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5 results on '"Stellacci F"'

1. FM19G11-Loaded Gold Nanoparticles Enhance the Proliferation and Self-Renewal of Ependymal Stem Progenitor Cells Derived from ALS Mice

Author

Marcuzzo S, Isaia D, Bonanno S, Malacarne C, Cavalcante P, Zacheo A, Laquintana V, Denora N, Sanavio B, Salvati E, Andreozzi P, Stellacci F, Krol S, Mellado-López M, Mantegazza R, Moreno-Manzano V, and Bernasconi P

Subjects
amyotrophic lateral sclerosis, nanoparticles, G93A-SOD1 mouse model, ependymal stem progenitor cells
Abstract

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease affecting motor neurons. In ALS mice, neurodegeneration is associated with the proliferative restorative attempts of ependymal stem progenitor cells (epSPCs) that normally lie in a quiescent in the spinal cord. Thus, modulation of the proliferation of epSPCs may represent a potential strategy to counteract neurodegeneration. Recent studies demonstrated that FM19G11, a hypoxia-inducible factor modulator, induces epSPC self-renewal and proliferation. The aim of the study was to investigate whether FM19G11-loaded gold nanoparticles (NPs) can affect self-renewal and proliferation processes in epSPCs isolated from G93A-SOD1 mice at disease onset. We discovered elevated levels of SOX2, OCT4, AKT1, and AKT3, key genes associated with pluripotency, self-renewal, and proliferation, in G93A-SOD1 epSPCs at the transcriptional and protein levels after treatment with FM19G11-loaded NPs. We also observed an increase in the levels of the mitochondrial uncoupling protein (UCP) gene in treated cells. FM19G11-loaded NPs treatment also affected the expression of the cell cycle-related microRNA (miR)-19a, along with its target gene PTEN, in G93A-SOD1 epSPCs. Overall our findings establish the significant impact of FM19G11-loaded NPs on the cellular pathways involved in self-renewal and proliferation in G93A-SOD1 epSPCs, thus providing an impetus to the design of novel tailored approaches to delay ALS disease progression.

Published
2019

2. FM19G11-Loaded Gold Nanoparticles Enhance the Proliferation and Self-Renewal of Ependymal Stem Progenitor Cells Derived from ALS Mice

Author

Marcuzzo, S, Isaia, D, Bonanno, S, Malacarne, C, Cavalcante, P, Zacheo, A, Laquintana, V, Denora, N, Sanavio, B, Salvati, E, Andreozzi, P, Stellacci, F, Krol, S, Mellado-López, M, Mantegazza, R, Moreno-Manzano, V, Bernasconi, P, Marcuzzo, Stefania, Isaia, Davide, Bonanno, Silvia, Malacarne, Claudia, Cavalcante, Paola, Zacheo, Antonella, Laquintana, Valentino, Denora, Nunzio, Sanavio, Barbara, Salvati, Elisa, Andreozzi, Patrizia, Stellacci, Francesco, Krol, Silke, Mellado-López, Maravillas, Mantegazza, Renato, Moreno-Manzano, Victoria, Bernasconi, Pia, Marcuzzo, S, Isaia, D, Bonanno, S, Malacarne, C, Cavalcante, P, Zacheo, A, Laquintana, V, Denora, N, Sanavio, B, Salvati, E, Andreozzi, P, Stellacci, F, Krol, S, Mellado-López, M, Mantegazza, R, Moreno-Manzano, V, Bernasconi, P, Marcuzzo, Stefania, Isaia, Davide, Bonanno, Silvia, Malacarne, Claudia, Cavalcante, Paola, Zacheo, Antonella, Laquintana, Valentino, Denora, Nunzio, Sanavio, Barbara, Salvati, Elisa, Andreozzi, Patrizia, Stellacci, Francesco, Krol, Silke, Mellado-López, Maravillas, Mantegazza, Renato, Moreno-Manzano, Victoria, and Bernasconi, Pia

