Evidence map›Paper›PMID 27793054›Full record

ArticleOncotarget2016

Cranial irradiation induces transient microglia accumulation, followed by long-lasting inflammation and loss of microglia.

Wei Han, Takashi Umekawa, Kai Zhou, Xing-Mei Zhang, Makiko Ohshima, Cecilia A Dominguez, Robert A Harris, Changlian Zhu, Klas Blomgren

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.1field-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

44 citing papers in PubMed, 86 citations in OpenAlex.

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  20. Microglia as Therapeutic Target for Radiation-Induced Brain Injury.International journal of molecular sciences · 2022
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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

9 authors at 4 institutions in 3 countries.

Wei HanDepartment of Pediatrics, Henan Provincial Women's and Children's Hospital, Zhengzhou, P.R. China.
Takashi UmekawaKarolinska Institutet, Department of Women's and Children's Health, Stockholm, Sweden.
Kai ZhouKarolinska Institutet, Department of Women's and Children's Health, Stockholm, Sweden.
Xing-Mei ZhangKarolinska Institutet, Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.
Makiko OhshimaKarolinska Institutet, Department of Women's and Children's Health, Stockholm, Sweden.
Cecilia A DominguezKarolinska Institutet, Department of Women's and Children's Health, Stockholm, Sweden.
Robert A HarrisKarolinska Institutet, Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska University Hospital, Stockholm, Sweden.
Changlian ZhuHenan Key Laboratory of Child Brain Injury, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, P.R. China.
Klas BlomgrenKarolinska Institutet, Department of Women's and Children's Health, Stockholm, Sweden.
Karolinska Institutet · SEKarolinska University Hospital · SEMie University · JPUniversity of Gothenburg · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The relative contribution of resident microglia and peripheral monocyte-derived macrophages in neuroinflammation after cranial irradiation is not known. A single dose of 8 Gy was administered to postnatal day 10 (juvenile) or 90 (adult) CX3CR1GFP/+ CCR2RFP/+ mouse brains. Microglia accumulated in the subgranular zone of the hippocampal granule cell layer, where progenitor cell death was prominent. The peak was earlier (6 h vs. 24 h) but less pronounced in adult brains. The increase in juvenile, but not adult, brains was partly attributed to proliferation. Microglia numbers then decreased over time to 39% (juvenile) and 58% (adult) of controls 30 days after irradiation, largely as a result of cell death. CD68 was expressed in 90% of amoeboid microglia in juvenile hippocampi but only in 9% of adult ones. Isolated hippocampal microglia revealed reduced CD206 and increased IL1-beta expression after irradiation, more pronounced in juvenile brains. CCL2 and IL-1 beta increased after irradiation, more in juvenile hippocampi, and remained elevated at all time points. In summary, microglia activation after irradiation was more pronounced, protracted and pro-inflammatory by nature in juvenile than in adult hippocampi. Common to both ages was long-lasting inflammation and the absence of monocyte-derived macrophages.

Indexed as

Age FactorsAnimalsAntigens, CDAntigens, Differentiation, MyelomonocyticCD68 MoleculeCell DeathCell ProliferationChemokine CCL2Cranial IrradiationCX3C Chemokine Receptor 1EncephalitisGreen Fluorescent ProteinsHippocampusInterleukin-1betaLuminescent ProteinsMice, Inbred C57BLAntigens, CDAntigens, Differentiation, MyelomonocyticCcl2 protein, mouseCcr2 protein, mouseCD68 MoleculeCD68 protein, mouseChemokine CCL2CX3C Chemokine Receptor 1Cx3cr1 protein, mouseGreen Fluorescent ProteinsIL1B protein, mouseInterleukin-1betaLuminescent ProteinsReceptors, CCR2Red Fluorescent Proteinirradiationmacrophagemicrogliamonocyteneurogenesisneuroinflammation

Identifiers

PMID27793054
PMCPMC5347693
OpenAlexW2545220750

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.