Evidence map›Paper›PMID 29196212›Full record

ArticleNeurobiology of disease2018

Axl activation attenuates neuroinflammation by inhibiting the TLR/TRAF/NF-κB pathway after MCAO in rats.

Guangyong Wu, Devin W McBride, John H Zhang

RetractedOpen access · greenAbstract readRetracted Publication
In one paragraph

Article in Neurobiology of disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

56 citing papers in PubMed, 116 citations in OpenAlex.

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  15. Growth arrest specific protein 6 alleviated white matter injury after experimental ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 2 countries.

Guangyong WuDepartments of Anesthesiology, Physiology & Pharmacology, Loma Linda University, Loma Linda, CA, USA; Department of Neurosurgery, the Third Xiangya Hospital, Central South University, Changsha, Hunan, China.
Devin W McBrideDepartments of Anesthesiology, Physiology & Pharmacology, Loma Linda University, Loma Linda, CA, USA.
John H ZhangDepartments of Anesthesiology, Physiology & Pharmacology, Loma Linda University, Loma Linda, CA, USA. Electronic address: jhzhang@llu.edu.
Loma Linda University · USCentral South University · CN

Funding

Vascular Biology Core FacilityP01NS082184 · NINDS · LOMA LINDA UNIVERSITY · PI PEARCE, WILLIAM J. · 2014 to 2018
$6.1M
Neurovascular Protection for Early Brain Injury after SAHR01NS081740 · NINDS · LOMA LINDA UNIVERSITY · PI ZHANG, JOHN H · 2013 to 2017
$1.6M
NINDS NIH HHS P01 NS082184NINDS NIH HHS R01 NS081740
6 · The paper itself

Abstract

background and purposeIschemic stroke activates Toll-like receptors (TLRs), triggering rapid inflammatory cytokine production. Axl signaling has multiple roles, including regulating cytokine secretion, clearing apoptotic cells, and maintaining cell survival, however, its role in inflammation after ischemic stroke has not been examined. We hypothesized that activation of Axl by recombinant Growth-arrest-specific protein 6 (rGas6) attenuates neuroinflammation by inhibiting the TLR/TRAF/NF-κB pathway after middle cerebral artery occlusion (MCAO) in rats. METH: Sprague-Dawley rats were subjected to 2h of MCAO. One hour after reperfusion, the rats were given an intranasal injection of rGas6, vehicle, or R428 (Axl receptor inhibitor). Neurological scores, infarct volumes, immunofluorescence staining, Morris Water Maze, rotarod test and histology alterations were analyzed. The expressions of proinflammatory cytokines, including IL-1β, IL-6, TNF-α, and Gas6, Axl, STAT1, SOCS1, SOCS3 and the TLR/TRAF/NF-κB pathway were quantified using Western blot.

resultsEndogenous expressions of Gas6 and Axl decreased significantly by 24h after MCAO. rGas6 reduced brain infarction and improved neurologic deficits scores, and increased expression of Axl and decreased the expressions of TRAF3, TRAF6 and inflammatory factors IL-1β, IL-6, and TNF-α. Four weeks after MCAO, rGas6 improved long-term neurological behavior and memory. Inhibition of the Axl/TLR/TRAF/NF-κB pathway reversed the brain protection by rGas6.

conclusionrGas6 reduced the neurological deficits by inhibiting neuroinflammation via the TLR/TRAF/NF-κB signaling pathway. rGas6 can be used as potential treatment to ischemic stroke.

Indexed as

AnimalsAnti-Inflammatory AgentsBrainEnzyme ActivationGrowth Arrest-Specific Protein 6Infarction, Middle Cerebral ArteryInflammationIntercellular Signaling Peptides and ProteinsMaleNeuroprotective AgentsNF-kappa BRatsRats, Sprague-DawleyReceptor Protein-Tyrosine KinasesRecombinant ProteinsSignal TransductionAnti-Inflammatory AgentsAxl protein, ratGrowth Arrest-Specific Protein 6Intercellular Signaling Peptides and ProteinsNeuroprotective AgentsNF-kappa BReceptor Protein-Tyrosine KinasesRecombinant ProteinsToll-Like ReceptorsTumor Necrosis Factor Receptor-Associated Peptides and ProteinsAxlGrowth-arrest-specific protein 6InflammationMiddle cerebral artery occlusionToll-like receptor

Identifiers

PMID29196212
PMCPMC5748011
OpenAlexW2770807583

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.