Abstract

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease affecting motor neurons. In ALS mice, neurodegeneration is associated with the proliferative restorative attempts of ependymal stem progenitor cells (epSPCs) that normally lie in a quiescent in the spinal cord. Thus, modulation of the proliferation of epSPCs may represent a potential strategy to counteract neurodegeneration. Recent studies demonstrated that FM19G11, a hypoxia-inducible factor modulator, induces epSPC self-renewal and proliferation. The aim of the study was to investigate whether FM19G11-loaded gold nanoparticles (NPs) can affect self-renewal and proliferation processes in epSPCs isolated from G93A-SOD1 mice at disease onset. We discovered elevated levels of SOX2, OCT4, AKT1, and AKT3, key genes associated with pluripotency, self-renewal, and proliferation, in G93A-SOD1 epSPCs at the transcriptional and protein levels after treatment with FM19G11-loaded NPs. We also observed an increase in the levels of the mitochondrial uncoupling protein (UCP) gene in treated cells. FM19G11-loaded NPs treatment also affected the expression of the cell cycle-related microRNA (miR)-19a, along with its target gene PTEN, in G93A-SOD1 epSPCs. Overall our findings establish the significant impact of FM19G11-loaded NPs on the cellular pathways involved in self-renewal and proliferation in G93A-SOD1 epSPCs, thus providing an impetus to the design of novel tailored approaches to delay ALS disease progression.

Published
2019

3. FM19G11-Loaded Gold Nanoparticles Enhance the Proliferation and Self-Renewal of Ependymal Stem Progenitor Cells Derived from ALS Mice

Author

Antonella Zacheo, Barbara Sanavio, Claudia Malacarne, Davide Isaia, Victoria Moreno-Manzano, Francesco Stellacci, Patrizia Andreozzi, Silke Krol, Stefania Marcuzzo, Nunzio Denora, Pia Bernasconi, Maravillas Mellado-López, Valentino Laquintana, Elisa Salvati, Renato Mantegazza, Silvia Bonanno, Paola Cavalcante, Marcuzzo, S, Isaia, D, Bonanno, S, Malacarne, C, Cavalcante, P, Zacheo, A, Laquintana, V, Denora, N, Sanavio, B, Salvati, E, Andreozzi, P, Stellacci, F, Krol, S, Mellado-López, M, Mantegazza, R, Moreno-Manzano, V, and Bernasconi, P

Subjects
Pluripotent Stem Cells, amyotrophic lateral sclerosis, Cell, AKT1, Metal Nanoparticles, Mice, Transgenic, AKT3, Article, Superoxide Dismutase-1, Nanoparticle, SOX2, Ependyma, microRNA, medicine, FM19G11, PTEN, Animals, Humans, Uncoupling Protein 2, Progenitor cell, Cell Self Renewal, lcsh:QH301-705.5, Amyotrophic lateral sclerosi, Cell Proliferation, biology, SOXB1 Transcription Factors, Stem Cells, Neurodegeneration, Cell Cycle, PTEN Phosphohydrolase, General Medicine, G93A-SOD1 mouse model, medicine.disease, Cell biology, MicroRNAs, medicine.anatomical_structure, Ependymal stem progenitor cell, Gene Expression Regulation, lcsh:Biology (General), Benzamides, biology.protein, nanoparticles, Gold, Octamer Transcription Factor-3, Proto-Oncogene Proteins c-akt, Biomarkers, ependymal stem progenitor cells
Abstract

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease affecting motor neurons. In ALS mice, neurodegeneration is associated with the proliferative restorative attempts of ependymal stem progenitor cells (epSPCs) that normally lie in a quiescent in the spinal cord. Thus, modulation of the proliferation of epSPCs may represent a potential strategy to counteract neurodegeneration. Recent studies demonstrated that FM19G11, a hypoxia-inducible factor modulator, induces epSPC self-renewal and proliferation. The aim of the study was to investigate whether FM19G11-loaded gold nanoparticles (NPs) can affect self-renewal and proliferation processes in epSPCs isolated from G93A-SOD1 mice at disease onset. We discovered elevated levels of SOX2, OCT4, AKT1, and AKT3, key genes associated with pluripotency, self-renewal, and proliferation, in G93A-SOD1 epSPCs at the transcriptional and protein levels after treatment with FM19G11-loaded NPs. We also observed an increase in the levels of the mitochondrial uncoupling protein (UCP) gene in treated cells. FM19G11-loaded NPs treatment also affected the expression of the cell cycle-related microRNA (miR)-19a, along with its target gene PTEN, in G93A-SOD1 epSPCs. Overall our findings establish the significant impact of FM19G11-loaded NPs on the cellular pathways involved in self-renewal and proliferation in G93A-SOD1 epSPCs, thus providing an impetus to the design of novel tailored approaches to delay ALS disease progression.

