Evidence map›Paper›PMID 18802113›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

Lipopolysaccharide-induced expression of matrix metalloproteinases in human monocytes is suppressed by IFN-gamma via superinduction of ATF-3 and suppression of AP-1.

Hao H Ho, Taras T Antoniv, Jong-Dae Ji, Lionel B Ivashkiv

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.6field-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

40 citing papers in PubMed, 79 citations in OpenAlex.

  1. Opsonization Improves Dual Proteomic Analysis ofJournal of proteome research · 2026
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  7. ABMC musculoskeletal disorders · 2022
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  19. Activating transcription factor-3 induction is involved in the anti-inflammatory action of berberine in RAW264.7 murine macrophages.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2016
    Article
  20. Article
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

4 authors at 2 institutions in 3 countries.

Hao H HoArthritis and Tissue Degeneration Program, Department of Medicine, Hospital for Special Surgery, New York University School of Medicine, New York, NY 10016, USA.
Taras T Antoniv
Jong-Dae Ji
Lionel B Ivashkiv
Hospital for Special Surgery · USNew York University · US

Funding

Inhibition of STAT3 and inflammatory cytokine productionR01AI044938 · NIAID · HOSPITAL FOR SPECIAL SURGERY · PI IVASHKIV, LIONEL B · 2000 to 2025
$9.2M
CYTOKINE REGULATION OF RA SYNOVIOCYTE PHENOTYPER01AR046713 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI IVASHKIV, LIONEL B · 1999 to 2025
$8.3M
NIAID NIH HHS R01 AI044938NIAMS NIH HHS R01 AR046713
6 · The paper itself

Abstract

Matrix metalloproteinases (MMPs) are induced during inflammatory responses and are important for immune regulation, angiogenesis, wound healing, and tissue remodeling. Expression of MMPs needs to be tightly controlled to avoid excessive tissue damage. In this study, we investigated the regulation of MMP expression by inflammatory factors in primary human monocytes and macrophages. IFN-gamma, which augments inflammatory cytokine production in response to macrophage-activating factors such as TLR ligands, instead broadly suppressed TLR-induced MMP expression. Inhibition of MMP expression was dependent on STAT1 and required de novo protein synthesis. IFN-gamma strongly enhanced TLR-induced expression of the transcriptional repressor activating transcription factor (ATF-3) in a STAT1-dependent manner, which correlated with recruitment of ATF-3 to the endogenous MMP-1 promoter as detected by chromatin immunoprecipitation assays. RNA interference experiments further supported a role for ATF-3 in suppression of MMP-1 expression. In addition, IFN-gamma suppressed DNA binding by AP-1 transcription factors that are known to promote MMP expression and a combination of supershift, RNA interference and overexpression experiments implicated AP-1 family member Fra-1 in the regulation of MMP-1 expression. These results define an IFN-gamma-mediated homeostatic loop that limits the potential for tissue damage associated with inflammation, and identify transcriptional factors that regulate MMP expression in myeloid cells in inflammatory settings.

Indexed as

Matrix Metalloproteinase InhibitorsActivating Transcription Factor 3Cell Line, TumorCells, CulturedDNA-Binding ProteinsDown-RegulationFeedback, PhysiologicalFos-Related Antigen 1Gene Expression RegulationHomeostasisHumansImmunity, InnateInflammation MediatorsInterferon-gammaLipopolysaccharidesMacrophagesActivating Transcription Factor 3ATF3 protein, humanDNA-Binding ProteinsFos-Related Antigen 1Inflammation MediatorsInterferon-gammaLipopolysaccharidesMatrix Metalloproteinase 1Matrix Metalloproteinase InhibitorsMMP1 protein, humanProto-Oncogene Proteins c-fosRepressor ProteinsTetradecanoylphorbol AcetateToll-Like ReceptorsTranscription Factor AP-1

Identifiers

PMID18802113
PMCPMC2610354
OpenAlexW1955758659

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.