Evidence map›Paper›PMID 29969654›Full record

ArticleMolecular and cellular neurosciences2018

Depletion of astrocytic transglutaminase 2 improves injury outcomes.

Alina Monteagudo, Julianne Feola, Heather Natola, Changyi Ji, Christoph Pröschel, Gail V W Johnson

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular neurosciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Alina MonteagudoDepartment of Pharmacology and Physiology, University of Rochester, Rochester, NY 14642, USA.
Julianne FeolaDepartment of Biomedical Genetics, University of Rochester, Rochester, NY 14642, USA.
Heather NatolaDepartment of Biomedical Genetics, University of Rochester, Rochester, NY 14642, USA.
Changyi JiDepartment of Anesthesiology and Perioperative Medicine, University of Rochester, Rochester, NY 14642, USA.
Christoph PröschelDepartment of Biomedical Genetics, University of Rochester, Rochester, NY 14642, USA; Stem Cell and Regenerative Medicine Institute, University of Rochester, Rochester, NY 14642, USA.
Gail V W JohnsonDepartment of Pharmacology and Physiology, University of Rochester, Rochester, NY 14642, USA; Department of Biomedical Genetics, University of Rochester, Rochester, NY 14642, USA; Department of Anesthesiology and Perioperative Medicine, University of Rochester, Rochester, NY 14642, USA. Electronic address: gail_johnsonvoll@urmc.rochester.edu.
University of Rochester · US

Funding

The attenuation of ischemic injury by transglutaminase 2R01NS065825 · NINDS · UNIVERSITY OF ROCHESTER · PI JOHNSON, GAIL V. W. · 2011 to 2015
$1.8M
TISSUE TRANSGLUTAMINASE--REGULATION AND DYSREGULATIONR01AG012396 · NIA · UNIVERSITY OF ROCHESTER · PI JOHNSON, GAIL V. W. · 1994 to 2006
$1.6M
The Role of Astrocytic Transglutaminase 2 in Mediating Ischemic Stroke DamageF31NS081894 · NINDS · UNIVERSITY OF ROCHESTER · PI FEOLA, JULIANNE M · 2012 to 2014
$127k
NIA NIH HHS R01 AG012396NINDS NIH HHS F31 NS081894NINDS NIH HHS R01 NS065825
6 · The paper itself

Abstract

Astrocytes play an indispensable role in maintaining a healthy, functional neural network in the central nervous system (CNS). A primary function of CNS astrocytes is to support the survival and function of neurons. In response to injury, astrocytes take on a reactive phenotype, which alters their molecular functions. Reactive astrocytes have been reported to be both beneficial and harmful to the CNS recovery process subsequent to injury. Understanding the molecular processes and regulatory proteins that determine the extent to which an astrocyte hinders or supports neuronal survival is important within the context of CNS repair. One protein that plays a role in modulating cellular survival is transglutaminase 2 (TG2). Global deletion of TG2 results in beneficial outcomes subsequent to in vivo ischemic brain injury. Ex vivo studies have also implicated TG2 as a negative regulator of astrocyte viability subsequent to injury. In this study we show that knocking down TG2 in astrocytes significantly increases their ability to protect neurons from oxygen glucose deprivation (OGD)/reperfusion injury. To begin to understand how deletion of TG2 in astrocytes improves their ability to protect neurons from injury, we performed transcriptome analysis of wild type and TG2

Indexed as

Nerve RegenerationAnimalsAstrocytesAxon GuidanceCell HypoxiaCells, CulturedGlucoseGTP-Binding ProteinsHEK293 CellsHumansMiceMice, Inbred C57BLNeuronsProtein Glutamine gamma Glutamyltransferase 2Spinal Cord InjuriesTranscription Factor AP-1GlucoseGTP-Binding ProteinsProtein Glutamine gamma Glutamyltransferase 2Transcription Factor AP-1TransglutaminasesAstrocytesCNS injuryNeuroprotectionTransglutaminase 2

Identifiers

PMID29969654
PMCPMC6218936
OpenAlexW2811013862

What OpenQuestion holds

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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.