Evidence map›Paper›PMID 22641100›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2012

CCL2 disrupts the adherens junction: implications for neuroinflammation.

Toni K Roberts, Eliseo A Eugenin, Lillie Lopez, Ignacio A Romero, Babette B Weksler, Pierre-Olivier Couraud, Joan W Berman

Open access · bronzeAbstract read
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

73 citing papers in PubMed, 111 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Roles of Microglia in Cerebral Small Vessel Disease.CNS neuroscience & therapeutics · 2026
    Review
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  20. Article

13 more citing papers are in PubMed but not listed here.

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 4 institutions in 3 countries.

Toni K RobertsDepartment of Pathology, The Albert Einstein College of Medicine, Bronx, NY, USA.
Eliseo A Eugenin
Lillie Lopez
Ignacio A Romero
Babette B Weksler
Pierre-Olivier Couraud
Joan W Berman
Albert Einstein College of Medicine · USCornell University · USInstitut Cochin · FRThe Open University · GB

Funding

Immunology/Pathology CoreP30AI051519 · NIAID · YESHIVA UNIVERSITY · PI GOLDSTEIN, HARRIS · 2003 to 2013
$18.6M
Astrocyte connexin43 containing channels amplify CNS dysfunction in NeuroAIDSR01MH096625 · NIMH · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI EUGENIN, ELISEO A · 2012 to 2020
$4.5M
Mechanisms of HAD:Role of CCL2 BBB & HIV InfectionR01MH075679 · NIMH · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI BERMAN, JOAN WEINBERGER · 2006 to 2016
$4.0M
Dopamine alters CNS migration of uninfected and HIV infected leukocytes to SDF-1R01DA025567 · NIDA · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI BERMAN, JOAN WEINBERGER · 2008 to 2012
$1.7M
The role of gap junction channels in NeuroAIDSK01MH076679 · NIMH · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI EUGENIN, ELISEO A · 2006 to 2010
$646k
Mechanisms of Transmigration of HIV Infected Cells Across the Blood Brain BarrierF31AI071326 · NIAID · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI ROBERTS, TONI KAY · 2007 to 2010
$183k
NIAID NIH HHS AI-051519NIAID NIH HHS AI071326NIAID NIH HHS F31 AI071326NIAID NIH HHS P30 AI051519NIDA NIH HHS DA025567NIDA NIH HHS R01 DA025567NIMH NIH HHS K01 MH076679NIMH NIH HHS MH075679NIMH NIH HHS MH076679NIMH NIH HHS MH096625NIMH NIH HHS R01 MH075679NIMH NIH HHS R01 MH096625
6 · The paper itself

Abstract

Alterations to blood-brain barrier (BBB) adhesion molecules and junctional integrity during neuroinflammation can promote central nervous system (CNS) pathology. The chemokine CCL2 is elevated during CNS inflammation and is associated with endothelial dysfunction. The effects of CCL2 on endothelial adherens junctions (AJs) have not been defined. We demonstrate that CCL2 transiently induces Src-dependent disruption of human brain microvascular endothelial AJ. β-Catenin is phosphorylated and traffics from the AJ to PECAM-1 (platelet endothelial cell adhesion molecule-1), where it is sequestered at the membrane. PECAM-1 is also tyrosine-phosphorylated, an event associated with recruitment of the phosphatase SHP-2 (Src homology 2 domain-containing protein phosphatase) to PECAM-1, β-catenin release from PECAM-1, and reassociation of β-catenin with the AJ. Surface localization of PECAM-1 is increased in response to CCL2. This may enable the endothelium to sustain CCL2-induced alterations in AJ and facilitate recruitment of leukocytes into the CNS. Our novel findings provide a mechanism for CCL2-mediated disruption of endothelial junctions that may contribute to BBB dysfunction and increased leukocyte recruitment in neuroinflammatory diseases.

Indexed as

Adherens JunctionsAntigens, CDbeta CateninBrainCadherin 5CadherinsCell LineCell Membrane PermeabilityChemokine CCL2EncephalitisEndothelial CellsFocal Adhesion Kinase 1HumansMicrovesselsPhosphorylationPlatelet Endothelial Cell Adhesion Molecule-1Antigens, CDbeta CateninCadherin 5CadherinsCCL2 protein, humanChemokine CCL2Focal Adhesion Kinase 1Platelet Endothelial Cell Adhesion Molecule-1Protein Tyrosine Phosphatase, Non-Receptor Type 11PTK2 protein, humanPTPN11 protein, humanRecombinant Proteins

Identifiers

PMID22641100
PMCPMC3409314
OpenAlexW2080520337

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.