Evidence map›Paper›PMID 24206054›Full record

ArticleAntioxidants & redox signaling2014

Heme oxygenase-1 is required for angiogenic function of bone marrow-derived progenitor cells: role in therapeutic revascularization.

Anna Grochot-Przeczek, Jerzy Kotlinowski, Magdalena Kozakowska, Katarzyna Starowicz, Jolanta Jagodzinska, Anna Stachurska, Oscar L Volger, Karolina Bukowska-Strakova, Urszula Florczyk, Magdalena Tertil and 7 more

Open access · hybridAbstract read
In one paragraph

Article in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 2 pooled it
2.8field-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

34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 55 citations in OpenAlex.

  1. Pooled it
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  14. The Protective Role of Heme Oxygenase-1 in Atherosclerotic Diseases.International journal of molecular sciences · 2019
    Review
  15. Targeting angiogenesis in Duchenne muscular dystrophy.Cellular and molecular life sciences : CMLS · 2019
    Review
  16. Article
  17. Article
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  19. A review on heme oxygenase-1 induction: is it a necessary evil.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018
    Review
  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

17 authors at 2 institutions in 3 countries.

Anna Grochot-Przeczek1 Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University , Krakow, Poland .
Jerzy Kotlinowski
Magdalena Kozakowska
Katarzyna Starowicz
Jolanta Jagodzinska
Anna Stachurska
Oscar L Volger
Karolina Bukowska-Strakova
Urszula Florczyk
Magdalena Tertil
Agnieszka Jazwa
Krzysztof Szade
Jacek Stepniewski
Agnieszka Loboda
Anton J G Horrevoets
Jozef Dulak
Alicja Jozkowicz
Jagiellonian University · PLUniversity Medical Center · US

Funding

Wellcome Trust
6 · The paper itself

Abstract

aimsHeme oxygenase-1 (HO-1) is a cytoprotective enzyme that can be down-regulated in diabetes. Its importance for mature endothelium has been described, but its role in proangiogenic progenitors is not well known. We investigated the effect of HO-1 on the angiogenic potential of bone marrow-derived cells (BMDCs) and on blood flow recovery in ischemic muscle of diabetic mice.

resultsLack of HO-1 decreased the number of endothelial progenitor cells (Lin(-)CD45(-)cKit(-)Sca-1(+)VEGFR-2(+)) in murine bone marrow, and inhibited the angiogenic potential of cultured BMDCs, affecting their survival under oxidative stress, proliferation, migration, formation of capillaries, and paracrine proangiogenic potential. Transcriptome analysis of HO-1(-/-) BMDCs revealed the attenuated up-regulation of proangiogenic genes in response to hypoxia. Heterozygous HO-1(+/-) diabetic mice subjected to hind limb ischemia exhibited reduced local expression of vascular endothelial growth factor (VEGF), placental growth factor (PlGF), stromal cell-derived factor 1 (SDF-1), VEGFR-1, VEGFR-2, and CXCR-4. This was accompanied by impaired revascularization of ischemic muscle, despite a strong mobilization of bone marrow-derived proangiogenic progenitors (Sca-1(+)CXCR-4(+)) into peripheral blood. Blood flow recovery could be rescued by local injections of conditioned media harvested from BMDCs, but not by an injection of cultured BMDCs. INNOVATION: This is the first report showing that HO-1 haploinsufficiency impairs tissue revascularization in diabetes and that proangiogenic in situ response, not progenitor cell mobilization, is important for blood flow recovery.

conclusionsHO-1 is necessary for a proper proangiogenic function of BMDCs. A low level of HO-1 in hyperglycemic mice decreases restoration of perfusion in ischemic muscle, which can be rescued by a local injection of conditioned media from cultured BMDCs.

Indexed as

Neovascularization, PhysiologicAnimalsApoptosisBone Marrow CellsCell MovementCell ProliferationCells, CulturedFemaleHaploinsufficiencyHeme Oxygenase-1HindlimbHyperglycemiaIschemiaMaleMembrane ProteinsMiceHeme Oxygenase-1Hmox1 protein, mouseMembrane Proteins

Identifiers

PMID24206054
PMCPMC3961799
OpenAlexW2009378013

What OpenQuestion holds

Textmetadata
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Registered trials

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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.