Evidence map›Paper›PMID 24747529›Full record

ArticlePloS one2014

C/EBPδ deficiency sensitizes mice to ionizing radiation-induced hematopoietic and intestinal injury.

Snehalata A Pawar, Lijian Shao, Jianhui Chang, Wenze Wang, Rupak Pathak, Xiaoyan Zhu, Junru Wang, Howard Hendrickson, Marjan Boerma, Esta Sterneck and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

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  9. Methionine dietary supplementation potentiates ionizing radiation-induced gastrointestinal syndrome.American journal of physiology. Gastrointestinal and liver physiology · 2020
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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

12 authors at 3 institutions in 1 country.

Snehalata A PawarDivision of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America.
Lijian ShaoDivision of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America.
Jianhui ChangDivision of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America.
Wenze WangDivision of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America.
Rupak PathakDivision of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America.
Xiaoyan ZhuDivision of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America.
Junru WangDivision of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America.
Howard HendricksonDepartment of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America.
Marjan BoermaDivision of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America.
Esta SterneckCenter for Cancer Research, National Cancer Institute, Frederick, Maryland, United States of America.
Daohong ZhouDivision of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America.
Martin Hauer-JensenDivision of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America; Surgical Service, Central Arkansas Veterans Healthcare System, Little Rock, Arkansas, United States of America.
University of Arkansas for Medical Sciences · USCentral Arkansas Veterans Healthcare System · USNational Cancer Institute · US

Funding

Understanding Hesitant AdoptersP20GM103429 · NIGMS · UNIV OF ARKANSAS FOR MED SCIS · PI Lawrence E Cornett, JERRY WARE · 2012 to 2026
$60.9M
VIRULENCE MECHANISMS IN ESCHERICHIA COLIP20RR016460 · NCRR · UNIV OF ARKANSAS FOR MED SCIS · PI HENSLEY, LORI · 2001 to 2011
$33.1M
Molecular Mechanisms Regulating Mouse Mammary Gland and Human Breast Tumor CellsZIABC010307 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI STERNECK, GISELA · 2009 to 2025
$22.1M
Study of the Cell-specific Inflammasome Responses During Defense Against Gram-negative BacteriaP20GM103625 · NIGMS · UNIV OF ARKANSAS FOR MED SCIS · PI SMELTZER, MARK S · 2012 to 2021
$21.5M
Intramural NIH HHSNCRR NIH HHS P20 RR016460NIGMS NIH HHS 1P20GM103625NIGMS NIH HHS P20 GM103429NIGMS NIH HHS P20 GM103625
6 · The paper itself

Abstract

Knowledge of the mechanisms involved in the radiation response is critical for developing interventions to mitigate radiation-induced injury to normal tissues. Exposure to radiation leads to increased oxidative stress, DNA-damage, genomic instability and inflammation. The transcription factor CCAAT/enhancer binding protein delta (Cebpd; C/EBPδ is implicated in regulation of these same processes, but its role in radiation response is not known. We investigated the role of C/EBPδ in radiation-induced hematopoietic and intestinal injury using a Cebpd knockout mouse model. Cebpd-/- mice showed increased lethality at 7.4 and 8.5 Gy total-body irradiation (TBI), compared to Cebpd+/+ mice. Two weeks after a 6 Gy dose of TBI, Cebpd-/- mice showed decreased recovery of white blood cells, neutrophils, platelets, myeloid cells and bone marrow mononuclear cells, decreased colony-forming ability of bone marrow progenitor cells, and increased apoptosis of hematopoietic progenitor and stem cells compared to Cebpd+/+ controls. Cebpd-/- mice exhibited a significant dose-dependent decrease in intestinal crypt survival and in plasma citrulline levels compared to Cebpd+/+ mice after exposure to radiation. This was accompanied by significantly decreased expression of γ-H2AX in Cebpd-/- intestinal crypts and villi at 1 h post-TBI, increased mitotic index at 24 h post-TBI, and increase in apoptosis in intestinal crypts and stromal cells of Cebpd-/- compared to Cebpd+/+ mice at 4 h post-irradiation. This study uncovers a novel biological function for C/EBPδ in promoting the response to radiation-induced DNA-damage and in protecting hematopoietic and intestinal tissues from radiation-induced injury.

Indexed as

Radiation ToleranceAnimalsApoptosisBlood CellsBone Marrow CellsCCAAT-Enhancer-Binding Protein-deltaCitrullineDNA DamageGene Expression RegulationHematopoietic Stem CellsHistonesIntestinesLeukocytes, MononuclearMiceMitosisMyeloid CellsCCAAT-Enhancer-Binding Protein-deltaCitrullinegamma-H2AX protein, mouseHistones

Identifiers

PMID24747529
PMCPMC3991713
OpenAlexW2016840431

What OpenQuestion holds

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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.