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15 results on '"Pieropan, Francesca"'

1. Amburana cearensis seed extract stimulates astrocyte glutamate homeostatic mechanisms in hippocampal brain slices and protects oligodendrocytes against ischemia

Author

Ferreira, Rafael Short, Ribeiro, Paulo Roberto, Silva, Juliana Helena Castro e, Hoppe, Juliana Bender, de Almeida, Monique Marylin Alves, de Lima Ferreira, Beatriz Correia, Andrade, Gustavo Borges, de Souza, Suzana Braga, Ferdandez, Luzimar Gonzaga, de Fátima Dias Costa, Maria, Salbego, Christianne Gazzana, Rivera, Andrea Domenico, Longoni, Aline, de Assis, Adriano Martimbianco, Pieropan, Francesca, Moreira, José Cláudio Fonseca, Costa, Silvia Lima, Butt, Arthur Morgan, and da Silva, Victor Diogenes Amaral

Published
2023
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3. Agathisflavone Modulates Reactive Gliosis After Trauma and Increases the Neuroblast Population at the Subventricular Zone.

Author

Castro e Silva, Juliana Helena, Pieropan, Francesca, Rivera, Andrea Domenico, Butt, Arthur Morgan, and Costa, Silvia Lima

Abstract

Background: Reactive astrogliosis and microgliosis are coordinated responses to CNS insults and are pathological hallmarks of traumatic brain injury (TBI). In these conditions, persistent reactive gliosis can impede tissue repopulation and limit neurogenesis. Thus, modulating this phenomenon has been increasingly recognized as potential therapeutic approach. Methods: In this study, we investigated the potential of the flavonoid agathisflavone to modulate astroglial and microglial injury responses and promote neurogenesis in the subventricular zone (SVZ) neurogenic niche. Agathisflavone, or the vehicle in controls, was administered directly into the lateral ventricles in postnatal day (P)8-10 mice by twice daily intracerebroventricular (ICV) injections for 3 days, and brains were examined at P11. Results: In the controls, ICV injection caused glial reactivity along the needle track, characterised immunohistochemically by increased astrocyte expression of glial fibrillary protein (GFAP) and the number of Iba-1+ microglia at the lesion site. Treatment with agathisflavone decreased GFAP expression, reduced both astrocyte reactivity and the number of Iba-1+ microglia at the core of the lesion site and the penumbra, and induced a 2-fold increase on the ratio of anti-inflammatory CD206+ to pro-inflammatory CD16/32+ microglia. Notably, agathisflavone increased the population of neuroblasts (GFAP+ type B cells) in all SVZ microdomains by up to double, without significantly increasing the number of neuronal progenitors (DCX+). Conclusions: Although future studies should investigate the underlying molecular mechanisms driving agathisflavone effects on microglial polarization and neurogenesis at different timepoints, these data indicate that agathisflavone could be a potential adjuvant treatment for TBI or central nervous system disorders that have reactive gliosis as a common feature. [ABSTRACT FROM AUTHOR]

Published
2024
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7. Modulation of the PI3K/Akt pathway in oligodendrogenesis

