Evidence map›Paper›PMID 25682599›Full record

ArticleHaematologica2015

Heme oxygenase-1 deficiency alters erythroblastic island formation, steady-state erythropoiesis and red blood cell lifespan in mice.

Stuart T Fraser, Robyn G Midwinter, Lucy A Coupland, Stephanie Kong, Birgit S Berger, Jia Hao Yeo, Osvaldo Cooley Andrade, Deborah Cromer, Cacang Suarna, Magda Lam and 4 more

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

Article in Haematologica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Altered Expression of Heme Oxygenase 2 in Heme Oxygenase 1-deficient Mouse Embryos.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2023
    Article
  6. Review
  7. The amino acid sensor GCN2 controls red blood cell clearance and iron metabolism through regulation of liver macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Frontiers in immunology · 2017
    Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 1 country.

Stuart T FraserLaboratory for Blood Cell Development, School of Medical Sciences (Physiology, Anatomy & Histology), Sydney Medical School, The University of Sydney, Australia.
Robyn G MidwinterCentre for Vascular Research, School of Medical Sciences (Pathology) and Bosch Institute, The University of Sydney, Australia.
Lucy A CouplandThe John Curtin School of Medical Research, The Australian National University, Canberra, Australia.
Stephanie KongVascular Biology Division, Victor Chang Cardiac Research Institute, Darlinghurst, Australia.
Birgit S BergerCentre for Vascular Research, School of Medical Sciences (Pathology) and Bosch Institute, The University of Sydney, Australia.
Jia Hao YeoLaboratory for Blood Cell Development, School of Medical Sciences (Physiology, Anatomy & Histology), Sydney Medical School, The University of Sydney, Australia.
Osvaldo Cooley AndradeLaboratory for Blood Cell Development, School of Medical Sciences (Physiology, Anatomy & Histology), Sydney Medical School, The University of Sydney, Australia.
Deborah CromerComplex Systems in Biology Group, Centre for Vascular Research, University of New South Wales, Kensington, Australia.
Cacang SuarnaCentre for Vascular Research, School of Medical Sciences (Pathology) and Bosch Institute, The University of Sydney, Australia Vascular Biology Division, Victor Chang Cardiac Research Institute, Darlinghurst, Australia.
Magda LamCentre for Vascular Research, School of Medical Sciences (Pathology) and Bosch Institute, The University of Sydney, Australia Vascular Biology Division, Victor Chang Cardiac Research Institute, Darlinghurst, Australia.
Ghassan J MaghzalCentre for Vascular Research, School of Medical Sciences (Pathology) and Bosch Institute, The University of Sydney, Australia Vascular Biology Division, Victor Chang Cardiac Research Institute, Darlinghurst, Australia School of Medical Sciences, Faculty of Medicine, University of New South Wales, Kensington.
Beng H ChongDepartment of Medicine, St George Clinical School, University of New South Wales, Kogarah, Australia.
Christopher R ParishThe John Curtin School of Medical Research, The Australian National University, Canberra, Australia.
Roland StockerCentre for Vascular Research, School of Medical Sciences (Pathology) and Bosch Institute, The University of Sydney, Australia Vascular Biology Division, Victor Chang Cardiac Research Institute, Darlinghurst, Australia School of Medical Sciences, Faculty of Medicine, University of New South Wales, Kensington r.stocker@victorchang.edu.au.
University of Sydney · AUUNSW Sydney · AUVictor Chang Cardiac Research Institute · AUAustralian National University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heme oxygenase-1 is critical for iron recycling during red blood cell turnover, whereas its impact on steady-state erythropoiesis and red blood cell lifespan is not known. We show here that in 8- to 14-week old mice, heme oxygenase-1 deficiency adversely affects steady-state erythropoiesis in the bone marrow. This is manifested by a decrease in Ter-119(+)-erythroid cells, abnormal adhesion molecule expression on macrophages and erythroid cells, and a greatly diminished ability to form erythroblastic islands. Compared with wild-type animals, red blood cell size and hemoglobin content are decreased, while the number of circulating red blood cells is increased in heme oxygenase-1 deficient mice, overall leading to microcytic anemia. Heme oxygenase-1 deficiency increases oxidative stress in circulating red blood cells and greatly decreases the frequency of macrophages expressing the phosphatidylserine receptor Tim4 in bone marrow, spleen and liver. Heme oxygenase-1 deficiency increases spleen weight and Ter119(+)-erythroid cells in the spleen, although α4β1-integrin expression by these cells and splenic macrophages positive for vascular cell adhesion molecule 1 are both decreased. Red blood cell lifespan is prolonged in heme oxygenase-1 deficient mice compared with wild-type mice. Our findings suggest that while macrophages and relevant receptors required for red blood cell formation and removal are substantially depleted in heme oxygenase-1 deficient mice, the extent of anemia in these mice may be ameliorated by the prolonged lifespan of their oxidatively stressed erythrocytes.

Indexed as

Anemia, HemolyticGrowth DisordersIron Metabolism DisordersAnimalsBone Marrow CellsCell CommunicationCell DifferentiationCell SurvivalErythroblastsErythrocyte IndicesErythrocytesErythropoiesisHeme Oxygenase-1ImmunophenotypingLiverMacrophagesHeme Oxygenase-1

Identifiers

PMID25682599
PMCPMC4420209
OpenAlexW2162377251

What OpenQuestion holds

Textmetadata
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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.