Evidence map›Paper›PMID 28694451›Full record

ArticleScientific reports2017

Polymorphic regulation of mitochondrial fission and fusion modifies phenotypes of microglia in neuroinflammation.

Mitsuhiko Katoh, Bao Wu, Huy Bang Nguyen, Truc Quynh Thai, Ryo Yamasaki, Haiyan Lu, Anna M Rietsch, Musab M Zorlu, Youichi Shinozaki, Yurika Saitoh and 6 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

61 citing papers in PubMed, 115 citations in OpenAlex.

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  20. Membrane Vesicles of ToxigenicAntioxidants (Basel, Switzerland) · 2023
    Article

1 more citing papers are in PubMed but not listed here.

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

16 authors at 4 institutions in 3 countries.

Mitsuhiko KatohDepartments of Anatomy and Molecular Histology, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo, Yamanashi, 409-3898, Japan.
Bao WuDepartments of Anatomy and Molecular Histology, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo, Yamanashi, 409-3898, Japan.
Huy Bang NguyenDepartments of Anatomy and Molecular Histology, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo, Yamanashi, 409-3898, Japan.
Truc Quynh ThaiDepartments of Anatomy and Molecular Histology, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo, Yamanashi, 409-3898, Japan.
Ryo YamasakiNeuroinflammation Research Center, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.
Haiyan LuNeuroinflammation Research Center, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.
Anna M RietschNeuroinflammation Research Center, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.
Musab M ZorluNeuroinflammation Research Center, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.ORCID 0000-0001-9076-9662
Youichi ShinozakiNeuropharmacology, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo, Yamanashi, 409-3898, Japan.
Yurika SaitohDepartments of Anatomy and Molecular Histology, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo, Yamanashi, 409-3898, Japan.
Sei SaitohDepartments of Anatomy and Molecular Histology, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo, Yamanashi, 409-3898, Japan.
Takashi SakohDepartments of Anatomy and Molecular Histology, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo, Yamanashi, 409-3898, Japan.
Kazuhiro IkenakaDivision of Neurobiology and Bioinformatics, National Institute for Physiological Sciences, Okazaki, Aichi, 444-8787, Japan.
Schuichi KoizumiNeuropharmacology, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo, Yamanashi, 409-3898, Japan.
Richard M RansohoffNeuroinflammation Research Center, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, 44195, USA.
Nobuhiko OhnoDepartments of Anatomy and Molecular Histology, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo, Yamanashi, 409-3898, Japan. nohno@nips.ac.jp.
University of Yamanashi · JPCleveland Clinic Lerner College of Medicine · USNational Institute for Physiological Sciences · JPChifeng University · CN

Funding

CHEMOKINES IN CNS INFLAMMATIONR01NS032151 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI RANSOHOFF, RICHARD M. · 1994 to 2013
$3.7M
NINDS NIH HHS R01 NS032151
6 · The paper itself

Abstract

Microglia are the resident macrophages of the central nervous system and play complex roles in the milieu of diseases including the primary diseases of myelin. Although mitochondria are critical for cellular functions and survival in the nervous system, alterations in and the roles of mitochondrial dynamics and associated signaling in microglia are still poorly understood. In the present study, by combining immunohistochemistry and 3D ultrastructural analyses, we show that mitochondrial fission/fusion in reactive microglia is differentially regulated from that in monocyte-derived macrophages and the ramified microglia of normal white matter in myelin disease models. Mouse cerebral microglia in vitro demonstrated that stimulation of TLR4 with lipopolysaccharide, widely used to examine microglial reactions, caused the activation of the mitochondrial fission protein, dynamin-related protein 1 (Drp1) and enhanced production of reactive oxygen species (ROS). The increase in the ROS level activated 5' adenosine monophosphate-activated protein kinase (AMPK), and facilitated elongation of mitochondria along the microtubule tracks. These results suggest that the polymorphic regulation of mitochondrial fission and fusion in reactive microglia is mediated by distinct signaling under inflammatory conditions, and modulates microglial phenotypes through the production of ROS.

Indexed as

Mitochondrial DynamicsPhenotypeAMP-Activated Protein KinasesAnimalsBiomarkersCentral Nervous SystemDemyelinating DiseasesDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalInflammationLipopolysaccharidesMacrophagesMiceMicrogliaMitochondriaReactive Oxygen SpeciesAMP-Activated Protein KinasesBiomarkersLipopolysaccharidesReactive Oxygen Species

Identifiers

PMID28694451
PMCPMC5503944
OpenAlexW2729815258

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.