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Your search keyword '"Muratori, Luisa"' showing total 29 results
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29 results on '"Muratori, Luisa"'

12. The Peptide A-3302-B Isolated from a Marine Bacterium Micromonospora sp. Inhibits HSV-2 Infection by Preventing the Viral Egress from Host Cells

Author

Sureram, Sanya, primary, Arduino, Irene, additional, Ueoka, Reiko, additional, Rittà, Massimo, additional, Francese, Rachele, additional, Srivibool, Rattanaporn, additional, Darshana, Dhanushka, additional, Piel, Jörn, additional, Ruchirawat, Somsak, additional, Muratori, Luisa, additional, Lembo, David, additional, Kittakoop, Prasat, additional, and Donalisio, Manuela, additional

Published
2022
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14. Elovl5 is required for proper action potential conduction along peripheral myelinated fibers

Author

Hoxha, Eriola, primary, Balbo, Ilaria, additional, Parolisi, Roberta, additional, Audano, Matteo, additional, Montarolo, Francesca, additional, Ravera, Francesco, additional, Guglielmotto, Michela, additional, Muratori, Luisa, additional, Raimondo, Stefania, additional, DiGregorio, Eleonora, additional, Buffo, Annalisa, additional, Brusco, Alfredo, additional, Borroni, Barbara, additional, Mitro, Nico, additional, Caruso, Donatella, additional, and Tempia, Filippo, additional

Published
2021
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15. Mesenchymal Stem Cell Treatment Perspectives in Peripheral Nerve Regeneration: Systematic Review

Author

Lavorato, Andrea, primary, Raimondo, Stefania, additional, Boido, Marina, additional, Muratori, Luisa, additional, Durante, Giorgia, additional, Cofano, Fabio, additional, Vincitorio, Francesca, additional, Petrone, Salvatore, additional, Titolo, Paolo, additional, Tartara, Fulvio, additional, Vercelli, Alessandro, additional, and Garbossa, Diego, additional

Published
2021
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16. Preclinical Validation of SilkBridgeTM for Peripheral Nerve Regeneration

Author

Fregnan, Federica, primary, Muratori, Luisa, additional, Bassani, Giulia A., additional, Crosio, Alessandro, additional, Biagiotti, Marco, additional, Vincoli, Valentina, additional, Carta, Giacomo, additional, Pierimarchi, Pasquale, additional, Geuna, Stefano, additional, Alessandrino, Antonio, additional, Freddi, Giuliano, additional, and Ronchi, Giulia, additional

Published
2020
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19. Mice harbouring a SCA28 patient mutation in AFG3L2 develop late-onset ataxia associated with enhanced mitochondrial proteotoxicity

Author

Mancini, Cecilia, primary, Hoxha, Eriola, additional, Iommarini, Luisa, additional, Brussino, Alessandro, additional, Richter, Uwe, additional, Montarolo, Francesca, additional, Cagnoli, Claudia, additional, Parolisi, Roberta, additional, Gondor Morosini, Diana Iulia, additional, Nicolò, Valentina, additional, Maltecca, Francesca, additional, Muratori, Luisa, additional, Ronchi, Giulia, additional, Geuna, Stefano, additional, Arnaboldi, Francesca, additional, Donetti, Elena, additional, Giorgio, Elisa, additional, Cavalieri, Simona, additional, Di Gregorio, Eleonora, additional, Pozzi, Elisa, additional, Ferrero, Marta, additional, Riberi, Evelise, additional, Casari, Giorgio, additional, Altruda, Fiorella, additional, Turco, Emilia, additional, Gasparre, Giuseppe, additional, Battersby, Brendan J., additional, Porcelli, Anna Maria, additional, Ferrero, Enza, additional, Brusco, Alfredo, additional, and Tempia, Filippo, additional

Published
2019
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21. Evaluation of Vascular Endothelial Growth Factor (VEGF) and Its Family Member Expression After Peripheral Nerve Regeneration and Denervation

Author

Muratori, Luisa, Gnavi, Sara, Fregnan, F., Mancardi, Anabella, Raimondo, Stefania, Perroteau, Isabelle, and Geuna, Stefano

