ArticleNeurotoxicity research2021
LncRNA JHDM1D-AS1 Suppresses MPP + -Induced Neuronal Injury in Parkinson's Disease via miR-134-5p/PIK3R3 Axis.
Article in Neurotoxicity research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Epigenetic mechanisms of Parkinson's disease and potential epigenetic-based therapeutics.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Review
- Non-coding RNAs in Parkinson's Disease: Pathogenesis, Exosomes, and Therapeutic Horizons.Cellular and molecular neurobiology · 2025Review
- MicroRNA-21-5p from induced pluripotent stem cells promotes neuroprotection of retinal ganglion cells in optic nerve crush model.BMC ophthalmology · 2025Article
- LncRNAs Orchestrating Neuroinflammation: A Comprehensive Review.Cellular and molecular neurobiology · 2025Review
- Blood-derived microRNAs are related to cognitive domains in the general population.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- KDM7A-DT induces genotoxic stress, tumorigenesis, and progression of p53 missense mutation-associated invasive breast cancer.Frontiers in oncology · 2024Article
- The Emerging Role of Autophagy-Associated lncRNAs in the Pathogenesis of Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- Crosstalk between regulatory non-coding RNAs and oxidative stress in Parkinson's disease.Frontiers in aging neuroscience · 2022Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is a multi-factorial neurodegenerative disease. Long noncoding RNAs (lncRNAs) have been revealed to be involved in the process of PD. Herein, this study aimed to investigate the potential function and mechanism of JHDM1D-AS1 (JHDM1D antisense 1) in PD process. 1-Methyl-4-phenylpyridinium (MPP +)-induced SK-N-SH cells were used to conduct expression and function analyses. Levels of genes and proteins were examined using real-time reverse transcription PCR (RT-qPCR) and Western blot. Cell viability and apoptosis were determined using CCK-8 assay, flow cytometry, and Western blot, respectively. ELISA analysis was performed for the detection of interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α. The contents of lactate dehydrogenase (LDH), superoxide dismutase (SOD), and malondialdehyde (MDA) were measured using commercial kits. The direct interactions between miR-134-5p and PIK3R3 (Phosphoinositide-3-Kinase Regulatory Subunit 3) or JHDM1D-AS1 were verified by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. JHDM1D-AS1 expression was decreased by MPP + in SK-N-SH cells in a dose- or time-dependent manner. Functionally, JHDM1D-AS1 overexpression attenuated MPP + -evoked neuronal apoptosis, inflammation, and oxidative stress. Mechanistically, JHDM1D-AS1 competitively bound to miR-134-5p to upregulate the expression of its target PIK3R3. Rescue experiments suggested that miR-134-5p upregulation reversed the inhibitory effects of JHDM1D-AS1 on MPP + -induced neuronal injury. Moreover, inhibition of miR-134-5p protected neurons against MPP + -induced neuronal apoptosis, inflammation, and oxidative stress, which were abolished by PIK3R3 silencing. JHDM1D-AS1 protected against MPP + -induced neuron injury via miR-134-5p/PIK3R3 axis, suggesting the potential involvement of this axis in PD process.
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