Evidence map›Paper›PMID 23650073›Full record

ArticleGlia2013

Evidence for miR-181 involvement in neuroinflammatory responses of astrocytes.

Emmette R Hutchison, Elisa M Kawamoto, Dennis D Taub, Ashish Lal, Kotb Abdelmohsen, Yongqing Zhang, William H Wood, Elin Lehrmann, Simonetta Camandola, Kevin G Becker and 2 more

Abstract read
In one paragraph

Article in Glia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
146citing papers in PubMed, 2 pooled it
8.9field-weighted citation impact, top 1% 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

146 citing papers in PubMed, 2 syntheses or guidelines pooled it, 241 citations in OpenAlex.

  1. Pooled it
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  3. Interaction of miR-181b andBioMed research international · 2020
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86 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

12 authors at 3 institutions in 1 country.

Emmette R HutchisonLaboratory of Neurosciences, National Institute on Aging, NIH, Baltimore, Maryland, 21224, USA.
Elisa M Kawamoto
Dennis D Taub
Ashish Lal
Kotb Abdelmohsen
Yongqing Zhang
William H Wood
Elin Lehrmann
Simonetta Camandola
Kevin G Becker
Myriam Gorospe
Mark P Mattson
National Institute on Aging · USBrown University · USNational Cancer Institute · US

Funding

Analysis of complex biological systems by microarray based gene expressionZICAG000616 · NIA · NATIONAL INSTITUTE ON AGING · PI DE, SUPRIYO · 2009 to 2025
$15.5M
RNA-binding Factors Implicated in Neurogenesis, Alzheimer's Disease, and other Neurodegenerative PathologiesZIAAG000518 · NIA · NATIONAL INSTITUTE ON AGING · PI GOROSPE, MYRIAM · 2009 to 2025
$11.6M
Neuroprotective And Neurorestorative Signaling Mechanisms in Alzheimer's DiseaseZIAAG000314 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$6.7M
Cellular And Molecular Pathogenesis Of Alzheimer's DiseaseZIAAG000312 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$6.4M
Intramural NIH HHS ZIA AG000312Intramural NIH HHS ZIA AG000314
6 · The paper itself

Abstract

Inflammation is a common component of acute injuries of the central nervous system (CNS) such as ischemia, and degenerative disorders such as Alzheimer's disease. Glial cells play important roles in local CNS inflammation, and an understanding of the roles for microRNAs in glial reactivity in injury and disease settings may therefore lead to the development of novel therapeutic interventions. Here, we show that the miR-181 family is developmentally regulated and present in high amounts in astrocytes compared to neurons. Overexpression of miR-181c in cultured astrocytes results in increased cell death when exposed to lipopolysaccharide (LPS). We show that miR-181 expression is altered by exposure to LPS, a model of inflammation, in both wild-type and transgenic mice lacking both receptors for the inflammatory cytokine TNF-α. Knockdown of miR-181 enhanced LPS-induced production of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β, IL-8) and HMGB1, while overexpression of miR-181 resulted in a significant increase in the expression of the anti-inflammatory cytokine IL-10. To assess the effects of miR-181 on the astrocyte transcriptome, we performed gene array and pathway analysis on astrocytes with reduced levels of miR-181b/c. To examine the pool of potential miR-181 targets, we employed a biotin pull-down of miR-181c and gene array analysis. We validated the mRNAs encoding MeCP2 and X-linked inhibitor of apoptosis as targets of miR-181. These findings suggest that miR-181 plays important roles in the molecular responses of astrocytes in inflammatory settings. Further understanding of the role of miR-181 in inflammatory events and CNS injury could lead to novel approaches for the treatment of CNS disorders with an inflammatory component.

Indexed as

AnimalsAstrocytesBiotinylationBrain-Derived Neurotrophic FactorCells, CulturedCerebral CortexCytokinesLipopolysaccharidesL-Lactate DehydrogenaseMaleMethyl-CpG-Binding Protein 2MiceMice, KnockoutMicroRNAsNeuroimmunomodulationNeuronsBrain-Derived Neurotrophic FactorCytokinesLipopolysaccharidesL-Lactate DehydrogenaseMecp2 protein, mouseMethyl-CpG-Binding Protein 2MicroRNAsmirn181 microRNA, mouseReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IITnfrsf1a protein, mouseX-Linked Inhibitor of Apoptosis Protein

Identifiers

PMID23650073
PMCPMC4624280
OpenAlexW2159268524

What OpenQuestion holds

Textmetadata
LicenceTDM
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.