Evidence map›Paper›PMID 24990649›Full record

ArticleAmerican journal of physiology. Cell physiology2014

Reduction of ARNT in myeloid cells causes immune suppression and delayed wound healing.

Christopher Scott, James Bonner, Danqing Min, Philip Boughton, Rebecca Stokes, Kuan Minn Cha, Stacey N Walters, Kendle Maslowski, Frederic Sierro, Shane T Grey and 3 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Cell physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. AhR promotes phosphorylation of ARNT isoform 1 in human T cell malignancies as a switch for optimal AhR activity.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  3. Article
  4. Hypoxia-inducible factors and diabetes.The Journal of clinical investigation · 2020
    Review
  5. Review
  6. Infection and immunity · 2019
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. 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

13 authors at 5 institutions in 2 countries.

Christopher ScottDiabetes and Transcription Factors Group, Department of Immunology and Inflammation, Garvan Institute of Medical Research, Sydney, New South Wales, Australia; Faculty of Medicine, University of Sydney, Sydney, New South Wales, Australia;
James BonnerDepartment of Endocrinology, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia;
Danqing MinDepartment of Endocrinology, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia;
Philip BoughtonSt. George Clinical School, St. George Hospital, Kogarah, New South Wales, Australia; Department of Biomedical Engineering, University of Sydney, Sydney, New South Wales, Australia;
Rebecca StokesDiabetes and Transcription Factors Group, Department of Immunology and Inflammation, Garvan Institute of Medical Research, Sydney, New South Wales, Australia;
Kuan Minn ChaDiabetes and Transcription Factors Group, Department of Immunology and Inflammation, Garvan Institute of Medical Research, Sydney, New South Wales, Australia;
Stacey N WaltersDepartment of Immunology and Inflammation, Garvan Institute of Medical Research, Sydney, New South Wales, Australia;
Kendle MaslowskiDepartment of Biochemistry, University of Lausanne, Lausanne, Switzerland;
Frederic SierroLiver Immunology, Centenary Institute, Sydney, New South Wales, Australia;
Shane T GreyDepartment of Immunology and Inflammation, Garvan Institute of Medical Research, Sydney, New South Wales, Australia;
Stephen TwiggFaculty of Medicine, University of Sydney, Sydney, New South Wales, Australia; Department of Endocrinology, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia;
Susan McLennanFaculty of Medicine, University of Sydney, Sydney, New South Wales, Australia; Department of Endocrinology, Royal Prince Alfred Hospital, Sydney, New South Wales, Australia;
Jenny E GuntonDiabetes and Transcription Factors Group, Department of Immunology and Inflammation, Garvan Institute of Medical Research, Sydney, New South Wales, Australia; Faculty of Medicine, University of Sydney, Sydney, New South Wales, Australia; St. Vincent's Clinical School, University of New South Wales, Sydney, New South Wales, Australia; and Department of Diabetes and Endocrinology, Westmead Hospital, Sydney, New South Wales, Australia jenny.gunton@sydney.edu.au j.gunton@garvan.org.au.
Garvan Institute of Medical Research · AURoyal Prince Alfred Hospital · AUThe University of Sydney · AUCentenary Institute · AUUniversity of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aryl hydrocarbon receptor nuclear translocator (ARNT) is a transcription factor that binds to partners to mediate responses to environmental signals. To investigate its role in the innate immune system, floxed ARNT mice were bred with lysozyme M-Cre recombinase animals to generate lysozyme M-ARNT (LAR) mice with reduced ARNT expression. Myeloid cells of LAR mice had altered mRNA expression and delayed wound healing. Interestingly, when the animals were rendered diabetic, the difference in wound healing between the LAR mice and their littermate controls was no longer present, suggesting that decreased myeloid cell ARNT function may be an important factor in impaired wound healing in diabetes. Deferoxamine (DFO) improves wound healing by increasing hypoxia-inducible factors, which require ARNT for function. DFO was not effective in wounds of LAR mice, again suggesting that myeloid cells are important for normal wound healing and for the full benefit of DFO. These findings suggest that myeloid ARNT is important for immune function and wound healing. Increasing ARNT and, more specifically, myeloid ARNT may be a therapeutic strategy to improve wound healing.

Indexed as

Immunity, InnateImmunocompromised HostTransplantation ToleranceWound HealingAgedAnimalsAryl Hydrocarbon Receptor Nuclear TranslocatorCase-Control StudiesCells, CulturedCytokinesDeferoxamineDermatitisDiabetes ComplicationsDiabetes Mellitus, ExperimentalFemaleGene Expression RegulationARNT protein, humanArnt protein, mouseAryl Hydrocarbon Receptor Nuclear TranslocatorCre recombinaseCytokinesDeferoxamineInflammation MediatorsIntegrasesMuramidaseRNA, Messengeraryl hydrocarbon receptor nuclear translocatordeferoxaminehypoxia-inducible factor-1α

Identifiers

PMID24990649
PMCPMC4137137
OpenAlexW1981252432

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.