Evidence map›Paper›PMID 24187597›Full record

ArticleTranslational stroke research2013

Role of the sphingosine metabolism pathway on neurons against experimental cerebral ischemia in rats.

Yu Hasegawa, Hidenori Suzuki, Orhan Altay, William Rolland, John H Zhang

Open access · greenAbstract read
In one paragraph

Article in Translational stroke research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

30 citing papers in PubMed, 51 citations in OpenAlex.

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  15. Immunoreactive Cells After Cerebral Ischemia.Frontiers in immunology · 2019
    Review
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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

5 authors at 1 institution in 1 country.

Yu HasegawaDepartment of Physiology, Loma Linda University School of Medicine, Loma Linda, California, USA.
Hidenori Suzuki
Orhan Altay
William Rolland
John H Zhang
Loma Linda University · US

Funding

Mechanisms of Hyperbaric Oxygen Induced Brain ProtectionR01NS043338 · NINDS · LOUISIANA STATE UNIV HSC SHREVEPORT · PI ZHANG, JOHN H · 2004 to 2014
$3.0M
Mechanisms of EPO-Induced NeuroprotectionR01NS054685 · NINDS · LOMA LINDA UNIVERSITY · PI ZHANG, JOHN H · 2007 to 2011
$1.8M
Neurovascular Protection for Subarachnoid HemorrhageR01NS053407 · NINDS · LOMA LINDA UNIVERSITY · PI ZHANG, JOHN H · 2006 to 2010
$1.8M
Neurovascular Protection for Early Brain Injury after SAHR01NS081740 · NINDS · LOMA LINDA UNIVERSITY · PI ZHANG, JOHN H · 2013 to 2017
$1.6M
NINDS NIH HHS NS053407NINDS NIH HHS R01 NS043338NINDS NIH HHS R01 NS053407NINDS NIH HHS R01 NS054685NINDS NIH HHS R01 NS081740
6 · The paper itself

Abstract

Although there is evidence that sphingosine-1-phosphate receptor-1 (S1P1) activation occurs following experimental brain injury, there is little information about its metabolic pathway in cerebral ischemia. The purpose of this study was to evaluate the role of the sphingosine metabolic pathway including S1P1, sphingosine kinases 1 (SphK1), and 2 (SphK2) in transient middle cerebral artery occlusion (MCAO). Fifty-eight male Sprague-Dawley rats were used to asses temporal profiles of S1P1, SphK1 and 2 on neurons in infarct and periinfarct cortices at pre-infarct state, 6, and 24 hours after MCAO. The animals were then treated with vehicle and 0.25 mg/kg FTY720, which is an agonist of S1P receptors, and evaluated regarding neurological function, infarct volume, and S1P1 expression on neurons at 24 hours after MCAO. The expressions of S1P1, SphK1, and SphK2 were significantly decreased after MCAO. Labeling of all markers were reduced in the infarct cortex but remained present in the periinfarct cortex, and some were found to be on neurons. Significant improvements of neurological function and brain injury were observed in the FTY720 group compared with the vehicle and untreated groups, although S1P1 expression on neurons was reduced in the FTY720 group compared with the vehicle group. We demonstrated that S1P1, SphK1, and SphK2 were downregulated in the infarct cortex, whereas they were preserved in the periinfarct cortex where FTY720 reduced neuronal injury possibly via S1P1 activation. Our findings suggest that activation of the sphingosine metabolic pathway may be neuroprotective in cerebral ischemia.

Indexed as

AnimalsBrain IschemiaDisease Models, AnimalFingolimod HydrochlorideImmunosuppressive AgentsInfarction, Middle Cerebral ArteryMaleNeuronsPhosphotransferases (Alcohol Group Acceptor)Propylene GlycolsRatsRats, Sprague-DawleySphingosineSphingosine KinaseFingolimod HydrochlorideImmunosuppressive AgentsPhosphotransferases (Alcohol Group Acceptor)Propylene GlycolsSphingosineSphingosine KinaseFTY720sphingosine 1-phosphate receptor-1sphingosine kinase 1sphingosine kinase 2transient middle cerebral artery occlusion

Identifiers

PMID24187597
PMCPMC3811943
OpenAlexW2016018848

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.