Evidence map›Paper›PMID 30563941›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2019

Neutral Sphingomyelinase Inhibition Alleviates LPS-Induced Microglia Activation and Neuroinflammation after Experimental Traumatic Brain Injury.

Asit Kumar, Rebecca J Henry, Bogdan A Stoica, David J Loane, Gelareh Abulwerdi, Shahnawaz A Bhat, Alan I Faden

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 66 citations in OpenAlex.

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  10. Natural resorcylic lactones derived from alternariol.Beilstein journal of organic chemistry · 2024
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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

7 authors at 1 institution in 1 country.

Asit KumarDepartment of Anesthesiology and Shock, Trauma and Anesthesiology Research (STAR) Center, University of Maryland School of Medicine, Baltimore, Maryland afaden1@som.umaryland.edu asitkumar14@gmail.com.
Rebecca J HenryDepartment of Anesthesiology and Shock, Trauma and Anesthesiology Research (STAR) Center, University of Maryland School of Medicine, Baltimore, Maryland.
Bogdan A StoicaDepartment of Anesthesiology and Shock, Trauma and Anesthesiology Research (STAR) Center, University of Maryland School of Medicine, Baltimore, Maryland.
David J LoaneDepartment of Anesthesiology and Shock, Trauma and Anesthesiology Research (STAR) Center, University of Maryland School of Medicine, Baltimore, Maryland.
Gelareh AbulwerdiDepartment of Anesthesiology and Shock, Trauma and Anesthesiology Research (STAR) Center, University of Maryland School of Medicine, Baltimore, Maryland.
Shahnawaz A BhatDepartment of Anesthesiology and Shock, Trauma and Anesthesiology Research (STAR) Center, University of Maryland School of Medicine, Baltimore, Maryland.
Alan I FadenDepartment of Anesthesiology and Shock, Trauma and Anesthesiology Research (STAR) Center, University of Maryland School of Medicine, Baltimore, Maryland afaden1@som.umaryland.edu asitkumar14@gmail.com.
University of Maryland, Baltimore · US

Funding

MODULATION OF INJURY BY METABOTROPIC GLUTAMATE RECEPTORSR01NS037313 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI FADEN, ALAN IRA · 1999 to 2019
$5.8M
miR-711 regulation of neuronal cell death after traumatic brain injuryR01NS096002 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI SABIRZHANOV, BORIS, STOICA, BOGDAN ADRIAN · 2016 to 2020
$1.7M
Microglial activation phenotypes and mechanisms of repair in the aged TBI brainR01NS082308 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI LOANE, DAVID J. · 2013 to 2016
$1.4M
NINDS NIH HHS R01 NS037313NINDS NIH HHS R01 NS082308NINDS NIH HHS R01 NS096002
6 · The paper itself

Abstract

Neuroinflammation is one of the key secondary injury mechanisms triggered by traumatic brain injury (TBI). Microglial activation, a hallmark of brain neuroinflammation, plays a critical role in regulating immune responses after TBI and contributes to progressive neurodegeneration and neurologic deficits following brain trauma. Here we evaluated the role of neutral sphingomyelinase (nSMase) in microglial activation by examining the effects of the nSMase inhibitors altenusin and GW4869 in vitro (using BV2 microglia cells and primary microglia), as well as in a controlled cortical injury (CCI) model in adult male C57BL/6 mice. Pretreatment of altenusin or GW4869 prior to lipopolysaccharide (LPS) stimulation for 4 or 24 hours, significantly downregulated gene expression of the pro-inflammatory mediators TNF-

Indexed as

AnimalsBrain Injuries, TraumaticCells, CulturedCell SurvivalDose-Response Relationship, DrugInflammation MediatorsLipopolysaccharidesMaleMiceMice, Inbred C57BLMicrogliaRatsRats, Sprague-DawleySphingomyelin PhosphodiesteraseInflammation MediatorsLipopolysaccharidesSphingomyelin Phosphodiesterase

Identifiers

PMID30563941
PMCPMC6367691
OpenAlexW2904497118

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.