Evidence map›Paper›PMID 31694961›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2020

Aberrant ER Stress Induced Neuronal-IFNβ Elicits White Matter Injury Due to Microglial Activation and T-Cell Infiltration after TBI.

Tanusree Sen, Pampa Saha, Rajaneesh Gupta, Lesley M Foley, Tong Jiang, Olena S Abakumova, T Kevin Hitchens, Nilkantha Sen

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed, 1 pooled it
8.5field-weighted citation impact, top 2% 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

104 citing papers in PubMed, 1 synthesis or guideline pooled it, 178 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Tanusree SenDepartment of Neurological Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania 15213, and tas215@pitt.edu senn@pitt.edu.
Pampa SahaDepartment of Neurological Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania 15213, and.ORCID 0000-0002-4926-9081
Rajaneesh GuptaDepartment of Neurological Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania 15213, and.
Lesley M FoleyAnimal Imaging Center, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania 15044.
Tong JiangDepartment of Neurological Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania 15213, and.
Olena S AbakumovaDepartment of Neurological Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania 15213, and.
T Kevin HitchensAnimal Imaging Center, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania 15044.
Nilkantha SenDepartment of Neurological Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania 15213, and tas215@pitt.edu senn@pitt.edu.ORCID 0000-0002-8383-8209
University of Pittsburgh · US

Funding

Molecular Mechanisms underlying vision impairment after TBIR01EY025622 · NEI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SEN, NILKANTHA · 2016 to 2020
$1.9M
Development of therapeutic strategy against TBI based on hydrogen sulfideR01NS094516 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SEN, NILKANTHA · 2016 to 2020
$1.7M
NEI NIH HHS R01 EY025622NINDS NIH HHS R01 NS094516
6 · The paper itself

Abstract

Persistent endoplasmic reticulum (ER) stress in neurons is associated with activation of inflammatory cells and subsequent neuroinflammation following traumatic brain injury (TBI); however, the underlying mechanism remains elusive. We found that induction of neuronal-ER stress, which was mostly characterized by an increase in phosphorylation of a protein kinase R-like ER kinase (PERK) leads to release of excess interferon (IFN)β due to atypical activation of the neuronal-STING signaling pathway. IFNβ enforced activation and polarization of the primary microglial cells to inflammatory M1 phenotype with the secretion of a proinflammatory chemokine CXCL10 due to activation of STAT1 signaling. The secreted CXCL10, in turn, stimulated the T-cell infiltration by serving as the ligand and chemoattractant for CXCR3

Indexed as

T-LymphocytesAnimalsBrain Injuries, TraumaticeIF-2 KinaseEndoplasmic Reticulum StressFemaleInterferon-betaMaleMiceMice, Inbred C57BLMicrogliaNeuronsSignal TransductionWhite MattereIF-2 KinaseInterferon-betaIFNmicroglianeuroinflammationtraumatic brain injurywhite matter injury

Identifiers

PMID31694961
PMCPMC6948950
OpenAlexW2983803664

What OpenQuestion holds

Textmetadata
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.