Evidence map›Paper›PMID 30275444›Full record

ArticleNature communications2018

Silencing of TGFβ signalling in microglia results in impaired homeostasis.

Tanja Zöller, Artur Schneider, Christian Kleimeyer, Takahiro Masuda, Phani Sankar Potru, Dietmar Pfeifer, Thomas Blank, Marco Prinz, Björn Spittau

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
126citing papers in PubMed, 1 pooled it
5.9field-weighted citation impact, top 3% 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

126 citing papers in PubMed, 1 synthesis or guideline pooled it, 186 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  8. iScience · 2026
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66 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

9 authors at 2 institutions in 1 country.

Tanja ZöllerInstitute for Anatomy and Cell Biology, Department of Molecular Embryology, Faculty of Medicine, University of Freiburg, 79104, Freiburg, Germany.
Artur SchneiderInstitute for Anatomy and Cell Biology, Department of Molecular Embryology, Faculty of Medicine, University of Freiburg, 79104, Freiburg, Germany.
Christian KleimeyerInstitute for Anatomy and Cell Biology, Department of Molecular Embryology, Faculty of Medicine, University of Freiburg, 79104, Freiburg, Germany.
Takahiro MasudaInstitute of Neuropathology, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, 79106, Freiburg, Germany.
Phani Sankar PotruFaculty of Biology, University of Freiburg, 79104, Freiburg, Germany.
Dietmar PfeiferDepartment of Hematology/Oncology, Faculty of Medicine, University of Freiburg, 79106, Freiburg, Germany.
Thomas BlankInstitute of Neuropathology, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, 79106, Freiburg, Germany.
Marco PrinzInstitute of Neuropathology, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, 79106, Freiburg, Germany.
Björn SpittauInstitute for Anatomy and Cell Biology, Department of Molecular Embryology, Faculty of Medicine, University of Freiburg, 79104, Freiburg, Germany. bjoern.spittau@med.uni-rostock.de.
University of Freiburg · DEUniversity of Rostock · DE

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) SP 1555/2-1
6 · The paper itself

Abstract

TGFβ1 has been implicated in regulating functional aspects of several distinct immune cell populations including central nervous system (CNS) resident microglia. Activation and priming of microglia have been demonstrated to contribute to the progression of neurodegenerative diseases and, thus, underlie stringent control by endogenous regulatory factors including TGFβ1. Here, we demonstrate that deletion of Tgfbr2 in adult postnatal microglia does neither result in impairment of the microglia-specific gene expression signatures, nor is microglial survival and maintenance affected. Tgfbr2-deficient microglia were characterised by distinct morphological changes and transcriptome analysis using RNAseq revealed that loss of TGFβ signalling results in upregulation of microglia activation and priming markers. Moreover, protein arrays demonstrated increased secretion of CXCL10 and CCL2 accompanied by activation of immune cell signalling as evidenced by increased phosphorylation of TAK1. Together, these data underline the importance of microglial TGFβ signalling to regulate microglia adaptive changes.

Indexed as

HomeostasisAnimalsChemokine CCL2Chemokine CXCL10Gene Expression ProfilingGene SilencingMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMiceMice, TransgenicMicrogliaPhosphorylationProtein Array AnalysisReceptor, Transforming Growth Factor-beta Type IISignal TransductionTransforming Growth Factor betaCcl2 protein, mouseChemokine CCL2Chemokine CXCL10Cxcl10 protein, mouseMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesReceptor, Transforming Growth Factor-beta Type IITgfbr2 protein, mouseTransforming Growth Factor beta

Identifiers

PMID30275444
PMCPMC6167353
OpenAlexW2892433402

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.