Mesenchymal stem cell exosomes rich in miR-23b-3p affect the Wnt signaling pathway and promote neuronal autophagy to alleviate PD symptoms
•miR-23b-3p-enriched exosomes promotes autophagy in MN9D cells in PD cell model.•Activation of the Wnt/β-Catenin pathway promotes neuronal autophagy in a cell model of PD.•MSC-exo rich in miR-23b-3p promote neuronal autophagy by regulating Wnt signaling pathway. This study aims to elucidate the role...
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Veröffentlicht in: | Neuroscience letters 2023-09, Vol.814, p.137437-137437, Article 137437 |
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Sprache: | eng |
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Zusammenfassung: | •miR-23b-3p-enriched exosomes promotes autophagy in MN9D cells in PD cell model.•Activation of the Wnt/β-Catenin pathway promotes neuronal autophagy in a cell model of PD.•MSC-exo rich in miR-23b-3p promote neuronal autophagy by regulating Wnt signaling pathway.
This study aims to elucidate the role of miR-23b-3p in mesenchymal stem cell exosomes in regulating the Wnt signaling pathway to promote autophagy of neurons and alleviate Parkinson's disease (PD) symptoms. We generated rat and cellular PD models with 6-OHDA, treated them with mesenchymal stem cell exosomes rich in miR-23b-3p and determined the expression of α-syn and Wnt/β-catenin pathway and autophagy-related genes. In the plasma of PD patients, the levels of miR-23b-3p and the Wnt/β-catenin pathway-related genes β-catenin and DAT were low, while α-syn expression was high. In the PD cell model, miR-23b-3p was downregulated, the Wnt pathway was inhibited, α-syn was upregulated, neuron autophagy was inhibited, and the revitalization of the Wnt/β-catenin pathway could promote the autophagy of neurons. Coculture of miR-23b-3p-enriched exosomes with MN9D cells confirmed that miR-23b-3p-enriched exosomes could promote autophagy in MN9D cells in a PD cell model. Moreover, animal experiments confirmed the results of the cell experiments. Therefore, miR-23b-3p-enriched mesenchymal stem cell exosomes promote neuronal autophagy by regulating the Wnt signaling pathway, thus alleviating PD progression and providing an important basis for the clinical treatment of PD. |
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ISSN: | 0304-3940 1872-7972 |
DOI: | 10.1016/j.neulet.2023.137437 |