ArticleNeurotoxicity research2016
Hair Cell Loss Induced by Sphingosine and a Sphingosine Kinase Inhibitor in the Rat Cochlea.
Article in Neurotoxicity research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
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.
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Who cites it
4 citing papers in PubMed, 14 citations in OpenAlex.
- Estradiol protects hair cells from cisplatin-induced ototoxicity via Nrf2 activation.Redox report : communications in free radical research · 2023Article
- Cisplatin induces calcium ion accumulation and hearing loss by causing functional alterations in calcium channels and exocytosis.American journal of translational research · 2019Article
- Loss of Sphingosine Kinase Alters Life History Traits and Locomotor Function inFrontiers in genetics · 2017Article
- Sphingosine 1-phosphate receptor 2 (S1P2) attenuates reactive oxygen species formation and inhibits cell death: implications for otoprotective therapy.Scientific reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sphingolipid metabolites including ceramide, sphingosine (Sph), and sphingosine-1-phosphate (S1P) play important roles in the regulation of cell survival and death. Sphingosine kinase (Sk) phosphorylates Sph to S1P. Sk is reportedly overexpressed in various cancer cells, and Sk inhibitors are therefore a target of anti-tumor therapy. However, the effects of Sph and Sk inhibitors on cochlear hair cells were unknown. In the present study, expression of Sk isotypes in the cochlea was examined. In addition, the changes in Sk activity induced by cisplatin (CDDP) and the effects of an Sk inhibitor, Sph, and S1P on CDDP ototoxicity were investigated using tissue culture techniques. Cochleae were dissected from Sprague–Dawley rats on postnatal days 3–5. Organ of Corti explants were exposed to 5 lM CDDP for 48 h with or without the Sk inhibitor, Sph, or S1P. Both Sk1 and Sk2 were expressed in the normal cochlea. CDDP activated Sk. The Sk inhibitor itself caused hair cell loss at a high concentration, and at lower concentrations, it increased CDDP-induced hair cell loss. Sph itself also induced hair cell death and increased hair cell loss induced by CDDP. However, S1P decreased hair cell loss induced by CDDP. Sk inhibitor has the function by increasing ototoxic Sph and decreasing otoprotective S1P and therefore potentially causes ototoxicity. Consideration of the possibility of ototoxicity is required in the usage of Sk inhibitors.
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Registered trials
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.