ArticleJournal of molecular neuroscience : MN2017
Let-7d microRNA Attenuates 6-OHDA-Induced Injury by Targeting Caspase-3 in MN9D Cells.
Article in Journal of molecular neuroscience : MN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Non-coding RNAs in Parkinson's Disease: Pathogenesis, Exosomes, and Therapeutic Horizons.Cellular and molecular neurobiology · 2025Review
- MicroRNAs in the Mouse Developing Retina.International journal of molecular sciences · 2023Review
- Chronic delta-9-tetrahydrocannabinol (THC) treatment counteracts SIV-induced modulation of proinflammatory microRNA cargo in basal ganglia-derived extracellular vesicles.Journal of neuroinflammation · 2022Article
- Crosstalk between regulatory non-coding RNAs and oxidative stress in Parkinson's disease.Frontiers in aging neuroscience · 2022Review
- Parkinson's disease and microRNAs - Lessons from model organisms and human studies.Experimental gerontology · 2021Review
- Non-Coding RNAs in the Brain-Heart Axis: The Case of Parkinson's Disease.International journal of molecular sciences · 2020Review
- Role of MicroRNAs in Parkinson's Disease.International journal of molecular sciences · 2019Review
- Wnt/β-Catenin Signaling Pathway Governs a Full Program for Dopaminergic Neuron Survival, Neurorescue and Regeneration in the MPTP Mouse Model of Parkinson's Disease.International journal of molecular sciences · 2018Review
- Comparison of Rat Primary Midbrain Neurons Cultured in DMEM/F12 and Neurobasal Mediums.Basic and clinical neuroscienceArticle
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Parkinson's disease (PD) mainly results from the progressive loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc), and the exact underlying mechanisms of the loss of DA neurons in PD remains largely unclear. The results of our previous work showed that let-7d was significantly downregulated in a 6-OHDA-induced cellular model of PD. However, the exact effect of let-7d on DA neural cells was unclear. In MN9D dopaminergic neuronal cells, we used a let-7d mimic and inhibitor to upregulate and downregulate the expression of let-7d, respectively, a cell counting kit to assess cell viability, and a TUNEL staining assay and flow cytometry to examine the cell death rate, and we found that let-7d could negatively regulate 6-OHDA-induced cell injury. Then, we verified that caspase-3 was a target gene of let-7d by using a dual-luciferase reporter system. Furthermore, using caspase-3 siRNA and a caspase-3-overexpression vector (without the 3'UTR) to respectively inhibit and increase the expression of caspase-3, we found that caspase-3 siRNA could reverse the cell injury induced by the let-7d inhibitor and that caspase-3 overexpression could reverse the protective effects of the let-7d mimic on 6-OHDA-induced cell injury. Taken together, these findings strongly suggest that let-7d plays an important role in DA neuronal cell injury and that the effects of let-7d are, at least in part, via the suppression of caspase-3 expression.
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