Evidence map›Paper›PMID 22028336›Full record

ArticleCardiovascular research2012

Tie2-dependent knockout of HIF-1 impairs burn wound vascularization and homing of bone marrow-derived angiogenic cells.

Kakali Sarkar, Sergio Rey, Xianjie Zhang, Raul Sebastian, Guy P Marti, Karen Fox-Talbot, Amanda V Cardona, Junkai Du, Yee Sun Tan, Lixin Liu and 4 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Cardiovascular research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Genome ofInternational journal of molecular sciences · 2022
    Article
  2. Article
  3. The Dynamics of the Skin's Immune System.International journal of molecular sciences · 2019
    Review
  4. Article
  5. Article
  6. Review
  7. Molecular mechanisms of ischemic preconditioning in the kidney.American journal of physiology. Renal physiology · 2015
    Review
  8. Kidney injury is independent of endothelial HIF-1α.Journal of molecular medicine (Berlin, Germany) · 2015
    Article
  9. microRNA and Wound Healing.Advances in experimental medicine and biology · 2015
    Article
  10. Article
  11. Hypoxic signaling during tissue repair and regenerative medicine.International journal of molecular sciences · 2014
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Endometriosis, a disease of the macrophage.Frontiers in immunology · 2013
    Article
  17. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 2 institutions in 2 countries.

Kakali SarkarVascular Program, Institute for Cell Engineering, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Sergio Rey
Xianjie Zhang
Raul Sebastian
Guy P Marti
Karen Fox-Talbot
Amanda V Cardona
Junkai Du
Yee Sun Tan
Lixin Liu
Frank Lay
Frank J Gonzalez
John W Harmon
Gregg L Semenza
Johns Hopkins University · USNational Institutes of Health · US

Funding

Xenobiotic ReceptorsZIABC005708 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GONZALEZ, FRANK J · 2009 to 2025
$16.4M
HIF-1-Regulated Endothelial Progenitor Cell Recruitment in Burn Wound HealingP20GM078494 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI SEMENZA, GREGG L · 2006 to 2010
$3.3M
NIGMS NIH HHS P20-GM078494
6 · The paper itself

Abstract

aimsHypoxia-inducible factor 1 (HIF-1) is a heterodimer composed of HIF-1α and HIF-1β subunits. HIF-1 is known to promote tissue vascularization by activating the transcription of genes encoding angiogenic factors, which bind to receptors on endothelial cells (ECs) and bone marrow-derived angiogenic cells (BMDACs). In this study, we analysed whether HIF-1 activity in the responding ECs and BMDACs is also required for cutaneous vascularization during burn wound healing. METHODS AND

resultsWe generated mice with floxed alleles at the Hif1a or Arnt locus encoding HIF-1α and HIF-1β, respectively. Expression of Cre recombinase was driven by the Tie2 gene promoter, which is expressed in ECs and bone marrow cells. Tie2Cre(+) and Tie2Cre(-) mice were subjected to burn wounds of reproducible diameter and depth. Deficiency of HIF-1α or HIF-1β in Tie2-lineage cells resulted in delayed wound closure, reduced vascularization, decreased cutaneous blood flow, impaired BMDAC mobilization, and decreased BMDAC homing to burn wounds.

conclusionHIF-1 activity in Tie2-lineage cells is required for the mobilization and homing of BMDACs to cutaneous burn wounds and for the vascularization of burn wound tissue.

Indexed as

AnimalsAryl Hydrocarbon Receptor Nuclear TranslocatorBase SequenceBone Marrow CellsBurnsCell MovementDNA PrimersGene Knockout TechniquesHypoxia-Inducible Factor 1, alpha SubunitMaleMiceMice, KnockoutNeovascularization, PhysiologicReceptor Protein-Tyrosine KinasesReceptor, TIE-2SkinArnt protein, mouseAryl Hydrocarbon Receptor Nuclear TranslocatorDNA PrimersHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitReceptor Protein-Tyrosine KinasesReceptor, TIE-2Tek protein, mouse

Identifiers

PMID22028336
PMCPMC3243042
OpenAlexW2066562452

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.