Evidence map›Paper›PMID 8642348›Full record

ArticleThe Journal of experimental medicine1996

Hyaluronan fragments activate an NF-kappa B/I-kappa B alpha autoregulatory loop in murine macrophages.

P W Noble, C M McKee, M Cowman, H S Shin

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed, 1 pooled it
4.7field-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

97 citing papers in PubMed, 1 synthesis or guideline pooled it, 326 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Prostaglandin EBiology · 2023
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Glycocalyx Impairment in Vascular Disease: Focus on Inflammation.Frontiers in cell and developmental biology · 2021
    Review
  13. Amphiregulin contributes to airway remodeling in chronic allograft dysfunction after lung transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2020
    Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. The CD44-HA axis and inflammation in atherosclerosis: A temporal perspective.Matrix biology : journal of the International Society for Matrix Biology · 2019
    Review

37 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

P W NobleDepartment of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
C M McKee
M Cowman
H S Shin
Johns Hopkins University · US

Funding

REGULATION OF MACROPHAGE PHENOTYPES IN LUNG REPAIRK11HL002880 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI NOBLE, PAUL WESLEY · 1992 to 1996
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PLATELET-MEDIATED CYTOTOXICITY:MECHANISMS &APPLICATIONSR01CA014113 · NCI · JOHNS HOPKINS UNIVERSITY · PI SHIN, HYUN S · 1985 to 1998
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NCI NIH HHS 5RO1CA1411320NHLBI NIH HHS K11HL02880
6 · The paper itself

Abstract

Macrophages play an important role in the acute tissue inflammatory response through the release of cytokines and growth factors in response to stimuli such as lipopolysaccharide (LPS). Macrophage inflammatory effector functions are also influenced by interactions with the extracellular matrix (ECM). Such macrophage-ECM interactions may be important in regulating chronic inflammatory responses. Recent evidence has suggested that hyaluronan (HA), a glycosaminoglycan (GAG) component of ECM can induce inflammatory gene expression in murine macrophages. HA exists in its native form as a large polymer, but is found as smaller fragments under inflammatory conditions. The NF-kappa B/I-kappa B transcriptional regulatory system has been shown to be a critical component of the host inflammatory response. We examined the effects of high molecular weight HA and lower molecular weight HA fragments on NF-kappa B activation in mouse macrophages. Only the smaller HA fragments were found to activate NF-kappa B DNA binding activity. After HA stimulation, I-kappa B alpha mRNA was induced and I-kappa B alpha protein levels, which initially decreased, were restored. The induction of I-kappa Balpha expression was not observed for other GAGs. The time course of I-kappa B alpha protein regeneration in response to HA fragments was consistent with an autoregulatory mechanism. In support of this mechanism, in vitro translated murine I-kappa B alpha inhibited HA fragment-induced NF-kappa B DNA binding activity. The NF-kappa B DNA binding complex in HA-stimulated extracts was found to contain p50 and p65 subunits. Activation of the NF-kappa B/I-kappa B system in macrophages by ECM fragments may be an important mechanism for propagating the tissue inflammatory response.

Indexed as

I-kappa B ProteinsAnimalsBase SequenceConsensus SequenceCycloheximideDNA-Binding ProteinsDNA, ComplementaryHomeostasisHumansHyaluronic AcidImmunoglobulin kappa-ChainsKineticsLipopolysaccharidesMacrophagesMiceMolecular Sequence DataCycloheximideDNA-Binding ProteinsDNA, ComplementaryHyaluronic AcidI-kappa B ProteinsImmunoglobulin kappa-ChainsLipopolysaccharidesNF-kappa BNF-KappaB Inhibitor alphaNFKBIA protein, humanNfkbia protein, mouseOligopeptidesRecombinant Proteins

Identifiers

PMID8642348
PMCPMC2192553
OpenAlexW2010427736

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.