationCells, CulturedChemokine CCL2FemaleGene ExpressionGray MatterHippocampusHistocompatibility Antigens Class IIHumansMale3'-O-(4-benzoyl)benzoyladenosine 5'-triphosphateAdenosine TriphosphateBromodeoxyuridineCCL2 protein, humanCCR2 protein, humanChemokine CCL2Histocompatibility Antigens Class IIMyelin Basic ProteinPlatelet Aggregation InhibitorsReceptors, CCR2

Identifiers

PMID25149422
PMCPMC4158064
OpenAlexW2107020854

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Registered trials

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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.