Evidence map›Paper›PMID 22613718›Full record

ArticleThe Journal of biological chemistry2012

Evidence that formation of vimentin mitogen-activated protein kinase (MAPK) complex mediates mast cell activation following FcεRI/CC chemokine receptor 1 cross-talk.

Masako Toda, Chuan-Hui Kuo, Satty K Borman, Ricardo Micheler Richardson, Akihito Inoko, Masaki Inagaki, Andrea Collins, Klaus Schneider, Santa Jeremy Ono

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
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  4. Extracellular vimentin amplifies inflammation: Perspectives for immune injury and therapeutics for periodontitis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Review
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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

9 authors at 5 institutions in 4 countries.

Masako TodaDivision of Allergy and Immunology, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio 45221-0097,USA.
Chuan-Hui Kuo
Satty K Borman
Ricardo Micheler Richardson
Akihito Inoko
Masaki Inagaki
Andrea Collins
Klaus Schneider
Santa Jeremy Ono
Aichi Cancer Center · JPCincinnati Children's Hospital Medical Center · USGlaxoSmithKline (United Kingdom) · GBNorth Carolina Central University · USUniversity of Cincinnati · US

Funding

Regulation of Chemokine Mediated Leukocyte FunctionsR01AI038910 · NIAID · NORTH CAROLINA CENTRAL UNIVERSITY · PI RICHARDSON, MICHELER RICARDO · 2002 to 2011
$2.3M
Roles of CC chemokine activity in mast cell responses and ocular allergyR01EY019630 · NEI · UNIVERSITY OF CINCINNATI · PI ONO, SANTA JEREMY · 2009 to 2012
$1.5M
REGULATION OF HUMAN INTERLEUKIN-8 RECEPTORSR29AI038910 · NIAID · DUKE UNIVERSITY · PI RICHARDSON, MICHELER RICARDO · 1996 to 2000
$107k
NEI NIH HHS R01 EY019630NEI NIH HHS R01-EY-019630-01NIAID NIH HHS AI-38910NIAID NIH HHS R01 AI038910NIAID NIH HHS R29 AI038910
6 · The paper itself

Abstract

Accumulating evidence points to cross-talk between FcεRI and CC chemokine receptor (CCR)-mediated signaling pathways in mast cells. Here, we propose that vimentin, a protein comprising type III intermediate filament, participates in such cross-talk for CCL2/monocyte chemotactic protein 1 (MCP-1) production in mast cells, which is a mechanism for allergic inflammation. Co-stimulation via FcεRI, using IgE/antigen, and CCR1, using recombinant CCL3/macrophage inflammatory protein-1α (MIP-1α), increased expression of phosphorylated, disassembled, and soluble vimentin in rat basophilic leukemia (RBL)-2H3 cells expressing human CCR1 (RBL-CCR1 cells) and bone marrow-derived murine mast cells, both models of mucosal type mast cells. Furthermore, co-stimulation enhanced production of CCL2 as well as phosphorylation of MAPK. Treating the cells with p38 MAPK inhibitor SB203580, but not with MEK inhibitor PD98058, reduced CCL2 production, suggesting that p38 MAPK, but not ERK1/2, plays a critical role in the chemokine production. Immunoprecipitation analysis showed that vimentin interacts with phosphorylated ERK1/2 and p38 MAPKs in the co-simulated cells. Preventing disassembly of the vimentin by aggregating vimentin filaments using β,β'-iminodipropionitrile reduced the interaction of vimentin with phosphorylated MAPKs as well as CCL2 production in the cells. Taken together, disassembled vimentin interacting with phosphorylated p38 MAPK could mediate CCL2 production in mast cells upon FcεRI and CCR1 activation.

Indexed as

AnimalsCell LineCell Line, TumorCells, CulturedChemokine CCL2Electrophoresis, Gel, Two-DimensionalEnzyme-Linked Immunosorbent AssayHumansImidazolesImmunoprecipitationMast CellsMiceMice, Inbred BALB CMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein KinasesChemokine CCL2ImidazolesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Mitogen-Activated Protein KinasesOrganic Chemicalsp38 Mitogen-Activated Protein KinasesPD 98058PyridinesReceptors, CCR1Receptors, IgGSB 203580Vimentin

Identifiers

PMID22613718
PMCPMC3397876
OpenAlexW1657172089

What OpenQuestion holds

Textmetadata
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.