Subjects
Vascular Endothelial Growth Factor A, Histology, Evolution, median nerve transaction, Median Neuropathy, Down-Regulation, Crush Injuries, Behavior and Systematics, Cell Movement, Peripheral Nerve Injuries, Animals, Rats, Wistar, VEGF receptors, crush injury, Cell Proliferation, Ecology, VEGF, Denervation, peripheral nerve regeneration, Neuropilin-1, Median Nerve, Nerve Regeneration, Neuropilin-2, Up-Regulation, end-to-end repair, neuropilin, Anatomy, Biotechnology, Ecology, Evolution, Behavior and Systematics, Receptors, Vascular Endothelial Growth Factor, Female, Schwann Cells
Abstract

Vascular endothelial growth factor (VEGF) represents one of the main factors involved not only in angiogenesis and vasculogenesis but also in neuritogenesis. VEGF plays its function acting via different receptors: VEGF receptor1 (VEGFR-1), VEGF receptor2 (VEGFR-2), VEGF receptor3 (VEGFR-3), and co-receptors Neuropilin-1 (NRP1) and Neuropilin-2 (NRP2). This study reports on the first in vivo analysis of the expression of VEGF and VEGF family molecules in peripheral nerve degeneration and regeneration: for this purpose, different models of nerve lesion in rat were adopted, the median nerve crush injury and the median nerve transaction followed or not by end-to end microsurgical repair. Results obtained by real time polymerase chain reaction showed that VEGF and VEGF family molecules are differentially expressed under regenerating and degenerating condition, furthermore, in order to study the modulation and involvement of these factors in two different regenerative models, crush injury and end-to-end repair, protein expression analysis was evaluated. In addition, immunohistochemical analysis allowed to state a glial localization of VEGF and VEGFR-2 after peripheral nerve crush injury. Finally in vitro assay on primary Schwann cells culture show that VEGF165 stimulation increases Schwann cells migration, a major process in the promotion of neurite outgrowth. Anat Rec, 301:1646-1656, 2018. © 2018 Wiley Periodicals, Inc.

Published
2017

23. Mice harboring a SCA28 patient mutation in AFG3L2 develop late-onset ataxia associated with enhanced mitochondrial proteotoxicity.

Author

Mancini, Cecilia, primary, Hoxha, Eriola, additional, Iommarini, Luisa, additional, Brussino, Alessandro, additional, Richter, Uwe, additional, Montarolo, Francesca, additional, Cagnoli, Claudia, additional, Parolisi, Roberta, additional, Gondor Morosini, Diana Iulia, additional, Nicolo, Valentina, additional, Maltecca, Francesca, additional, Muratori, Luisa, additional, Ronchi, Giulia, additional, Geuna, Stefano, additional, Arnaboldi, Francesca, additional, Donetti, Elena, additional, Giorgio, Elisa, additional, Cavalieri, Simona, additional, Di Gregorio, Eleonora, additional, Pozzi, Elisa, additional, Ferrero, Marta, additional, Riberi, Evelise, additional, Casari, Giorgio, additional, Altruda, Fiorella, additional, Turco, Emilia, additional, Gasparre, Giuseppe, additional, Battersby, Brendan J, additional, Porcelli, Anna Maria, additional, Ferrero, Enza, additional, Brusco, Alfredo, additional, and Tempia, Filippo, additional

Published
2018
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24. Generation of New Neurons in Dorsal Root Ganglia in Adult Rats after Peripheral Nerve Crush Injury

Author

Muratori, Luisa, Ronchi, Giulia, Raimondo, Stefania, Geuna, Stefano, Giacobini-Robecchi, Maria Giuseppina, and Fornaro, Michele

Subjects
Pathology, medicine.medical_specialty, Article Subject, Sensory Receptor Cells, Neurogenesis, Cell Count, Sensory system, Biology, lcsh:RC321-571, Lesion, Dorsal root ganglion, Peripheral Nerve Injuries, Ganglia, Spinal, medicine, Animals, Rats, Wistar, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, Nestin, Nerve injury, medicine.disease, Rats, medicine.anatomical_structure, Neurology, nervous system, Crush injury, Female, Neurology (clinical), medicine.symptom, Neuroscience, Research Article
Abstract

