Evidence map›Paper›PMID 24003215›Full record

ArticleThe Journal of biological chemistry2013

Gremlin-1 is an inhibitor of macrophage migration inhibitory factor and attenuates atherosclerotic plaque growth in ApoE-/- Mice.

Iris Müller, Tanja Schönberger, Martina Schneider, Oliver Borst, Melanie Ziegler, Peter Seizer, Christoph Leder, Karin Müller, Michael Lang, Florian Appenzeller and 13 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

  1. Pooled it
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  15. Gremlin: a complex molecule regulating wound healing and fibrosis.Cellular and molecular life sciences : CMLS · 2021
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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

23 authors at 4 institutions in 2 countries.

Iris MüllerFrom the Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard Karls Universität, 72076 Tübingen, Germany.
Tanja Schönberger
Martina Schneider
Oliver Borst
Melanie Ziegler
Peter Seizer
Christoph Leder
Karin Müller
Michael Lang
Florian Appenzeller
Oleg Lunov
Berthold Büchele
Manuela Fahrleitner
Marcus Olbrich
Harald Langer
Tobias Geisler
Florian Lang
Madhumita Chatterjee
Jan Freark de Boer
Uwe J F Tietge
Jürgen Bernhagen
Thomas Simmet
Meinrad Gawaz
University of Tübingen · DEUniversität Ulm · DEUniversity Medical Center Groningen · NLRWTH Aachen University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Monocyte infiltration and macrophage formation are pivotal steps in atherosclerosis and plaque vulnerability. Gremlin-1/Drm is crucial in embryo-/organogenesis and has been shown to be expressed in the adult organism at sites of arterial injury and to inhibit monocyte migration. The purpose of the present study was to evaluate and characterize the role of Gremlin-1 in atherosclerosis. Here we report that Gremlin-1 is highly expressed primarily by monocytes/macrophages in aortic atherosclerotic lesions of ApoE(-/-) mice and is secreted from activated monocytes and during macrophage development in vitro. Gremlin-1 reduces macrophage formation by inhibiting macrophage migration inhibitory factor (MIF), a cytokine critically involved in atherosclerotic plaque progression and vulnerability. Gremlin-1 binds with high affinity to MIF (KD = 54 nm), as evidenced by surface plasmon resonance analysis and co-immunoprecipitation, and reduces MIF-induced release of TNF-α from macrophages. Treatment of ApoE(-/-) mice with a dimeric recombinant fusion protein, mGremlin1-Fc, but not with equimolar control Fc or inactivated mGremlin1-Fc, reduced TNF-α expression, the content of monocytes/macrophages of atherosclerotic lesions, and attenuated atheroprogression. The present data disclose that Gremlin-1 is an endogenous antagonist of MIF and define a role for Gremlin-1/MIF interaction in atherosclerosis.

Indexed as

Apolipoproteins EGene Expression RegulationAnimalsCHO CellsCricetinaeCricetulusCytokinesHumansIntercellular Signaling Peptides and ProteinsIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMacrophagesMiceMice, KnockoutPlaque, AtheroscleroticRecombinant Fusion ProteinsApolipoproteins ECytokinesGREM1 protein, humanGrem1 protein, mouseIntercellular Signaling Peptides and ProteinsIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMIF protein, humanMif protein, mouseRecombinant Fusion ProteinsTumor Necrosis Factor-alphaAtherosclerosisChemokinesInflammationMonocytesVascular Biology

Identifiers

PMID24003215
PMCPMC3814759
OpenAlexW2137586290

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.