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Your search keyword '"Fornai, Francesco"' showing total 28 results
Start Over Author "Fornai, Francesco" Journal international journal of molecular sciences
28 results on '"Fornai, Francesco"'

2. Methamphetamine Increases Tubulo-Vesicular Areas While Dissipating Proteins from Vesicles Involved in Cell Clearance.

Author

Lazzeri, Gloria, Lenzi, Paola, Busceti, Carla L., Puglisi-Allegra, Stefano, Ferrucci, Michela, and Fornai, Francesco

Subjects
PARKINSON'S disease, ORGANELLES, LYSOSOMES, DEGENERATION (Pathology), DRUGS of abuse
Abstract

Cytopathology induced by methamphetamine (METH) is reminiscent of degenerative disorders such as Parkinson's disease, and it is characterized by membrane organelles arranged in tubulo-vesicular structures. These areas, appearing as clusters of vesicles, have never been defined concerning the presence of specific organelles. Therefore, the present study aimed to identify the relative and absolute area of specific membrane-bound organelles following a moderate dose (100 µM) of METH administered to catecholamine-containing PC12 cells. Organelles and antigens were detected by immunofluorescence, and they were further quantified by plain electron microscopy and in situ stoichiometry. This analysis indicated an increase in autophagosomes and damaged mitochondria along with a decrease in lysosomes and healthy mitochondria. Following METH, a severe dissipation of hallmark proteins from their own vesicles was measured. In fact, the amounts of LC3 and p62 were reduced within autophagy vacuoles compared with the whole cytosol. Similarly, LAMP1 and Cathepsin-D within lysosomes were reduced. These findings suggest a loss of compartmentalization and confirm a decrease in the competence of cell clearing organelles during catecholamine degeneration. Such cell entropy is consistent with a loss of energy stores, which routinely govern appropriate subcellular compartmentalization. [ABSTRACT FROM AUTHOR]

Published
2024
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4. Damage to the Locus Coeruleus Alters the Expression of Key Proteins in Limbic Neurodegeneration.

Author

Biagioni, Francesca, Ferrucci, Michela, Lazzeri, Gloria, Scioli, Mariarosaria, Frati, Alessandro, Puglisi-Allegra, Stefano, and Fornai, Francesco

Subjects
LOCUS coeruleus, ALZHEIMER'S disease, NEURODEGENERATION, PROTEIN expression, PARKINSON'S disease, ALPHA-synuclein
Abstract

The present investigation was designed based on the evidence that, in neurodegenerative disorders, such as Alzheimer's dementia (AD) and Parkinson's disease (PD), damage to the locus coeruleus (LC) arising norepinephrine (NE) axons (LC-NE) is documented and hypothesized to foster the onset and progression of neurodegeneration within target regions. Specifically, the present experiments were designed to assess whether selective damage to LC-NE axons may alter key proteins involved in neurodegeneration within specific limbic regions, such as the hippocampus and piriform cortex, compared with the dorsal striatum. To achieve this, a loss of LC-NE axons was induced by the neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4) in C57 Black mice, as assessed by a loss of NE and dopamine-beta-hydroxylase within target regions. In these experimental conditions, the amount of alpha-synuclein (alpha-syn) protein levels were increased along with alpha-syn expressing neurons within the hippocampus and piriform cortex. Similar findings were obtained concerning phospho-Tau immunoblotting. In contrast, a decrease in inducible HSP70-expressing neurons and a loss of sequestosome (p62)-expressing cells, along with a loss of these proteins at immunoblotting, were reported. The present data provide further evidence to understand why a loss of LC-NE axons may foster limbic neurodegeneration in AD and limbic engagement during PD. [ABSTRACT FROM AUTHOR]

Published
2024
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9. In Pancreatic Adenocarcinoma Alpha-Synuclein Increases and Marks Peri-Neural Infiltration

Author

Bianchini, Matteo, primary, Giambelluca, Maria, additional, Scavuzzo, Maria Concetta, additional, Di Franco, Gregorio, additional, Guadagni, Simone, additional, Palmeri, Matteo, additional, Furbetta, Niccolò, additional, Gianardi, Desirée, additional, Costa, Aurelio, additional, Gentiluomo, Manuel, additional, Gaeta, Raffaele, additional, Pollina, Luca Emanuele, additional, Falcone, Alfredo, additional, Vivaldi, Caterina, additional, Di Candio, Giulio, additional, Biagioni, Francesca, additional, Busceti, Carla Letizia, additional, Soldani, Paola, additional, Puglisi-Allegra, Stefano, additional, Morelli, Luca, additional, and Fornai, Francesco, additional

Published
2022
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16. Brain Overexpression of Uncoupling Protein-2 (UCP2) Delays Renal Damage and Stroke Occurrence in Stroke-Prone Spontaneously Hypertensive Rats

Author

Busceti, Carla L., primary, Cotugno, Maria, additional, Bianchi, Franca, additional, Forte, Maurizio, additional, Stanzione, Rosita, additional, Marchitti, Simona, additional, Battaglia, Giuseppe, additional, Nicoletti, Ferdinando, additional, Fornai, Francesco, additional, and Rubattu, Speranza, additional

Published
2020
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21. Prion Protein in Glioblastoma Multiforme

Author

Ryskalin, Larisa, primary, Busceti, Carla L., additional, Biagioni, Francesca, additional, Limanaqi, Fiona, additional, Familiari, Pietro, additional, Frati, Alessandro, additional, and Fornai, Francesco, additional

Published
2019
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28. The CXCL2/IL8/CXCR2 Pathway Is Relevant for Brain Tumor Malignancy and Endothelial Cell Function.

Author

Urbantat, Ruth M., Blank, Anne, Kremenetskaia, Irina, Vajkoczy, Peter, Acker, Güliz, Brandenburg, Susan, and Fornai, Francesco

Subjects
ENDOTHELIAL cells, CELL physiology, BRAIN tumors, NEOVASCULARIZATION, CELL receptors, SURVIVAL analysis (Biometry)
Abstract

We aimed to evaluate the angiogenic capacity of CXCL2 and IL8 affecting human endothelial cells to clarify their potential role in glioblastoma (GBM) angiogenesis. Human GBM samples and controls were stained for proangiogenic factors. Survival curves and molecule correlations were obtained from the TCGA (The Cancer Genome Atlas) database. Moreover, proliferative, migratory and angiogenic activity of peripheral (HUVEC) and brain specific (HBMEC) primary human endothelial cells were investigated including blockage of CXCR2 signaling with SB225502. Gene expression analyses of angiogenic molecules from endothelial cells were performed. Overexpression of VEGF and CXCL2 was observed in GBM patients and associated with a survival disadvantage. Molecules of the VEGF pathway correlated but no relation for CXCR1/2 and CXCL2/IL8 was found. Interestingly, receptors of endothelial cells were not induced by addition of proangiogenic factors in vitro. Proliferation and migration of HUVEC were increased by VEGF, CXCL2 as well as IL8. Their sprouting was enhanced through VEGF and CXCL2, while IL8 showed no effect. In contrast, brain endothelial cells reacted to all proangiogenic molecules. Additionally, treatment with a CXCR2 antagonist led to reduced chemokinesis and sprouting of endothelial cells. We demonstrate the impact of CXCR2 signaling on endothelial cells supporting an impact of this pathway in angiogenesis of glioblastoma. [ABSTRACT FROM AUTHOR]

Published
2021
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