The evidence of neurons generatedex novoin sensory ganglia of adult animals is still debated. In the present study, we investigated, using high resolution light microscopy and stereological analysis, the changes in the number of neurons in dorsal root ganglia after 30 days from a crush lesion of the rat brachial plexus terminal branches. Results showed, as expected, a relevant hypertrophy of dorsal root ganglion neurons. In addition, we reported, for the first time in the literature, that neuronal hypertrophy was accompanied by massive neuronal hyperplasia leading to a 42% increase of the number of primary sensory neurons. Moreover, ultrastructural analyses on sensory neurons showed that there was not a relevant neuronal loss as a consequence of the nerve injury. The evidence of BrdU-immunopositive neurons and neural progenitors labeled with Ki67, nanog, nestin, and sox-2 confirmed the stereological evidence of posttraumatic neurogenesis in dorsal root ganglia. Analysis of morphological changes following axonal damage in addition to immunofluorescence characterization of cell phenotype suggested that the neuronal precursors which give rise to the newly generated neurons could be represented by satellite glial cells that actively proliferate after the lesion and are able to differentiate toward the neuronal lineage.

Published
2015

25. Pig decellularized peripheral nerve supports fiber regeneration.

Author

Raimondo, Stefania, Muratori, Luisa, Ronchi, Giulia, Crosio, Alessandro, and Lovati, Arianna

Abstract

The article focuses on the development of a new decellularization protocol for pig nerves that preserves the nerve extracellular matrix (ECM) and its subsequent use in repairing rat median nerves, demonstrating its potential for treating severe nerve injuries.

Published
2023

26. Strategies to improve cavernous nerve regeneration after radical prostatectomy.

Author

Muratori, Luisa, Fregnan, Federica, Crosio, Alessandro, Zen, Federica, Manfredi, Matteo, Tonazzini, Ilaria, Meziere, Juliette, Porpiglia, Francesco, Geuna, Stefano, and Raimondo, Stefania

Abstract

The article focuses on strategies to improve cavernous nerve regeneration after radical prostatectomy, with a specific focus on the use of chitosan membranes, which have been shown to promote nerve regeneration in clinical and experimental settings.

Published
2023

28. Mice harbouring a SCA28 patient mutation in AFG3L2 develop late-onset ataxia associated with enhanced mitochondrial proteotoxicity

Author

Brendan J. Battersby, Luisa Iommarini, Alfredo Brusco, Eriola Hoxha, Emilia Turco, Stefano Geuna, Giuseppe Gasparre, Cecilia Mancini, Francesca Montarolo, Valentina Nicolò, Simona Cavalieri, Giorgio Casari, Diana Iulia Gondor Morosini, Uwe Richter, Luisa Muratori, Elena Donetti, Alessandro Brussino, Elisa Pozzi, Francesca Maltecca, Francesca Arnaboldi, Evelise Riberi, Enza Ferrero, Fiorella Altruda, Claudia Cagnoli, Filippo Tempia, Roberta Parolisi, Marta Ferrero, Giulia Ronchi, Elisa Giorgio, Eleonora Di Gregorio, Anna Maria Porcelli, Mancini, Cecilia, Hoxha, Eriola, Iommarini, Luisa, Brussino, Alessandro, Richter, Uwe, Montarolo, Francesca, Cagnoli, Claudia, Parolisi, Roberta, Gondor Morosini, Diana Iulia, Nicolò, Valentina, Maltecca, Francesca, Muratori, Luisa, Ronchi, Giulia, Geuna, Stefano, Arnaboldi, Francesca, Donetti, Elena, Giorgio, Elisa, Cavalieri, Simona, Di Gregorio, Eleonora, Pozzi, Elisa, Ferrero, Marta, Riberi, Evelise, Casari, Giorgio, Altruda, Fiorella, Turco, Emilia, Gasparre, Giuseppe, Battersby, Brendan J., Porcelli, Anna Maria, Ferrero, Enza, Brusco, Alfredo, Tempia, Filippo, and Morosini, Diana Iulia Gondor

