Evidence map›Paper›PMID 34071440›Full record

ArticleBiomolecules2021

Disulfide and Fully Reduced HMGB1 Induce Different Macrophage Polarization and Migration Patterns.

Henna Salo, Heshuang Qu, Dimitra Mitsiou, Hannah Aucott, Jinming Han, Xing-Mei Zhang, Cecilia Aulin, Helena Erlandsson Harris

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Pathophysiology of Status Epilepticus Revisited.International journal of molecular sciences · 2025
    Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. 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

8 authors at 1 institution in 1 country.

Henna SaloDepartment of Medicine, Solna, Rheumatology Unit, Centre for Molecular Medicine, Karolinska Institutet, 17176 Stockholm, Sweden.
Heshuang QuDepartment of Medicine, Solna, Rheumatology Unit, Centre for Molecular Medicine, Karolinska Institutet, 17176 Stockholm, Sweden.ORCID 0000-0001-6011-5588
Dimitra MitsiouDepartment of Medicine, Solna, Rheumatology Unit, Centre for Molecular Medicine, Karolinska Institutet, 17176 Stockholm, Sweden.
Hannah AucottDepartment of Medicine, Solna, Rheumatology Unit, Centre for Molecular Medicine, Karolinska Institutet, 17176 Stockholm, Sweden.
Jinming HanDepartment of Clinical Neuroscience, Centre for Molecular Medicine, Karolinska Institutet, 17176 Stockholm, Sweden.ORCID 0000-0002-6084-3275
Xing-Mei ZhangDepartment of Clinical Neuroscience, Centre for Molecular Medicine, Karolinska Institutet, 17176 Stockholm, Sweden.
Cecilia AulinDepartment of Medicine, Solna, Rheumatology Unit, Centre for Molecular Medicine, Karolinska Institutet, 17176 Stockholm, Sweden.
Helena Erlandsson HarrisDepartment of Medicine, Solna, Rheumatology Unit, Centre for Molecular Medicine, Karolinska Institutet, 17176 Stockholm, Sweden.
Karolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophage plasticity enables cells to obtain different functions over a broad proinflammatory and repairing spectrum. In different conditions, macrophages can be induced by high-mobility group box 1 (HMGB1), a nuclear DNA-binding protein that activates innate immunity, to polarize towards a pro- (M1) or anti-inflammatory (M2) phenotype. In this study, we investigated the phenotypes of murine bone-marrow-derived macrophages (BMDMs) induced by different HMGB1 redox isoforms in depth. Our results demonstrate that disulfide HMGB1 (dsHMGB1) induces a unique macrophage phenotype that secretes pro-inflammatory cytokines, rather than inducing metabolic changes leading to nitric oxide production. Fully reduced HMGB1 (frHMGB1) did not induce macrophage polarization. The migrating function of BMDMs was measured by scratch assay after the stimulation with dsHMGB1 and frHMGB1. Both dsHMGB1 and frHMGB1 induced cell migration. We found that dsHMGB1 mediates cytokine secretion and cellular motility, mainly through toll-like receptor 4 (TLR4). Importantly, our data shows that dsHMGB1 and frHMGB1 induce distinct BMDM polarization phenotypes, and that dsHMGB1 induces a unique phenotype differing from the classical proinflammatory macrophage phenotype.

Indexed as

HMGB1 ProteinAnimalsCell MovementDisulfidesFemaleMacrophagesMiceOxidation-ReductionToll-Like Receptor 4DisulfidesHMGB1 ProteinHMGB1 protein, mouseTlr4 protein, mouseToll-Like Receptor 4dsHMGB1frHMGB1HMGB1inflammationmacrophagesmigrationpolarizationRAGETLR4

Identifiers

PMID34071440
PMCPMC8229957
OpenAlexW3165320590

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.