ArticleFrontiers in cellular neuroscience2021
MiR-30c-5p/ATG5 Axis Regulates the Progression of Parkinson's Disease.
Article in Frontiers in cellular neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 21 citations in OpenAlex.
- Mitochondria-Associated MicroRNAs: Emerging Roles in the Pathogenesis of Parkinson's Disease.Biomedicines · 2026Review
- Role of microRNAs in major brain diseases, focusing on neuroinflammation and neuronal apoptosis.Iranian journal of basic medical sciences · 2026Review
- Navigating the Autophagy Maze: ATG and Their Impact on Neurodegenerative Diseases.Molecular neurobiology · 2025Review
- Non-coding RNAs in Parkinson's Disease: Pathogenesis, Exosomes, and Therapeutic Horizons.Cellular and molecular neurobiology · 2025Review
- Relationship of Autophagic Dysfunction With the Quality of Life and Sleep, Depression and Disease Severity in Patients With Restless Legs Syndrome.Brain and behavior · 2025Article
- Unraveling Dysregulated Cell Signaling Pathways, Genetic and Epigenetic Mysteries of Parkinson's Disease.Molecular neurobiology · 2024Review
- STM2457 Inhibits METTL3-Mediated m6A Modification of miR-30c to Alleviate Spinal Cord Injury by Inducing the ATG5-Mediated Autophagy.Neurospine · 2024Article
- Autophagy-associated non-coding RNAs: Unraveling their impact on Parkinson's disease pathogenesis.CNS neuroscience & therapeutics · 2024Review
- MicroRNAs regulating autophagy: opportunities in treating neurodegenerative diseases.Frontiers in neuroscience · 2024Review
- Gender differences in microRNA expression in levodopa-naive PD patients.Journal of neurology · 2023Article
- Autophagy‑regulating miRNAs: Novel therapeutic targets for Parkinson's disease (Review).International journal of molecular medicine · 2023Review
- ATG5 provides host protection acting as a switch in the atg8ylation cascade between autophagy and secretion.Developmental cell · 2023Article
- Emerging Role of MicroRNA-30c in Neurological Disorders.International journal of molecular sciences · 2022Review
- Article
- Insulin-like growth factor 2 and autophagy gene expression alteration arise as potential biomarkers in Parkinson's disease.Scientific reports · 2022Article
- Influence of age and sex on microRNA response and recovery in the hippocampus following sepsis.Aging · 2022Article
- miRNA and antisense oligonucleotide-based α-synuclein targeting as disease-modifying therapeutics in Parkinson's disease.Frontiers in pharmacology · 2022Review
- Non-coding RNAs and their bioengineering applications for neurological diseases.Bioengineered · 2021Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Serum miR-30c-5p correlates with Parkinson's disease (PD), yet its role has not been illustrated. This research analyzed the function of miR-30c-5p in PD. The behavioral evaluation was performed on MPTP-treated PD mice transfected with miR-30c-5p agomiR, antagomiR, siATG5, or 3-MA (an autophagy inhibitor). Oxidative stress-related factors, miR-30c-5p, and apoptosis- and autophagy-associated proteins in brain tissues or cells were determined by molecular experiments. Tyrosine hydroxylase (TH) and dopamine metabolic markers were detected using immunofluorescence and Diode Array Detector (DAD), respectively. Effects of miR-30c-5p and its target gene Autophagy-related gene (ATG) 5 protein (ATG5) on MPP+-treated SH-SY5Y cells were determined through a series of molecular experiments. MiR-30c-5p was upregulated but ATG5 was downregulated in PD mice. MiR-30c-5p antagomiR attenuated the decrease of ATG5 in PD mice. MiR-30c-5p antagomiR partly alleviated the behavioral symptoms and inhibited the increases of malondialdehyde (MDA), catalase (CAT), and SOD in PD mice. The levels of Bcl-2, dopamine, dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), TH, and LC3 II were downregulated in PD mice, while Bax, cleaved caspase-3, P62, and LC3 I were upregulated. However, miR-30c-5p antagomiR partly reversed the levels of these factors in PD mice. 3-MA could block the effects of miR-30c-5p antagomiR on PD mice. MiR-30c-5p antagomiR attenuated apoptosis and induced autophagy in brain tissues of MPTP-treated mice by targeting ATG5.
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