Evidence map›Paper›PMID 26042591›Full record

ArticlePloS one2015

Consequences of low dose ionizing radiation exposure on the hippocampal microenvironment.

Munjal M Acharya, Neal H Patel, Brianna M Craver, Katherine K Tran, Erich Giedzinski, Bertrand P Tseng, Vipan K Parihar, Charles L Limoli

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
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  11. Microglia as Therapeutic Target for Radiation-Induced Brain Injury.International journal of molecular sciences · 2022
    Review
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  19. Long-term neurocognitive benefits of FLASH radiotherapy driven by reduced reactive oxygen species.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
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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

8 authors at 1 institution in 1 country.

Munjal M AcharyaDepartment of Radiation Oncology, University of California Irvine, Irvine, CA, 92697-2695, United States of America.
Neal H PatelDepartment of Radiation Oncology, University of California Irvine, Irvine, CA, 92697-2695, United States of America.
Brianna M CraverDepartment of Radiation Oncology, University of California Irvine, Irvine, CA, 92697-2695, United States of America.
Katherine K TranDepartment of Radiation Oncology, University of California Irvine, Irvine, CA, 92697-2695, United States of America.
Erich GiedzinskiDepartment of Radiation Oncology, University of California Irvine, Irvine, CA, 92697-2695, United States of America.
Bertrand P TsengDepartment of Radiation Oncology, University of California Irvine, Irvine, CA, 92697-2695, United States of America.
Vipan K PariharDepartment of Radiation Oncology, University of California Irvine, Irvine, CA, 92697-2695, United States of America.
Charles L LimoliDepartment of Radiation Oncology, University of California Irvine, Irvine, CA, 92697-2695, United States of America.
University of California, Irvine · US

Funding

University of California Health Participation in the National COVID Cohort Collaborative (N3C)UL1TR001414 · NCATS · UNIVERSITY OF CALIFORNIA-IRVINE · PI COOPER, DAN M, VILAIN, ERIC J. · 2015 to 2023
$35.1M
NCATS NIH HHS UL1 TR001414
6 · The paper itself

Abstract

The response of the brain to irradiation is complex, involving a multitude of stress inducible pathways that regulate neurotransmission within a dynamic microenvironment. While significant past work has detailed the consequences of CNS radiotherapy following relatively high doses (≥ 45 Gy), few studies have been conducted at much lower doses (≤ 2 Gy), where the response of the CNS (like many other tissues) may differ substantially from that expected from linear extrapolations of high dose data. Low dose exposure could elicit radioadaptive modulation of critical CNS processes such as neurogenesis, that provide cellular input into hippocampal circuits known to impact learning and memory. Here we show that mice deficient for chemokine signaling through genetic disruption of the CCR2 receptor exhibit a neuroprotective phenotype. Compared to wild type (WT) animals, CCR2 deficiency spared reductions in hippocampal neural progenitor cell survival and stabilized neurogenesis following exposure to low dose irradiation. While radiation-induced changes in microglia levels were not found in WT or CCR2 deficient animals, the number of Iba1+ cells did differ between each genotype at the higher dosing paradigms, suggesting that blockade of this signaling axis could moderate the neuroinflammatory response. Interestingly, changes in proinflammatory gene expression were limited in WT animals, while irradiation caused significant elevations in these markers that were attenuated significantly after radioadaptive dosing paradigms in CCR2 deficient mice. These data point to the importance of chemokine signaling under low dose paradigms, findings of potential significance to those exposed to ionizing radiation under a variety of occupational and/or medical scenarios.

Indexed as

Radiation ExposureRadiation, IonizingAnimalsBiomarkersCell ProliferationCell SurvivalCellular MicroenvironmentCerebral CortexDentate GyrusDose-Response Relationship, RadiationGene Expression RegulationHippocampusInflammation MediatorsMice, Inbred C57BLMice, KnockoutMicrogliaBiomarkersCcr2 protein, mouseInflammation MediatorsReceptors, CCR2

Identifiers

PMID26042591
PMCPMC4456101
OpenAlexW1538599062

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.