MicroRNA-124 loaded nanoparticles enhance brain repair in Parkinson's disease
Open accessAbstract
Modulation of the subventricular zone (SVZ) neurogenic niche can enhance brain repair in several disorders including Parkinson's disease (PD). Herein, we used biocompatible and traceable polymeric nanoparticles (NPs) containing perfluoro-1,5-crown ether (PFCE) and coated with protamine sulfate to complex microRNA-124 (miR-124), a neuronal fate determinant. The ability of NPs to efficiently deliver miR-124 and prompt SVZ neurogenesis and brain repair in PD was evaluated. In vitro, miR-124 NPs were efficiently internalized by neural stem/progenitors cells and neuroblasts and promoted their neuronal commitment and maturation. The expression of Sox9 and Jagged1, two miR-124 targets and stemness-related genes, were also decreased upon miR-124 NP treatment. In vivo, the intracerebral administration of miR-124 NPs increased the number of migrating neuroblasts that reached the granule cell layer of the olfactory bulb, both in healthy and in a 6-hydroxydopamine (6-OHDA) mouse model for PD. MiR-124 NPs were also able to induce migration of neurons into the lesioned striatum of 6-OHDA-treated mice. Most importantly, miR-124 NPs proved to ameliorate motor symptoms of 6-OHDA mice, monitored by the apomorphine-induced rotation test. Altogether, we provide clear evidences to support the use of miR-124 NPs as a new therapeutic approach to boost endogenous brain repair mechanisms in a setting of neurodegeneration.
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Neural stem cells of subventricular zone treated with miR-124 NPs showed significant proliferation of neuroblasts but lower number of proliferating glial cells or astrocyte-like cells than control.
“Neural stem cells of the subventricular zone treated with microRNA miR-124 NPs showed significant proliferation of neuroblasts (Ki67+/DCX+) but a lower number of proliferating glial cells or astrocyte-like cells (Ki67+/GFAP+) than in the control.”
From Targeted therapy in chronic diseases using nanomaterial-based drug delivery vehicles (2019) · cites this paper as [132]
Apomorphine-induced rotation behavior test confirmed role of miR-124 NPs in ameliorating motor symptoms in PD mouse model.
“An apomorphine-induced rotation behavior test confirmed the role of miR-124 NPs in ameliorating motor symptoms in a PD mouse model (Fig. 4h).132”
From Targeted therapy in chronic diseases using nanomaterial-based drug delivery vehicles (2019) · cites this paper as [132]
A 2.5-fold increase in number of mature neurons indicated that miR-124 NPs promote neuronal differentiation.
“A 2.5-fold increase in the number of mature neurons indicated that miR-124 NPs promote neuronal differentiation.”
From Targeted therapy in chronic diseases using nanomaterial-based drug delivery vehicles (2019) · cites this paper as [132]
Decreased expression of SOX-9 and Jagged1 was observed after miR-124 NPs, which promotes neurogenesis by modulating other signaling pathways.
“Furthermore, decreased expression of SOX-9 and Jagged1 was observed, which promotes neurogenesis by modulating other signaling pathways (Fig. 4c, d).”
From Targeted therapy in chronic diseases using nanomaterial-based drug delivery vehicles (2019) · cites this paper as [132]
miR-124 NPs induced migration of neurons into compromised striatum of PD model.
“miR-124 NPs also induced the migration of neurons into the compromised striatum of the PD model (Fig. 4f, g).”
From Targeted therapy in chronic diseases using nanomaterial-based drug delivery vehicles (2019) · cites this paper as [132]
Polymeric nanoparticles containing perfluoro-1,5-crown ether mediated miR-124 delivery and increased number of migrating neuroblasts in healthy mice and 6-OHDA mouse models for PD.
“Polymeric nanoparticles containing perfluoro-1,5-crown ether mediated miR-124 delivery and increased the number of migrating neuroblasts both in healthy mice and in 6-OHDA mouse models for PD.”
From Targeted therapy in chronic diseases using nanomaterial-based drug delivery vehicles (2019) · cites this paper as [132]
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- Authors
- Saraiva, C., Paiva, J., Santos, T., Ferreira, L., & Bernardino, L.
- Affiliations
- University of Beira Interior (PT)
- Biocant – Associação de Transferência de Tecnologia (PT)
- Corresponding author
- Bernardino, L.
- Venue
- Journal of Controlled Release
- Publisher
- Elsevier BV
- Published
- 2016-08
- Volume
- 235
- Pages
- 291-305
- ISSN
- 0168-3659 (ISSN-L)
- OpenAlex
- W2409318878
- Cited by
- 169
- References
- 69
- Citations by year
- 2026: 4 · 2025: 15 · 2024: 14 · 2023: 25 · 2022: 23 · 2021: 17 · 2020: 22 · 2019: 23 · 2018: 13 · 2017: 10 · 2016: 3
- FWCI
- 8.35
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Licence
- Locations
- Journal of Controlled Release (publishedVersion)
- PubMed (publishedVersion)
- Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) (submittedVersion, other-oa)
- Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) (submittedVersion)
- Funders
- Programa Operacional Temático Factores de Competitividade (EXPL/BIM-MED/0822/2013, FCOMP-01-0124-FEDER-041099, SFRH/BD/79526/2011, SFRH/BD/90365/2012)
- European Commission
- European Research Council (307384)
- Fundação para a Ciência e a Tecnologia
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Interference and Gene Delivery
- Physical Sciences › Materials Science › Biomaterials › Nanoparticle-Based Drug Delivery
- Keywords
- miR-124, Parkinson's disease, polymeric nanoparticles, neural stem/progenitor cells, neuronal differentiation, SOX9, Jagged1, striatum, motor symptoms, brain repair, neurodegeneration, nanoparticle drug delivery
- MeSH terms
- Jagged-1 Protein, Animals, Brain, Disease Models, Animal, Male, Mice, Inbred C57BL, Parkinson Disease, Secondary, Oxidopamine, Lateral Ventricles, MicroRNAs, Nanoparticles, Neurogenesis, SOX9 Transcription Factor, Neural Stem Cells
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