Evidence map›Paper›PMID 28794441›Full record

ArticleScientific reports2017

TGFβ signaling is associated with changes in inflammatory gene expression and perineuronal net degradation around inhibitory neurons following various neurological insults.

Soo Young Kim, Vladimir V Senatorov, Christapher S Morrissey, Kristina Lippmann, Oscar Vazquez, Dan Z Milikovsky, Feng Gu, Isabel Parada, David A Prince, Albert J Becker and 3 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 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 4% 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

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 135 citations in OpenAlex.

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9 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

13 authors at 6 institutions in 4 countries.

Soo Young KimDepartment of Integrative Biology, University of California Berkeley, Berkeley, CA, 94720, USA. sooykim29@gmail.com.ORCID 0000-0002-2111-4619
Vladimir V SenatorovHelen Wills Neuroscience Institute, University of California Berkeley, Berkeley, CA, 94720, USA.
Christapher S MorrisseyDepartment of Integrative Biology, University of California Berkeley, Berkeley, CA, 94720, USA.
Kristina LippmannInstitute of Neurophysiology, Charité Universitätsmedizin Berlin, Berlin, D10117, Germany.
Oscar VazquezHelen Wills Neuroscience Institute, University of California Berkeley, Berkeley, CA, 94720, USA.
Dan Z MilikovskyDepartments of Cognitive and Brain Sciences, Physiology and Cell Biology, Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva, 84105, Israel.
Feng GuDepartment of Neurology and Neurological Sciences, , Stanford University School of Medicine, Stanford, CA, 94305, USA.
Isabel ParadaDepartment of Neurology and Neurological Sciences, , Stanford University School of Medicine, Stanford, CA, 94305, USA.
David A PrinceDepartment of Neurology and Neurological Sciences, , Stanford University School of Medicine, Stanford, CA, 94305, USA.
Albert J BeckerDepartment of Neuropathology, University of Bonn Medical Center, Bonn, 53105, Germany.
Uwe HeinemannInstitute of Neurophysiology, Charité Universitätsmedizin Berlin, Berlin, D10117, Germany.
Alon FriedmanDepartments of Cognitive and Brain Sciences, Physiology and Cell Biology, Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, Beer-Sheva, 84105, Israel.
Daniela KauferDepartment of Integrative Biology, University of California Berkeley, Berkeley, CA, 94720, USA. danielak@berkeley.edu.
University of California, Berkeley · USStanford University · USBen-Gurion University of the Negev · ILCharité - Universitätsmedizin Berlin · DECanadian Institute for Advanced Research · CAUniversity of Bonn · DE

Funding

Training in Basic Research on Aging and Age-Related DiseaseT32AG000266 · NIA · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI Lisa M Ellerby · 1998 to 2026
$13.8M
MODULATION OF NEOCORTICAL INTERNEURONAL FUNCTIONR01NS039579 · NINDS · STANFORD UNIVERSITY · PI HUGUENARD, JOHN R, PRINCE, DAVID ALLAN · 2000 to 2013
$4.3M
Effects of TrkB Activation on Abnormalities in Neocortical FS InterneuronsR01NS082644 · NINDS · STANFORD UNIVERSITY · PI PRINCE, DAVID ALLAN · 2013 to 2022
$3.7M
Effects of pregabalin and thrombospondins on enhanced excitatory connectivity, new synapse formation and epileptogenesis after neocortical injuryR01NS090076 · NINDS · STANFORD UNIVERSITY · PI PRINCE, DAVID ALLAN · 2014 to 2018
$1.9M
TGF-beta Mediated Inflammatory Signaling: a critical role in epileptogenesisR56NS066005 · NINDS · UNIVERSITY OF CALIFORNIA BERKELEY · PI KAUFER, DANIELA · 2014 to 2014
$534k
Modulation of Neocortical Interneuronal FunctionR56NS039579 · NINDS · STANFORD UNIVERSITY · PI PRINCE, DAVID ALLAN · 2014 to 2014
$402k
NIA NIH HHS T32 AG000266NINDS NIH HHS R01 NS039579NINDS NIH HHS R01 NS082644NINDS NIH HHS R01 NS090076NINDS NIH HHS R56 NS039579NINDS NIH HHS R56 NS066005
6 · The paper itself

Abstract

Brain damage due to stroke or traumatic brain injury (TBI), both leading causes of serious long-term disability, often leads to the development of epilepsy. Patients who develop post-injury epilepsy tend to have poor functional outcomes. Emerging evidence highlights a potential role for blood-brain barrier (BBB) dysfunction in the development of post-injury epilepsy. However, common mechanisms underlying the pathological hyperexcitability are largely unknown. Here, we show that comparative transcriptome analyses predict remodeling of extracellular matrix (ECM) as a common response to different types of injuries. ECM-related transcriptional changes were induced by the serum protein albumin via TGFβ signaling in primary astrocytes. In accordance with transcriptional responses, we found persistent degradation of protective ECM structures called perineuronal nets (PNNs) around fast-spiking inhibitory interneurons, in a rat model of TBI as well as in brains of human epileptic patients. Exposure of a naïve brain to albumin was sufficient to induce the transcriptional and translational upregulation of molecules related to ECM remodeling and the persistent breakdown of PNNs around fast-spiking inhibitory interneurons, which was contingent on TGFβ signaling activation. Our findings provide insights on how albumin extravasation that occurs upon BBB dysfunction in various brain injuries can predispose neural circuitry to the development of chronic inhibition deficits.

Indexed as

Gene ExpressionSignal TransductionAstrocytesBlood-Brain BarrierBrain Injuries, TraumaticCerebral CortexComputational BiologyExtracellular MatrixGene Expression ProfilingHippocampusHumansInflammationInterneuronsLosartanNeuronsReceptor, Transforming Growth Factor-beta Type ILosartanReceptor, Transforming Growth Factor-beta Type ITGFBR1 protein, humanTransforming Growth Factor beta

Identifiers

PMID28794441
PMCPMC5550510
OpenAlexW2743499986

What OpenQuestion holds

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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.