Author

Pieropan, Francesca and Butt, Arthur Morgan

Abstract

Oligodendrocytes are highly specialised cells that ensure the rapid and efficient conduction of impulses by producing myelin, a phospholipid substance that enwraps and insulates the axons. Myelin disruption and oligodendrocytes impairment are hallmarks of many neurodegenerative diseases, such as multiple sclerosis, stroke and Alzheimer's disease. Identifying the multiple aspects that regulate oligodendrogenesis is therefore relevant for new therapies to neurodegenerative diseases. The PI3K/Akt signalling pathway is downstream of multiple factors that regulate oligodendrocyte precursor cells (OPCs) proliferation, survival and differentiation into myelinating oligodendrocytes in the developing CNS. However, its role in the adult CNS is still poorly understood. In this thesis, I used the adult optic nerve and postnatal cerebellar slice ex vivo organotypic culture models to investigate the impact on oligodendrocyte lineage cells by targeting the PI3K/Akt pathway. Transgenic mice models in which expression of fluorescent reporters was driven by the Sox10 and proteolipid protein (PLP) genes, together with microarray, (RT)-qPCR and immunoassays were utilised to identify and evaluate the role of this pathway in driving oligodendrocyte generation. Inhibition of PI3K/Akt was achieved with LY294002, a well-known PI3K inhibitor, and the effects were compared with 3'-O-methylepicatechin, a flavonoid that has been shown to be neuroprotective acting via PI3K/Akt. The results showed that strong inhibition of PI3K/Akt by LY294002 resulted in a dramatic loss of oligodendrocyte lineage cells, whereas partial inhibition of PI3K/Akt by lower doses of LY294002 proved beneficial. Notably, 3'-O-methylepicatechin was also shown to inhibit PI3K/Akt and to be cytoprotective for mature oligodendrocytes and increased MBP mRNA expression. A key objective of this PhD was to synthesise 3,3',4',5,7- pentaacetyl epicatechin, a less hydrophilic derivative of the flavonoid (-)- epicatechin, in order to increase its membrane permeability and potentially facilitate its uptake across the blood-brain barrier. In silico molecular modelling demonstrated that 3,3',4',5,7-pentaacetyl epicatechin had a greater affinity than that of LY294002, epicatechin and 3'-O-methylepicatechin at the ATP-binding site of PI3K, the site of enzyme inhibitions. In addition, immunoassays determined that 3,3',4',5,7-pentaacetyl epicatechin was 200-fold more efficient than LY294002 inducing PI3K/Akt inhibition. Furthermore, 3,3',4',5,7-pentaacetyl epicatechin was shown to be cytoprotective and increase MBP mRNA at nanomolar concentrations, compared to micromolar concentrations for LY294002 and 3'-O-methylepicatechin. This study identified the PI3K/Akt/mTOR pathway as the common mechanism by which LY294002 and the derivatives of epicatechin might exert protective or proliferative effects on oligodendrocytes. Altogether, these findings indicated a potential new strategy to target oligodendrocyte and myelin via development of new pharmacological agents aimed to modulate the PI3K/Akt/mTOR signalling pathway.

Published
2016

8. Additional file 2 of Amburana cearensis seed extract stimulates astrocyte glutamate homeostatic mechanisms in hippocampal brain slices and protects oligodendrocytes against ischemia

Author

Ferreira, Rafael Short, Ribeiro, Paulo Roberto, Silva, Juliana Helena Castro e, Hoppe, Juliana Bender, de Almeida, Monique Marylin Alves, de Lima Ferreira, Beatriz Correia, Andrade, Gustavo Borges, de Souza, Suzana Braga, Ferdandez, Luzimar Gonzaga, de Fátima Dias Costa, Maria, Salbego, Christianne Gazzana, Rivera, Andrea Domenico, Longoni, Aline, de Assis, Adriano Martimbianco, Pieropan, Francesca, Moreira, José Cláudio Fonseca, Costa, Silvia Lima, Butt, Arthur Morgan, and da Silva, Victor Diogenes Amaral

Abstract

Additional file 2: Supplementary Table S1. Characterization of coumarin chemical structure.

Published
2023
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9. Additional file 1 of Amburana cearensis seed extract stimulates astrocyte glutamate homeostatic mechanisms in hippocampal brain slices and protects oligodendrocytes against ischemia

Author

Ferreira, Rafael Short, Ribeiro, Paulo Roberto, Silva, Juliana Helena Castro e, Hoppe, Juliana Bender, de Almeida, Monique Marylin Alves, de Lima Ferreira, Beatriz Correia, Andrade, Gustavo Borges, de Souza, Suzana Braga, Ferdandez, Luzimar Gonzaga, de Fátima Dias Costa, Maria, Salbego, Christianne Gazzana, Rivera, Andrea Domenico, Longoni, Aline, de Assis, Adriano Martimbianco, Pieropan, Francesca, Moreira, José Cláudio Fonseca, Costa, Silvia Lima, Butt, Arthur Morgan, and da Silva, Victor Diogenes Amaral

Abstract

Additional file 1: Supplementary Figure S1. Chemicalcharacterization of Amburana cearensis extract (EDAC).

Published
2023
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10. Amburana cearensis seed extract stimulates astrocyte glutamate homeostatic mechanisms in hippocampal brain slices and protects oligodendrocytes against ischemia

Author

Ferreira, Rafael Short, primary, Ribeiro, Paulo Roberto, additional, Silva, Juliana Helena Castro e, additional, Hoppe, Juliana Bender, additional, Almeida, Monique Marylin Alves, additional, Ferreira, Beatriz Correia Lima, additional, Andrade, Gustavo Borges, additional, Souza, Suzana Braga, additional, Ferdandez, Luzimar Gonzaga, additional, Costa, Maria de Fátima Dias, additional, Salbego, Christianne Gazzana, additional, Rivera, Andrea Domenico, additional, Longoni, Aline, additional, De Assis, Adriano Martimbianco, additional, Pieropan, Francesca, additional, Moreira, José Cláudio Fonseca, additional, Costa, Silvia Lima, additional, Butt, Arthur Morgan, additional, and Silva, Victor Diogenes Amaral, additional

