ArticleMolecular medicine reports2017
The involvement of Eag1 potassium channels and miR-34a in rotenone-induced death of dopaminergic SH-SY5Y cells.
Article in Molecular medicine reports, 2017. 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, 17 citations in OpenAlex.
- MicroRNA‑34a‑5p expression in the plasma and in its extracellular vesicle fractions in subjects with Parkinson's disease: An exploratory study.International journal of molecular medicine · 2021Trial
- New insights into the physiological, pathological and pharmacological roles of voltage‑gated potassium channel Kv10.1 in cancer (Review).International journal of oncology · 2026Review
- Amitriptyline inhibits EAG1 channels by binding to their PAS domains and exerts EAG1-dependent anti-tumorigenic effects.Cancer gene therapy · 2026Article
- Neuronal dysfunction and gene modulation by non-coding RNA in Parkinson's disease and synucleinopathies.Frontiers in cellular neuroscience · 2023Review
- Modulation of miR-181 influences dopaminergic neuronal degeneration in a mouse model of Parkinson's disease.Molecular therapy. Nucleic acids · 2022Article
- Non-Coding RNAs in the Brain-Heart Axis: The Case of Parkinson's Disease.International journal of molecular sciences · 2020Review
- miR-129-5p and miR-130a-3p Regulate VEGFR-2 Expression in Sensory and Motor Neurons during Development.International journal of molecular sciences · 2020Article
- Voltage-Gated Potassium Channels as Regulators of Cell Death.Frontiers in cell and developmental biology · 2020Review
- Excessive Treadmill Training Enhances Brain-Specific MicroRNA-34a in the Mouse Hippocampus.Frontiers in molecular neuroscience · 2020Article
- A Novel Anti-Kv10.1 Nanobody Fused to Single-Chain TRAIL Enhances Apoptosis Induction in Cancer Cells.Frontiers in pharmacology · 2020Article
- miR-34a in Neurophysiology and Neuropathology.Journal of molecular neuroscience : MN · 2019Review
- Signature of Aberrantly Expressed microRNAs in the Striatum of Rotenone-Induced Parkinsonian Rats.Neurochemical research · 2018Article
- Delivery of miRNA-Targeted Oligonucleotides in the Rat Striatum by Magnetofection with NeuromagMolecules (Basel, Switzerland) · 2018Article
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3 authors at 1 institution in 1 country.
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Abstract
The loss of dopaminergic neurons and the resultant motor impairment are hallmarks of Parkinson's disease. The SH‑SY5Y cell line is a model of dopaminergic neurons, and allows for the study of dopaminergic neuronal injury. Previous studies have revealed changes in Ether à go‑go 1 (Eag1) potassium channel expression during p53-induced SH‑SY5Y apoptosis, and the regulatory involvement of microRNA‑34a (miR‑34a) was demonstrated. In the present study, the involvement of Eag1 and miR‑34a in rotenone‑induced SH‑SY5Y cell injury was investigated. Rotenone is a neurotoxin, which is often used to generate models of Parkinson's disease, since it causes the death of nigrostriatal neurons by inducing intracellular aggregation of alpha synuclein and ubiquitin. In the present study, rotenone resulted in a dose‑dependent decrease in cell viability, as revealed by 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyltetrazolium bromide (MTT) and trypan blue cell counting assays. In addition, Eag1 was demonstrated to be constitutively expressed by SH‑SY5Y cells, and involved in cell viability. Suppression of Eag1 with astemizole resulted in a dose‑dependent decrease in cell viability, as revealed by MTT assay. Astemizole also enhanced the severity of rotenone‑induced injury in SH‑SY5Y cells. RNA interference against Eag1, using synthetic small interfering RNAs (siRNAs), corroborated this finding, as siRNAs potentiated rotenone‑induced injury. Eag1‑targeted siRNAs (kv10.1‑3 or EAG1hum_287) resulted in a statistically significant 16.4‑23.5% increase in vulnerability to rotenone. An increased number of apoptotic nuclei were observed in cells transfected with EAG1hum_287. Notably, this siRNA intensified rotenone‑induced apoptosis, as revealed by an increase in caspase 3/7 activity. Conversely, a miR‑34a inhibitor was demonstrated to exert neuroprotective effects. The viability of cells exposed to rotenone for 24 or 48 h and treated with miR‑34a inhibitor was restored by 8.4‑8.8%. In conclusion, Eag1 potassium channels and miR‑34a are involved in the response to rotenone-induced injury in SH‑SY5Y cells. The neuroprotective effect of mir‑34a inhibitors merits further investigations in animal models of Parkinson's disease.
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