Evidence map›Paper›PMID 24833787›Full record

ArticleAnnals of the rheumatic diseases2015

Characterising the expression and function of CCL28 and its corresponding receptor, CCR10, in RA pathogenesis.

Zhenlong Chen, Seung-Jae Kim, Abdul B Essani, Michael V Volin, Olga M Vila, William Swedler, Shiva Arami, Suncica Volkov, Latriese V Sardin, Nadera Sweiss and 1 more

Open access · greenAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

44 citing papers in PubMed, 66 citations in OpenAlex.

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  10. Bone Marrow-Derived GCAAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
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  16. [Role of the CCL28-CCR10 pathway in monocyte migration in rheumatoid arthritis].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2022
    Article
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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

11 authors at 2 institutions in 1 country.

Zhenlong ChenDivision of Rheumatology, Department of Medicine, University of Illinois, Chicago, Illinois, USA.
Seung-Jae KimDivision of Rheumatology, Department of Medicine, University of Illinois, Chicago, Illinois, USA.
Abdul B EssaniDivision of Rheumatology, Department of Medicine, University of Illinois, Chicago, Illinois, USA.
Michael V VolinDepartment of Microbiology & Immunology, Midwestern University, Chicago College of Osteopathic Medicine, Downers Grove, Illinois, USA.
Olga M VilaDivision of Rheumatology, Department of Medicine, University of Illinois, Chicago, Illinois, USA.
William SwedlerDivision of Rheumatology, Department of Medicine, University of Illinois, Chicago, Illinois, USA.
Shiva AramiDivision of Rheumatology, Department of Medicine, University of Illinois, Chicago, Illinois, USA.
Suncica VolkovDivision of Rheumatology, Department of Medicine, University of Illinois, Chicago, Illinois, USA.
Latriese V SardinDivision of Rheumatology, Department of Medicine, University of Illinois, Chicago, Illinois, USA.
Nadera SweissDivision of Rheumatology, Department of Medicine, University of Illinois, Chicago, Illinois, USA.
Shiva ShahraraDivision of Rheumatology, Department of Medicine, University of Illinois, Chicago, Illinois, USA.
University of Illinois Chicago · USMidwestern University · US

Funding

Role of Stress-Response Protein gp96 in the Persistence of Rheumatoid ArthritisR01AR055240 · NIAMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI POPE, RICHARD M. · 2008 to 2012
$1.7M
The Role of IL-17 in Monocyte MigrationR03AR056099 · NIAMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI SHAHRARA, SHIVA · 2009 to 2011
$229k
NIAMS NIH HHS AR055240NIAMS NIH HHS R03 AR056099
6 · The paper itself

Abstract

objectiveThis study was conducted to determine the expression pattern, regulation and function of CCL28 and CCR10 in rheumatoid arthritis (RA) pathogenesis.

methodsExpression of CCL28 and CCR10 was assessed in RA compared with other arthritis synovial tissues (STs) or fluids (SFs) by histology or ELISA. The factors modulating CCL28 and CCR10 expression were identified in RA myeloid and endothelial cells by ELISA, FACS and Western blotting. The mechanism by which CCL28 ligation promotes RA angiogenesis was examined in control and CCR10-knockdown endothelial cell chemotaxis and capillary formation.

resultsCCL28 and/or CCR10 expression levels were accentuated in STs and SFs of patients with joint disease compared with normal controls and they were predominately coexpressed in RA myeloid and endothelial cells. We show that protein expression of CCL28 and CCR10 was modulated by tumour necrosis factor (TNF)-α and toll-like receptor 4 ligation in RA monocytes and endothelial cells and by interleukin (IL)-6 stimulation in RA macrophages. Neutralisation of CCL28 in RA SF or blockade of CCR10 on human endothelial progenitor cells (EPCs) significantly reduced SF-induced endothelial migration and capillary formation, demonstrating that ligation of joint CCL28 to endothelial CCR10+ cells is involved in RA angiogenesis. We discovered that angiogenesis driven by ligation of CCL28 to CCR10 is linked to the extracellular signal regulated kinase (ERK) cascade, as CCR10-knockdown cells exhibit dysfunctional CCL28-induced ERK signalling, chemotaxis and capillary formation.

conclusionsThe overexpression of CCL28 and CCR10 in RA ST and their contribution to EPC migration into RA joints support the CCL28/CCR10 cascade as a potential therapeutic target for RA.

Indexed as

AdultAgedArthritis, RheumatoidCells, CulturedChemokines, CCChemotaxisEndothelial CellsEndothelium, VascularFemaleGene Expression RegulationGene SilencingHumansJointsMacrophagesMaleMAP Kinase Signaling SystemCCL28 protein, humanCCR10 protein, humanChemokines, CCReceptors, CCR10RNA, MessengerChemokinesInflammationRheumatoid ArthritisSynovial fluidTNF-alpha

Identifiers

PMID24833787
PMCPMC4282625
OpenAlexW2159929729

What OpenQuestion holds

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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.