ArticleMedical science monitor : international medical journal of experimental and clinical research2020
Overexpression of MicroRNA-133a Inhibits Apoptosis and Autophagy in a Cell Model of Parkinson's Disease by Downregulating Ras-Related C3 Botulinum Toxin Substrate 1 (RAC1).
Article in Medical science monitor : international medical journal of experimental and clinical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Gentisic acid ameliorates lumbar disc herniation by regulating M1/M2 Polarization via the MAPK14/S100A9/Rac1/2 pathway.Cell biology and toxicology · 2025Article
- The Potential of Targeting Autophagy-Related Non-coding RNAs in the Treatment of Alzheimer's and Parkinson's Diseases.Cellular and molecular neurobiology · 2024Review
- The role of microRNAs in neurodegenerative diseases: a review.Cell biology and toxicology · 2023Review
- Amorfrutin B Protects Mouse Brain Neurons from Hypoxia/Ischemia by Inhibiting Apoptosis and Autophagy Processes Through Gene Methylation- and miRNA-Dependent Regulation.Molecular neurobiology · 2023Article
- miR-133a-3p/TRPM4 axis improves palmitic acid induced vascular endothelial injury.Frontiers in pharmacology · 2023Article
- Autophagy and Its Association with Genetic Mutations in Parkinson Disease.Medical science monitor : international medical journal of experimental and clinical research · 2022Review
- Overexpression of MicroRNA-133a Inhibits Apoptosis and Autophagy in a Cell Model of Parkinson's Disease by Downregulating Ras-Related C3 Botulinum Toxin Substrate 1 (RAC1).Medical science monitor : international medical journal of experimental and clinical research · 2022Article
- The Role of Non-Coding RNAs in the Pathogenesis of Parkinson's Disease: Recent Advancement.Pharmaceuticals (Basel, Switzerland) · 2022Review
- MicroRNAs in the pathophysiology of Alzheimer's disease and Parkinson's disease: an overview.Molecular neurobiology · 2022Review
- miR-133a targets YES1 to reduce cisplatin resistance in ovarian cancer by regulating cell autophagy.Cancer cell international · 2022Article
- Crosstalk between regulatory non-coding RNAs and oxidative stress in Parkinson's disease.Frontiers in aging neuroscience · 2022Review
- Virus, Exosome, and MicroRNA: New Insights into Autophagy.Advances in experimental medicine and biology · 2022Article
- Parkinson's disease and microRNAs - Lessons from model organisms and human studies.Experimental gerontology · 2021Review
Corrections and comments
- Retracted
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Parkinson's disease (PD) is a movement disorder. microRNA (miR)-133 expression is reduced in PD patients and in mice with a dopamine neuron deficiency. We aimed to identify the mechanism of miR-133a in apoptosis and autophagy in PD. MATERIAL AND METHODS The optimal concentration of MPP⁺ (1-methyl-4-phenylpyridinium ion) was initially determined to construct a PD cell model. Gain-of function experiments were carried out to evaluate the role of miR-133a in PD. The levels of miR-133a, RAC1 (Ras-related C3 botulinum toxin substrate 1), apoptosis-related factors, and autophagy-related factors were detected after detection of cell proliferation, cell cycle, and apoptosis. Transmission electron microscopy was applied to observe autophagosomes, and immunofluorescence staining was performed to detect LC3 and further analyze the effect of miR-133a on autophagy in a PD cell model. RESULTS Low miR-133a expression was detected in a cell model of MPP⁺-induced PD. After overexpressing miR-133a, cell proliferation increased, and apoptosis (cleaved caspase-3 and Bax levels decreased, while Bcl2 levels increased) and autophagy was inhibited (LC3II/I and Beclin-1 levels decreased, while p62 levels increased). MiR-133a targeted RAC1. RACY upregulation attenuated the inhibitory effects of miR-133a on PC12 cell apoptosis and autophagy. CONCLUSIONS Our data highlighted that miR-133a overexpression prevented apoptosis and autophagy in a cell model of MPP⁺-induced PD by inhibiting RAC1 expression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.