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Published on: October 3, 2012
miR-29c-3p regulates TET2 expression and inhibits autophagy process in Parkinson's disease models
Ruili Wang1, Jie Yao1, Fuhua Gong1
1Department of Geriatric Neurology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Abstract:
Autophagy in dopamine (DA) neurons is concerned to be associated with Parkinson's disease (PD), but the detailed mechanism remains unknown. Herein, we aimed to investigate the function of microRNA (miR)-29c-3p in autophagy in PD models. Intraperitoneal injection of MPTP (20 mg/kg) was given to C57BL/6 mice to establish PD mouse model. SH-SY5Y cells were treated with MPP+ (1 mmol/L) to establish in vitro PD model. The results indicated that in the substantia nigra pars compacta (SNpc) DA neurons of PD mice, autophagy was activated accompanied by down-regulated miR-29c-3p and up-regulated ten-eleven translocation 2 (TET2) expression. Up-regulation of miR-29c-3p inhibited TET2 expression and SNpc (including DA neurons) autophagy in PD mice. In vitro PD model confirmed that MPP+ treatment markedly down-regulated miR-29c-3p expression and up-regulated TET2 expression in SH-SY5Y cells in a dose/time-dependent manner. Moreover, miR-29c-3p up-regulation also inhibited autophagy and TET2 expression in vitro. Additionally, TET2 was proved to be targeted and down-regulated by miR-29c-3p. TET2 knockdown inhibited MPP+ -induced autophagy, whereas TET2 over-expression reversed the effects of miR-29c-3p over-expression on SH-SY5Y cell autophagy. Overall, miR-29c-3p over-expression inhibits autophagy in PD models, which may be mediated by TET2. Our finding may provide new insights for regulating autophagy to improve PD progression.
Insights
MicroRNA-29c-3p, when upregulated, inhibits autophagy in Parkinson's disease models by targeting TET2. This finding offers new strategies for managing Parkinson's disease progression through autophagy regulation.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Autophagy dysfunction in dopamine (DA) neurons is linked to Parkinson's disease (PD), but underlying mechanisms require elucidation.
- MicroRNA-29c-3p (miR-29c-3p) and ten-eleven translocation 2 (TET2) are implicated in cellular processes relevant to neurodegeneration.
Purpose of the Study:
- To investigate the role of miR-29c-3p in regulating autophagy within Parkinson's disease models.
- To determine the mechanistic link between miR-29c-3p, TET2, and autophagy in the context of PD.
Main Methods:
- Establishment of in vivo (MPTP-induced) and in vitro (MPP+-treated SH-SY5Y cells) Parkinson's disease models.
- Analysis of miR-29c-3p and TET2 expression levels and their correlation with autophagy markers.
- Experimental manipulation of miR-29c-3p and TET2 levels (upregulation, knockdown, overexpression) to assess effects on autophagy.
Main Results:
- Parkinson's disease models exhibited decreased miR-29c-3p and increased TET2 expression, alongside activated autophagy in DA neurons.
- Upregulation of miR-29c-3p suppressed TET2 expression and inhibited autophagy in both in vivo and in vitro PD models.
- TET2 was identified as a direct target of miR-29c-3p, and its knockdown mimicked the inhibitory effects of miR-29c-3p on autophagy.
Conclusions:
- miR-29c-3p acts as a negative regulator of autophagy in Parkinson's disease models, potentially through its inhibition of TET2.
- Modulating the miR-29c-3p/TET2 axis presents a potential therapeutic avenue for managing Parkinson's disease progression by controlling autophagy.
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