ArticleAging2024
miR-101a-3p/ROCK2 axis regulates neuronal injury in Parkinson's disease models.
Article in Aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Translating Exosomal microRNAs from Bench to Bedside in Parkinson's Disease.Brain sciences · 2025Review
- Protective effects of harpagoside on mitochondrial functions in rotenone‑induced cell models of Parkinson's disease.Biomedical reports · 2025Article
- Corydaline Alleviates 1-Methyl-4-Phenylpyridium (MPPNeurochemical research · 2025Article
- New insights on the regulators and inhibitors of RhoA-ROCK signalling in Parkinson's disease.Metabolic brain disease · 2025Review
- Reduced levels of nitrated α-synuclein in the protective effect of harpagoside on rotenone-induced cellular models of Parkinson's disease.Frontiers in cell and developmental biology · 2025Article
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Authors and funding
7 authors.
Funding
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Abstract
backgroundParkinson's disease (PD) is a neurodegenerative disease characterized by the loss of dopaminergic neurons in substantia nigra pars compacta (SNpc). This study focuses on deciphering the role of microRNA (miR)-101a-3p in the neuronal injury of PD and its regulatory mechanism.
methodsWe constructed a mouse model of PD by intraperitoneal injection of 1-methyl 4-phenyl 1, 2, 3, 6-tetrahydropyridine hydrochloride (MPTP), and used 1-methyl-4-phenylpyridinium (MPP+) to treat Neuro-2a cells to construct an
resultsLow miR-101a-3p expression and high ROCK2 expression were found in the brain tissues of PD mice and MPP+-treated Neuro-2a cells; PD mice showed decreased neurological disorders, and apoptosis of Neuro-2a cells was increased after MPP+ treatment, both of which were accompanied by increased accumulation of α-synuclein protein. After miR-101a-3p was overexpressed, the neurological function of PD mice was improved, and the apoptosis of Neuro-2a cells induced by MPP+ was alleviated, and the accumulation of α-synuclein protein was reduced; ROCK2 overexpression counteracted the protective effect of miR-101a-3p. Additionally, ROCK2 was identified as the direct target of miR-101a-3p.
conclusionMiR-101a-3p can reduce neuronal apoptosis and neurological deficit in PD mice by inhibiting ROCK2 expression, suggesting that miR-101a-3p is a promising therapeutic target for PD.
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