Published
2019

4. Antiviral Mechanism of Virucidal Sialic Acid Modified Cyclodextrin.

Author

Zhu Y, Sysoev AA, Silva PHJ, Batista M, and Stellacci F

Abstract

We have reported that CD-6'SLN [6-sialyllactosamine (6'SLN)-modified β-cyclodextrin (CD)] can be a potential anti-influenza drug because it irreversibly deactivates virions. Indeed, in vivo, CD-6'SLN improved mice survival in an H1N1 infection model even when administered 24 h post-infection. Although CD-6'SLN was designed to target the viral envelope protein hemagglutinin (HA), a natural receptor of 6'SLN, it remains unclear whether other targets exist. In this study, we confirm that CD-6'SLN inhibits the influenza virus through an extracellular mechanism by interacting with HA, but not with neuraminidase (NA), despite the latter also having a binding pocket for the sialyl group. We find that CD-6'SLN interacts with the viral envelope as it elicits the release of a fluorophore embedded in the membrane. Two similar compounds were designed to test separately the effect of 6'SLN and of the undecyl moiety that links the CD to 6'SLN. Neither showed any interaction with the membrane nor the irreversible viral inhibition (virucidal), confirming that both components are essential to membrane interaction and virucidal action. Unlike similar antiviral cyclodextrins developed against other viruses, CD-6'SLN was not able to decapsulate viral RNA. Our findings support that combining viral protein-specific epitopes with hydrophobic linkers provides a strategy for developing antiviral drugs with a virucidal mechanism.

Published
2023
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5. The Clustering of mApoE Anti-Amyloidogenic Peptide on Nanoparticle Surface Does Not Alter Its Performance in Controlling Beta-Amyloid Aggregation.

Author

Corti R, Cox A, Cassina V, Nardo L, Salerno D, Marrano CA, Missana N, Andreozzi P, Silva PJ, Stellacci F, Dal Magro R, Re F, and Mantegazza F

Subjects
Alzheimer Disease metabolism, Amyloid metabolism, Brain metabolism, Cluster Analysis, Gold chemistry, Humans, Plaque, Amyloid metabolism, Protein Binding physiology, Amyloid beta-Peptides metabolism, Apolipoproteins E metabolism, Metal Nanoparticles chemistry, Peptide Fragments metabolism
Abstract

The deposition of amyloid-β (Aβ) plaques in the brain is a significant pathological signature of Alzheimer's disease, correlating with synaptic dysfunction and neurodegeneration. Several compounds, peptides, or drugs have been designed to redirect or stop Aβ aggregation. Among them, the trideca-peptide CWG-LRKLRKRLLR (mApoE), which is derived from the receptor binding sequence of apolipoprotein E, is effectively able to inhibit Aβ aggregation and to promote fibril disaggregation. Taking advantage of Atomic Force Microscopy (AFM) imaging and fluorescence techniques, we investigate if the clustering of mApoE on gold nanoparticles (AuNP) surface may affect its performance in controlling Aβ aggregation/disaggregation processes. The results showed that the ability of free mApoE to destroy preformed Aβ fibrils or to hinder the Aβ aggregation process is preserved after its clustering on AuNP. This allows the possibility to design multifunctional drug delivery systems with clustering of anti-amyloidogenic molecules on any NP surface without affecting their performance in controlling Aβ aggregation processes., Competing Interests: The authors declare no conflict of interest.

Published
2020
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