Subjects
0301 basic medicine, Ataxia, Mutant, Mutation, Missense, Biology, medicine.disease_cause, Proteotoxicity, lcsh:RC321-571, Mitochondrial Proteins, 03 medical and health sciences, Purkinje Cells, SCA28, 0302 clinical medicine, ATP-Dependent Proteases, Mitochondrial dynamic, medicine, Missense mutation, Animals, Spinocerebellar Ataxias, Gene Knock-In Techniques, Allele, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, AFG3L2, 030304 developmental biology, Membrane Potential, Mitochondrial, 0303 health sciences, Mutation, Cerebellar ataxia, Mouse knock-in, medicine.disease, Molecular biology, Phenotype, Mitochondria, Mice, Inbred C57BL, Disease Models, Animal, 030104 developmental biology, Neurology, SCA28 AFG3L2 Mouse knock-in Mitochondrial dynamics Proteotoxicity, Spinocerebellar ataxia, Mitochondrial dynamics, ATPases Associated with Diverse Cellular Activities, Female, medicine.symptom, 030217 neurology & neurosurgery
Abstract

Spinocerebellar ataxia 28 is an autosomal dominant neurodegenerative disorder caused by missense mutations affecting the proteolytic domain of AFG3L2, a major component of the mitochondrial m-AAA protease. However, little is known of the underlying pathogenetic mechanisms or how to treat patients with SCA28. Currently available Afg3l2 mutant mice harbour deletions that lead to severe, early-onset neurological phenotypes that do not faithfully reproduce the late-onset and slowly progressing SCA28 phenotype. Here we describe production and detailed analysis of a new knock-in murine model harbouring an Afg3l2 allele carrying the p.Met665Arg patient-derived mutation. Heterozygous mutant mice developed normally but signs of ataxia were detectable by beam test at 18 months. Cerebellar pathology was negative; electrophysiological analysis showed increased spontaneous firing in Purkinje cells from heterozygous mutants with respect to wild-type controls, although not statistically significant. As homozygous mutants died perinatally with evidence of cardiac atrophy, for each genotype we generated mouse embryonic fibroblasts (MEFs) to investigate mitochondrial function. MEFs from mutant mice showed altered mitochondrial bioenergetics, with decreased basal oxygen consumption rate, ATP synthesis and mitochondrial membrane potential. Mitochondrial network formation and morphology was also altered, in line with greatly reduced expression of Opa1 fusogenic protein L-isoforms. The mitochondrial alterations observed in MEFs were also detected in cerebella of 18-month-old heterozygous mutants, suggesting they may be a hallmark of disease. Pharmacological inhibition of de novo mitochondrial protein translation with chloramphenicol caused reversal of mitochondrial morphology in homozygous mutant MEFs, supporting the relevance of mitochondrial proteotoxicity for SCA28 pathogenesis and therapy development.

Published
2019

29. Preclinical Validation of SilkBridge TM for Peripheral Nerve Regeneration.

Author

Fregnan F, Muratori L, Bassani GA, Crosio A, Biagiotti M, Vincoli V, Carta G, Pierimarchi P, Geuna S, Alessandrino A, Freddi G, and Ronchi G

Abstract

Silk fibroin ( Bombyx mori ) was used to manufacture a nerve conduit (SilkBridge TM ) characterized by a novel 3D architecture. The wall of the conduit consists of two electrospun layers (inner and outer) and one textile layer (middle), perfectly integrated at the structural and functional level. The manufacturing technology conferred high compression strength on the device, thus meeting clinical requirements for physiological and pathological compressive stresses. As demonstrated in a previous work, the silk material has proven to be able to provide a valid substrate for cells to grow on, differentiate and start the fundamental cellular regenerative activities in vitro and, in vivo , at the short time point of 2 weeks, to allow the starting of regenerative processes in terms of good integration with the surrounding tissues and colonization of the wall layers and of the lumen with several cell types. In the present study, a 10 mm long gap in the median nerve was repaired with 12 mm SilkBridge TM conduit and evaluated at middle (4 weeks) and at longer time points (12 and 24 weeks). The SilkBridge TM conduit led to a very good functional and morphological recovery of the median nerve, similar to that observed with the reference autograft nerve reconstruction procedure. Taken together, all these results demonstrated that SilkBridge TM has an optimized balance of biomechanical and biological properties, which allowed proceeding with a first-in-human clinical study aimed at evaluating safety and effectiveness of using the device for the reconstruction of digital nerve defects in humans., (Copyright © 2020 Fregnan, Muratori, Bassani, Crosio, Biagiotti, Vincoli, Carta, Pierimarchi, Geuna, Alessandrino, Freddi and Ronchi.)

Published
2020
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