ArticleInternational journal of nanomedicine2025
Extracellular Vesicles Derived from FGF2-Primed Astrocytes Against Mitochondrial and Synaptic Toxicities in Parkinson's Disease.
Article in International journal of nanomedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- A Novel Reporter Mouse for Astrocyte-Derived Extracellular Vesicles Reveals Enrichment of Cargo at Neuronal Mitochondria.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Article
- Protocol for ultracentrifugation-based isolation and characterization of extracellular vesicles from FGF2-primed astrocytes.STAR protocols · 2026Article
- Olfactory Mucosa MSCs-Derived Exosomal RPL6 Attenuates Seizure-Induced Neuronal Damage via FGF2-Mediated Oxidative Stress and Mitophagy.Neurochemical research · 2026Article
- Small Extracellular Vesicles from Neural Cells: Physiological and Pathological Roles, and Potential in Neurodegenerative Therapy.Advanced healthcare materials · 2026Review
- A novel reporter mouse for astrocyte-derived extracellular vesicles reveals trafficking of cargo to neuronal mitochondria.bioRxiv : the preprint server for biology · 2026Article
- Dysregulated circRNA-miRNA-mRNA networks reveal stage-specific mRNA expression changes in Parkinson's disease.Molecular brain · 2025Article
- Astrocyte alterations in α-synucleinopathies.Frontiers in cellular neuroscience · 2025Review
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8 authors.
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Abstract
Purpose: Mitochondrial dysfunction associated with neuronal degeneration and subsequent synaptic disconnection are essential for the development of Parkinson's disease (PD). Considering that astrocytes play key roles in synaptogenesis during development, we hypothesized that fibroblast growth factor - 2 (FGF2), a key factor for astrocyte development, could reverse the toxic phenotype of reactive astrocytes, and the extracellular vesicles (EVs) derived from FGF2-primed astrocytes would enhance synaptogenesis in PD model. The present study was to test this hypothesis. Methods: EVs isolated from FGF2-primed astrocytes (FGF2-EVs) were characterized by transmission electron microscopy and nanoparticle tracking analysis. FGF2-EVs were applied to both in vitro and in vivo models of PD. EVs derived from naïve astrocytes (CON-EV) were used as control. Mitochondrial alterations, neuronal survival, synaptogenesis, and mice behavior were subsequently evaluated by quantitative real-time polymerase chain reaction, Western-blotting, immunohistochemistry, and CatWalk gait analysis. To dissect the underlying mechanisms, proteomic analysis and small interfering RNA (siRNA) mediated gene silencing were adopted. Results: FGF2 treatment restored the expression of neural progenitor markers and suppressed the levels of A1 astrocytic markers in MPP Conclusion: EVs from FGF2-primed astrocytes are superior in protecting PD mice against mitochondrial and synaptic toxicities, possibly through NCAM1, which could be used as a therapeutic strategy for PD.
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