Evidence map›Paper›PMID 27080739›Full record

ArticleScientific reports2016

Sphingosine 1-phosphate receptor 2 (S1P2) attenuates reactive oxygen species formation and inhibits cell death: implications for otoprotective therapy.

Deron R Herr, Marie J Y Reolo, Yee Xin Peh, Wei Wang, Chang-Wook Lee, Rich Rivera, Ian C Paterson, Jerold Chun

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 53 citations in OpenAlex.

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  6. Activation of S1PCell proliferation · 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

8 authors at 3 institutions in 3 countries.

Deron R HerrDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597.
Marie J Y ReoloDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597.
Yee Xin PehDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597.
Wei WangDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117597.
Chang-Wook LeeDepartment of Molecular and Cellular Neuroscience, Dorris Neuroscience Center, The Scripps Research Institute, La Jolla, CA, USA.
Rich RiveraDepartment of Molecular and Cellular Neuroscience, Dorris Neuroscience Center, The Scripps Research Institute, La Jolla, CA, USA.
Ian C PatersonDepartment of Oral Biology and Biomedical Sciences and Oral Cancer Research &Coordinating Centre, Faculty of Dentistry, University of Malaya, Kuala Lumpur, Malaysia.
Jerold ChunDepartment of Molecular and Cellular Neuroscience, Dorris Neuroscience Center, The Scripps Research Institute, La Jolla, CA, USA.
National University of Singapore · SGScripps Research Institute · USUniversity of Malaya · MY

Funding

Receptor-mediated S1P signaling in the embryonic brainR01DA019674 · NIDA · SCRIPPS RESEARCH INSTITUTE, THE · PI CHUN, JEROLD · 2006 to 2010
$1.9M
NIDA NIH HHS DA019674NIDA NIH HHS R01 DA019674
6 · The paper itself

Abstract

Ototoxic drugs, such as platinum-based chemotherapeutics, often lead to permanent hearing loss through apoptosis of neuroepithelial hair cells and afferent neurons of the cochlea. There is no approved therapy for preventing or reversing this process. Our previous studies identified a G protein-coupled receptor (GPCR), S1P2, as a potential mediator of otoprotection. We therefore sought to identify a pharmacological approach to prevent cochlear degeneration via activation of S1P2. The cochleae of S1pr2(-/-) knockout mice were evaluated for accumulation of reactive oxygen species (ROS) with a nitro blue tetrazolium (NBT) assay. This showed that loss of S1P2 results in accumulation of ROS that precedes progressive cochlear degeneration as previously reported. These findings were supported by in vitro cell-based assays to evaluate cell viability, induction of apoptosis, and accumulation of ROS following activation of S1P2 in the presence of cisplatin. We show for the first time, that activation of S1P2 with a selective receptor agonist increases cell viability and reduces cisplatin-mediated cell death by reducing ROS. Cumulatively, these results suggest that S1P2 may serve as a therapeutic target for attenuating cisplatin-mediated ototoxicity.

Indexed as

AnimalsCell DeathCell SurvivalCochleaMiceMice, KnockoutReactive Oxygen SpeciesReceptors, LysosphingolipidSignal TransductionReactive Oxygen SpeciesReceptors, Lysosphingolipid

Identifiers

PMID27080739
PMCPMC4832229
OpenAlexW2340709304

What OpenQuestion holds

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LicenceCC BY
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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.