Please use this identifier to cite or link to this item: https://doi.org/10.1038/srep24541
Title: Sphingosine 1-phosphate receptor 2 (S1P2) attenuates reactive oxygen species formation and inhibits cell death: Implications for otoprotective therapy
Authors: Herr, D.R 
Reolo, M.J.Y 
Peh, Y.X 
Wang, W 
Lee, C.-W
Rivera, R
Paterson, I.C
Chun, J
Keywords: reactive oxygen metabolite
sphingosine 1 phosphate receptor
agonists
animal
cell death
cell survival
cochlea
drug effects
genetics
knockout mouse
metabolism
mouse
pathology
signal transduction
Animals
Cell Death
Cell Survival
Cochlea
Mice
Mice, Knockout
Reactive Oxygen Species
Receptors, Lysosphingolipid
Signal Transduction
Issue Date: 2016
Publisher: Nature Publishing Group
Citation: Herr, D.R, Reolo, M.J.Y, Peh, Y.X, Wang, W, Lee, C.-W, Rivera, R, Paterson, I.C, Chun, J (2016). Sphingosine 1-phosphate receptor 2 (S1P2) attenuates reactive oxygen species formation and inhibits cell death: Implications for otoprotective therapy. Scientific Reports 6 : 24541. ScholarBank@NUS Repository. https://doi.org/10.1038/srep24541
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.
Source Title: Scientific Reports
URI: https://scholarbank.nus.edu.sg/handle/10635/174977
ISSN: 20452322
DOI: 10.1038/srep24541
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