Evidence map›Paper›PMID 25603016›Full record

ArticleStem cells and development2015

Catalase inhibits ionizing radiation-induced apoptosis in hematopoietic stem and progenitor cells.

Xia Xiao, Hongmei Luo, Kenneth N Vanek, Amanda C LaRue, Bradley A Schulte, Gavin Y Wang

Open access · greenAbstract read
In one paragraph

Article in Stem cells and development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

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  15. Oxidative stress induces senescence in breast cancer stem cells.Biochemical and biophysical research communications · 2019
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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

6 authors at 1 institution in 1 country.

Xia Xiao1Department of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, South Carolina.
Hongmei Luo1Department of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, South Carolina.
Kenneth N Vanek4Department of Radiation Oncology, Medical University of South Carolina, Charleston, South Carolina.
Amanda C LaRue1Department of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, South Carolina.
Bradley A Schulte1Department of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, South Carolina.
Gavin Y Wang1Department of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, South Carolina.
Medical University of South Carolina · US

Funding

Translational Science Laboratory Shared ResourceP30CA138313 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RAYMOND N. DUBOIS · 2009 to 2026
$42.7M
Targeting the ROS-p38 MAPK Pathway as a Novel Strategy for Stem Cell ExpansionR21HL106451 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI WANG, GAVIN YONG · 2011 to 2012
$404k
NCI NIH HHS P30 CA138313NHLBI NIH HHS HL106451NHLBI NIH HHS R21 HL106451
6 · The paper itself

Abstract

Hematologic toxicity is a major cause of mortality in radiation emergency scenarios and a primary side effect concern in patients undergoing chemo-radiotherapy. Therefore, there is a critical need for the development of novel and more effective approaches to manage this side effect. Catalase is a potent antioxidant enzyme that coverts hydrogen peroxide into hydrogen and water. In this study, we evaluated the efficacy of catalase as a protectant against ionizing radiation (IR)-induced toxicity in hematopoietic stem and progenitor cells (HSPCs). The results revealed that catalase treatment markedly inhibits IR-induced apoptosis in murine hematopoietic stem cells and hematopoietic progenitor cells. Subsequent colony-forming cell and cobble-stone area-forming cell assays showed that catalase-treated HSPCs can not only survive irradiation-induced apoptosis but also have higher clonogenic capacity, compared with vehicle-treated cells. Moreover, transplantation of catalase-treated irradiated HSPCs results in high levels of multi-lineage and long-term engraftments, whereas vehicle-treated irradiated HSPCs exhibit very limited hematopoiesis reconstituting capacity. Mechanistically, catalase treatment attenuates IR-induced DNA double-strand breaks and inhibits reactive oxygen species. Unexpectedly, we found that the radioprotective effect of catalase is associated with activation of the signal transducer and activator of transcription 3 (STAT3) signaling pathway and pharmacological inhibition of STAT3 abolishes the protective activity of catalase, suggesting that catalase may protect HSPCs against IR-induced toxicity via promoting STAT3 activation. Collectively, these results demonstrate a previously unrecognized mechanism by which catalase inhibits IR-induced DNA damage and apoptosis in HSPCs.

Indexed as

ApoptosisHematopoiesisAnimalsAntioxidantsCatalaseCells, CulturedDNA DamageHematopoietic Stem CellsMaleMiceMice, Inbred C57BLRadiation, IonizingSignal TransductionSTAT3 Transcription FactorAntioxidantsCatalaseStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID25603016
PMCPMC4440990
OpenAlexW2029844548

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.