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Exosomes derived from mesenchymal stem cells overexpressing miR-210 inhibits neuronal inflammation and contribute to neurite outgrowth through modulating microglia polarization
- Source :
- Open Medicine, Vol 18, Iss 1, Pp 6138-35 (2023)
- Publication Year :
- 2023
- Publisher :
- De Gruyter, 2023.
-
Abstract
- Inflammatory responses play a critical role in the progress of neurodegenerative disorders. MSC-Exos is considered to have an anti-inflammatory effect on the treatment strategy for brain injury. However, the therapeutic effect and possible mechanism of Exosomal miR-210 on microglia polarization-induced neuroinflammation and neurite outgrowth have not been reported. MSC-Exos were isolated by ultracentrifugation, identified by Nanosight NS300, transmission electron microscopy, and western bolt. In vitro, to explore the protective mechanism of MSC-Exos against neuroinflammation, the microglial BV2 cell was exposed to lipopolysaccharide to assess inflammatory changes. The intake of 1,1’-dioctadecyl-3,3,3’,3’-tetramethylindocarbocyanine perchlorate (Dil)-MSC-Exos into microglia was observed by fluorescence microscopy. The results showed that Exosomal miR-210 treatment significantly inhibited the production of nitric oxide and pro-inflammatory cytokines. Exosomal miR-210 treatment also increased the number of M2 microglia cells and inhibited M1 microglia polarization. In addition, western blot demonstrated that Exosomal miR-210 reduced neuronal apoptosis. Thus, Exosomal miR-210 attenuated neuronal inflammation and promoted neurite outgrowth. Exosomal miR-210 from MSCs attenuated neuronal inflammation and contributed to neurogenesis possibly by inhibiting microglial M1 polarization.
- Subjects :
- exosomes
mesenchymal stem cells
microglia polarization
mir-210
Medicine
Subjects
Details
- Language :
- English
- ISSN :
- 23915463 and 20220618
- Volume :
- 18
- Issue :
- 1
- Database :
- Directory of Open Access Journals
- Journal :
- Open Medicine
- Publication Type :
- Academic Journal
- Accession number :
- edsdoj.83ea28cc7e49159e3f2cec9a9204e6
- Document Type :
- article
- Full Text :
- https://doi.org/10.1515/med-2022-0618