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1.
Med Sci Monit ; 28: e938747, 2022 Oct 26.
Artículo en Inglés | MEDLINE | ID: mdl-36285562

RESUMEN

The manuscript is being retracted due to non-original and duplicated content in the figure images, which raise concerns regarding the credibility of the study. Reference: Wusheng Lu, Jinhuang Lin, Dequan Zheng, Chunyong Hong, Laishun Ke, Xinyu Wu, Peineng Chen. 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). Med Sci Monit, 2020; 26: e922032. DOI: 10.12659/MSM.922032.


Asunto(s)
MicroARNs , Enfermedad de Parkinson , Humanos , Proteína de Unión al GTP rac1/genética , Proteína de Unión al GTP rac1/metabolismo , MicroARNs/genética , Enfermedad de Parkinson/genética , Autofagia/genética , Apoptosis
2.
Med Sci Monit ; 26: e922032, 2020 Jul 27.
Artículo en Inglés | MEDLINE | ID: mdl-32713934

RESUMEN

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.


Asunto(s)
MicroARNs/genética , Enfermedad de Parkinson/genética , 1-Metil-4-fenilpiridinio/farmacología , Animales , Apoptosis/genética , Autofagia/genética , Proliferación Celular/efectos de los fármacos , MicroARNs/metabolismo , Células PC12 , Enfermedad de Parkinson/metabolismo , Enfermedad de Parkinson/patología , Ratas , Receptor IGF Tipo 1/genética , Receptor IGF Tipo 1/metabolismo , Proteína de Unión al GTP rac1/genética , Proteína de Unión al GTP rac1/metabolismo
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