Published
2022
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11. Agathisflavone Modifies Microglial Activation State and Myelination in Organotypic Cerebellar Slices Culture

Author

de Almeida, Monique Marylin Alves, primary, Pieropan, Francesca, additional, Footz, Tim, additional, David, Jorge Mauricio, additional, David, Juceni Pereira, additional, da Silva, Victor Diogenes Amaral, additional, dos Santos Souza, Cleide, additional, Voronova, Anastassia, additional, Butt, Arthur Morgan, additional, and Costa, Silvia Lima, additional

Published
2021
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14. Disruption of Oligodendrocyte Progenitor Cells is an Early Sign of Pathology in the Triple Transgenic Mouse Model of Alzheimer's Disease

Author

Neurociencias, Neurozientziak, Vanzulli, Ilaria, Papanikolaou, Maria, Chacón de la Rocha, Irene, Pieropan, Francesca, Rivera, Andrea D., Gómez Nicola, Diego, Verkhratsky, Alexei, Rodríguez Arellano, José Julio, Butt, Arthur M., Neurociencias, Neurozientziak, Vanzulli, Ilaria, Papanikolaou, Maria, Chacón de la Rocha, Irene, Pieropan, Francesca, Rivera, Andrea D., Gómez Nicola, Diego, Verkhratsky, Alexei, Rodríguez Arellano, José Julio, and Butt, Arthur M.

Abstract

There is increasing evidence that myelin disruption is related to cognitive decline in Alzheimer's disease (AD). In the CNS, myelin is produced by oligodendrocytes, which are generated throughout life by adult oligodendrocyte progenitor cells (OPCs), also known as NG2-glia. To address whether alterations in myelination are related to age-dependent changes in OPCs, we analyzed NG2 and myelin basic protein (MBP) immunolabelling in the hippocampus of 3xTg-AD mice at 6 and 24 months of age, compared with non-Tg age-matched controls. There was an age-related decrease in MBP immunostaining and OPC density, together with a decline in the number of OPC sister cells, a measure of OPC replication. Notably, the loss of myelin and OPC sister cells occurred earlier at 6 months in 3xTg-AD, suggesting accelerated aging, although there was not a concomitant decline in OPC numbers at this age, suggesting the observed changes in myelin were not a consequence of replicative exhaustion, but possibly of OPC disruption or senescence. In line with this, a key finding is that compared to age-match controls, OPC displayed marked morphological atrophy at 6 months in 3xTg-AD followed by morphological hypertrophy at 24 months, as deduced from significant changes in total cell surface area, total cell volume, somata volume and branching of main processes. Moreover, we show that hypertrophic OPCs surround and infiltrate amyloid-beta (A beta) plaques, a key pathological hallmark of AD. The results indicate that OPCs undergo complex age-related remodeling in the hippocampus of the 3xTg-AD mouse model. We conclude that OPC disruption is an early pathological sign in AD and is a potential factor in accelerated myelin loss and cognitive decline.

Published
2020

15. Pharmacogenomic identification of small molecules for lineage specific manipulation of subventricular zone germinal activity

