ArticlePloS one2012
Zebrafish chemical screening reveals the impairment of dopaminergic neuronal survival by cardiac glycosides.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Neuronal autosis is NaCell death & disease · 2024Article
- Small molecule regulators of microRNAs identified by high-throughput screen coupled with high-throughput sequencing.Nature communications · 2023Article
- NaBiomedicines · 2023Review
- Application of the Transcriptional Disease Signature (TDSs) to Screen Melanoma-Effective Compounds in a Small Fish Model.Scientific reports · 2019Article
- Tp53 gene mediates distinct dopaminergic neuronal damage in different dopaminergic neurotoxicant models.Neural regeneration research · 2017Review
- Advancing toxicology research using in vivo high throughput toxicology with small fish models.ALTEX · 2016Article
- Compartmentalized Platforms for Neuro-Pharmacological Research.Current neuropharmacology · 2016Review
- Cardiotonic Steroids as Modulators of Neuroinflammation.Frontiers in endocrinology · 2016Review
- A High-Content Larval Zebrafish Brain Imaging Method for Small Molecule Drug Discovery.PloS one · 2016Article
- Article
- Analysis of oxidative stress in zebrafish embryos.Journal of visualized experiments : JoVE · 2014Article
- α3Na+/K+-ATPase deficiency causes brain ventricle dilation and abrupt embryonic motility in zebrafish.The Journal of biological chemistry · 2013Article
- Synthetic molecules: helping to unravel plant signal transduction.Journal of chemical biology · 2013Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Parkinson's disease is a neurodegenerative disorder characterized by the prominent degeneration of dopaminergic (DA) neurons among other cell types. Here we report a first chemical screen of over 5,000 compounds in zebrafish, aimed at identifying small molecule modulators of DA neuron development or survival. We find that Neriifolin, a member of the cardiac glycoside family of compounds, impairs survival but not differentiation of both zebrafish and mammalian DA neurons. Cardiac glycosides are inhibitors of Na(+)/K(+) ATPase activity and widely used for treating heart disorders. Our data suggest that Neriifolin impairs DA neuronal survival by targeting the neuronal enriched Na(+)/K(+) ATPase α3 subunit (ATP1A3). Modulation of ionic homeostasis, knockdown of p53, or treatment with antioxidants protects DA neurons from Neriifolin-induced death. These results reveal a previously unknown effect of cardiac glycosides on DA neuronal survival and suggest that it is mediated through ATP1A3 inhibition, oxidative stress, and p53. They also elucidate potential approaches for counteracting the neurotoxicity of this valuable class of medications.
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Registered trials
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