Evidence map›Paper›PMID 23633118›Full record

ArticleArthritis and rheumatism2013

Evidence that CXCL16 is a potent mediator of angiogenesis and is involved in endothelial progenitor cell chemotaxis : studies in mice with K/BxN serum-induced arthritis.

Takeo Isozaki, Ali S Arbab, Christian S Haas, M Asif Amin, Monica D Arendt, Alisa E Koch, Jeffrey H Ruth

Open access · bronzeAbstract read
In one paragraph

Article in Arthritis and rheumatism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

46 citing papers in PubMed, 80 citations in OpenAlex.

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  12. IL-34 and protein-tyrosine phosphatase receptor type-zeta-dependent mechanisms limit arthritis in mice.Laboratory investigation; a journal of technical methods and pathology · 2022
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  19. The Role of CXCL16 in the Pathogenesis of Cancer and Other Diseases.International journal of molecular sciences · 2021
    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

7 authors at 2 institutions in 1 country.

Takeo IsozakiUniversity of Michigan Medical School, Ann Arbor, MI, USA.
Ali S Arbab
Christian S Haas
M Asif Amin
Monica D Arendt
Alisa E Koch
Jeffrey H Ruth
University of Michigan–Ann Arbor · USHenry Ford Hospital · US

Funding

Vector CoreP30AR048310 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FOX, DAVID ALAN · 2001 to 2010
$5.9M
Understanding Mechanisms of Resistance to Anti-angiogenic TreatmentsR01CA160216 · NCI · HENRY FORD HEALTH SYSTEM · PI ARBAB, ALI SYED · 2012 to 2016
$1.8M
IL-18 in rheumatoid inflammation and angiogenesisR01AR048267 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KOCH, ALISA E · 2003 to 2007
$1.4M
IL 4 AND IL 13 GENE THERAPY FOR ARTHRITISR01AI040987 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KOCH, ALISA E · 1998 to 2006
$1.3M
Cellular MRI in Glioma and Radiation NecrosisR01CA122031 · NCI · HENRY FORD HEALTH SYSTEM · PI ARBAB, ALI SYED · 2007 to 2010
$992k
In vivo detection of involvement of endogenous BM progenitor cells in gliomaR01CA172048 · NCI · HENRY FORD HEALTH SYSTEM · PI ARBAB, ALI SYED · 2012 to 2014
$894k
NOVEL ANGIOGENIC CYTOKINE INDUCED ENDOTHELIAL ANTIGENR01HL058695 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KOCH, ALISA E · 1999 to 2002
$640k
IL 4 AND IL 13 GENE THERAPY FOR ARTHRITISR21AI040987 · NIAID · NORTHWESTERN UNIVERSITY · PI KOCH, ALISA E · 1997 to 1997
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NCI NIH HHS R01 CA122031NCI NIH HHS R01-CA-122031NCI NIH HHS R01 CA160216NCI NIH HHS R01 CA172048NHLBI NIH HHS HL-58694NHLBI NIH HHS R01 HL058695NIAID NIH HHS AI-40987NIAID NIH HHS R01 AI040987NIAMS NIH HHS AR-48267NIAMS NIH HHS P30 AR048310NIAMS NIH HHS P30-AR-048310NIAMS NIH HHS R01 AR048267
6 · The paper itself

Abstract

objectiveTo examine the possibility that CXCL16 recruits endothelial cells (ECs) to developing neovasculature in rheumatoid arthritis (RA) synovium.

methodsWe utilized the RA synovial tissue SCID mouse chimera system to examine human microvascular EC (HMVEC) and human endothelial progenitor cell (EPC) recruitment into engrafted human synovium that was injected intragraft with CXCL16-immunodepleted RA synovial fluid (SF). CXCR6-deficient and wild-type (WT) C57BL/6 mice were primed to develop K/BxN serum-induced arthritis and evaluated for angiogenesis. HMVECs and EPCs from human cord blood were also examined for CXCR6 expression, by immunofluorescence and assessment of CXCL16 signaling activity.

resultsCXCR6 was prominently expressed on human EPCs and HMVECs, and its expression on HMVECs could be up-regulated by interleukin-1β. SCID mice injected with CXCL16-depleted RA SF exhibited a significant reduction in EPC recruitment. In experiments using the K/BxN serum-induced inflammatory arthritis model, CXCR6(-/-) mice showed profound reductions in hemoglobin levels, which correlated with reductions in monocyte and T cell recruitment to arthritic joint tissue compared to that observed in WT mice. Additionally, HMVECs and EPCs responded to CXCL16 stimulation, but exhibited unique signal transduction pathways and homing properties.

conclusionThese results indicate that CXCL16 and its receptor CXCR6 may be a central ligand/receptor pair that is closely associated with EPC recruitment and blood vessel formation in the RA joint.

Indexed as

AnimalsArthritis, ExperimentalArthritis, RheumatoidChemokine CXCL16Chemokine CXCL6Chemokines, CXCChemotaxisEndothelial CellsHumansInterleukin-1betaMiceMice, Inbred C57BLMice, SCIDMice, TransgenicNeovascularization, PathologicReceptors, ChemokineChemokine CXCL16Chemokine CXCL6Chemokines, CXCCXCL16 protein, humanCxcl16 protein, mouseCXCR6 protein, humanCxcr6 protein, mouseInterleukin-1betaReceptors, ChemokineReceptors, CXCRReceptors, CXCR6Receptors, ScavengerReceptors, Virus

Identifiers

PMID23633118
PMCPMC3701743
OpenAlexW1953734276

What OpenQuestion holds

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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.