Author

Azim, Kasum, Angonin, Diane, Marcy, Guillaume, Pieropan, Francesca, Rivera, Andrea, Donega, Vanessa, Cantù, Claudio, Williams, Gareth, Berninger, Benedikt, Butt, Arthur M, Raineteau, Olivier, Bodescot, Myriam, Brain Research Institute [Zurich, Suisse], Eidgenössische Technische Hochschule - Swiss Federal Institute of Technology [Zürich] (ETH Zürich)-Universität Zürich [Zürich] = University of Zurich (UZH), Adult Neurogenesis and Cellular Reprogramming [Mayence, Allemagne], Institute of Physiological Chemistry [Mayence, Allemagne], University Medical Centre [Mayence, Allemagne], Johannes Gutenberg - Universität Mainz = Johannes Gutenberg University (JGU)-Johannes Gutenberg - Universität Mainz = Johannes Gutenberg University (JGU)-University Medical Centre [Mayence, Allemagne], Johannes Gutenberg - Universität Mainz = Johannes Gutenberg University (JGU)-Johannes Gutenberg - Universität Mainz = Johannes Gutenberg University (JGU), Focus Program Translational Neuroscience [Mayence, Allemagne], Johannes Gutenberg - Universität Mainz = Johannes Gutenberg University (JGU), Institut cellule souche et cerveau (U846 Inserm - UCBL1), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Recherche Agronomique (INRA), School of Pharmacy and Biomedical Sciences [Portsmouth, Royaume-Uni], University of Portsmouth, Institute of Molecular Life Sciences [Zurich, Suisse] (IMLS), Universität Zürich [Zürich] = University of Zurich (UZH), Wolfson Centre for Age-Related Diseases [Londres, Royaume-Uni], Guy's Campus [Londres, Royaume-Uni], King‘s College London-King‘s College London, Biotechnology and Biological Sciences Research Council (BBSRC) http://www.bbsrc.ac.uk/ (grant number BB/M029379/1). Funding to AB lab. Multiple Sclerosis Society of UK https://www.mssociety.org.uk/ms-research/for-researchers (grant number 40). Funding to AB lab. Investissements d'Avenir/French National Research Agency (ANR) http://www.agence-nationale-recherche.fr/ (grant number ANR-11-IDEX-0007). Program 'Investissements d'Avenir' to OR lab. Swiss National Science Foundation (SNF) http://www.nrp63.ch/en (grant number 406340_128291). SNF project grant NRP63 to OR lab. Swiss National Science Foundation (SNF) http://www.snf.ch/en/funding/careers/advanced-postdoc-mobility/Pages/default.aspx (grant number P300P3_154614). Advanced Post-doc mobility fellowship to KA., Johannes Gutenberg - Universität Mainz (JGU)-Johannes Gutenberg - Universität Mainz (JGU)-University Medical Centre [Mayence, Allemagne], Johannes Gutenberg - Universität Mainz (JGU)-Johannes Gutenberg - Universität Mainz (JGU), Johannes Gutenberg - Universität Mainz (JGU), Institut National de la Recherche Agronomique (INRA)-Université Claude Bernard Lyon 1 (UCBL), and Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
animal diseases, Gene Identification and Analysis, Genetic Networks, APC-PAID, Mice, Neural Stem Cells, Cell Signaling, Lateral Ventricles, Databases, Genetic, Gene Regulatory Networks, Biology (General), WNT Signaling Cascade, Notch Signaling, Organic Compounds, BB/M029379/1, Genomics, Signaling Cascades, Oligodendroglia, Chemistry, BBSRC, Physical Sciences, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Network Analysis, Neurovetenskaper, Signal Transduction, Research Article, Biotechnology, Computer and Information Sciences, Signal Inhibition, QH301-705.5, Neurogenesis, Research and Analysis Methods, Small Molecule Libraries, Genetics, Animals, Adults, Cell Lineage, Computer Simulation, [SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Molecular Biology Techniques, Molecular Biology, Organic Chemistry, Gene Mapping, Chemical Compounds, Neurosciences, Biology and Life Sciences, RCUK, Biomedical Sciences, Cell Biology, Nerve Regeneration, Signaling Networks, Gene Expression Regulation, nervous system, Small Molecules, Age Groups, People and Places, Population Groupings, Transcriptome
Abstract

Strategies for promoting neural regeneration are hindered by the difficulty of manipulating desired neural fates in the brain without complex genetic methods. The subventricular zone (SVZ) is the largest germinal zone of the forebrain and is responsible for the lifelong generation of interneuron subtypes and oligodendrocytes. Here, we have performed a bioinformatics analysis of the transcriptome of dorsal and lateral SVZ in early postnatal mice, including neural stem cells (NSCs) and their immediate progenies, which generate distinct neural lineages. We identified multiple signaling pathways that trigger distinct downstream transcriptional networks to regulate the diversity of neural cells originating from the SVZ. Next, we used a novel in silico genomic analysis, searchable platform-independent expression database/connectivity map (SPIED/CMAP), to generate a catalogue of small molecules that can be used to manipulate SVZ microdomain-specific lineages. Finally, we demonstrate that compounds identified in this analysis promote the generation of specific cell lineages from NSCs in vivo, during postnatal life and adulthood, as well as in regenerative contexts. This study unravels new strategies for using small bioactive molecules to direct germinal activity in the SVZ, which has therapeutic potential in neurodegenerative diseases., PLoS Biology, 15 (3), ISSN:1544-9173, ISSN:1545-7885

Published
2017
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