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18 results on '"Torcinaro, Alessio"'

5. Repurposing of Trimetazidine for amyotrophic lateral sclerosis: A study in SOD1 G93A mice

Author

Scaricamazza, Silvia, primary, Salvatori, Illari, additional, Amadio, Susanna, additional, Nesci, Valentina, additional, Torcinaro, Alessio, additional, Giacovazzo, Giacomo, additional, Primiano, Aniello, additional, Gloriani, Michela, additional, Candelise, Niccolò, additional, Pieroni, Luisa, additional, Loeffler, Jean‐Philippe, additional, Renè, Frederique, additional, Quessada, Cyril, additional, Tefera, Tesfaye W., additional, Wang, Hao, additional, Steyn, Frederik J., additional, Ngo, Shyuan T., additional, Dobrowolny, Gabriella, additional, Lepore, Elisa, additional, Urbani, Andrea, additional, Musarò, Antonio, additional, Volonté, Cinzia, additional, Ferraro, Elisabetta, additional, Coccurello, Roberto, additional, Valle, Cristiana, additional, and Ferri, Alberto, additional

Published
2022
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6. Corrigendum to “Proneurogenic and neuroprotective effect of a multi strain probiotic mixture in a mouse model of acute inflammation: Involvement of the gut-brain axis” [Pharmacol. Res. 172 (2021) 105795]

Author

Petrella, Carla, primary, Strimpakos, Georgios, additional, Torcinaro, Alessio, additional, Middei, Sivlia, additional, Ricci, Valentina, additional, Gargari, Giorgio, additional, Mora, Diego, additional, De Santa, Francesco, additional, and Farioli-Vecchioli, Stefano, additional

Published
2021
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8. Role of Lamin A/C as Candidate Biomarker of Aggressiveness and Tumorigenicity in Glioblastoma Multiforme

Author

Gatti, Giuliana, primary, Vilardo, Laura, additional, Musa, Carla, additional, Di Pietro, Chiara, additional, Bonaventura, Fabrizio, additional, Scavizzi, Ferdinando, additional, Torcinaro, Alessio, additional, Bucci, Barbara, additional, Saporito, Raffaele, additional, Arisi, Ivan, additional, De Santa, Francesca, additional, Raspa, Marcello, additional, Guglielmi, Loredana, additional, and D’Agnano, Igea, additional

Published
2021
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10. Repurposing of Trimetazidine for amyotrophic lateral sclerosis: A study in SOD1G93A mice.

Author

Scaricamazza, Silvia, Salvatori, Illari, Amadio, Susanna, Nesci, Valentina, Torcinaro, Alessio, Giacovazzo, Giacomo, Primiano, Aniello, Gloriani, Michela, Candelise, Niccolò, Pieroni, Luisa, Loeffler, Jean‐Philippe, Renè, Frederique, Quessada, Cyril, Tefera, Tesfaye W., Wang, Hao, Steyn, Frederik J., Ngo, Shyuan T., Dobrowolny, Gabriella, Lepore, Elisa, and Urbani, Andrea

Subjects
MOTOR neuron diseases, AMYOTROPHIC lateral sclerosis, TRIMETAZIDINE, MOTOR neurons, SPINAL nerves, PERIPHERAL nervous system
Abstract

Background and Purpose: Amyotrophic lateral sclerosis (ALS), a neurodegenerative disease characterized by the degeneration of upper and lower motor neurons, progressive wasting and paralysis of voluntary muscles and is currently incurable. Although considered to be a pure motor neuron disease, increasing evidence indicates that the sole protection of motor neurons by a single targeted drug is not sufficient to improve the pathological phenotype. We therefore evaluated the therapeutic potential of the multi‐target drug used to treatment of coronary artery disease, trimetazidine, in SOD1G93A mice. Experimental Approach As a metabolic modulator, trimetazidine improves glucose metabolism. Furthermore, trimetazidine enhances mitochondrial metabolism and promotes nerve regeneration, exerting an anti‐inflammatory and antioxidant effect. We orally treated SOD1G93A mice with trimetazidine, solubilized in drinking water at a dose of 20 mg kg−1, from disease onset. We assessed the impact of trimetazidine on disease progression by studying metabolic parameters, grip strength and histological alterations in skeletal muscle, peripheral nerves and the spinal cord. Key Results: Trimetazidine administration delays motor function decline, improves muscle performance and metabolism, and significantly extends overall survival of SOD1G93A mice (increased median survival of 16 days and 12.5 days for male and female respectively). Moreover, trimetazidine prevents the degeneration of neuromuscular junctions, attenuates motor neuron loss and reduces neuroinflammation in the spinal cord and in peripheral nerves. Conclusion and Implications: In SOD1G93A mice, therapeutic effect of trimetazidine is underpinned by its action on mitochondrial function in skeletal muscle and spinal cord. [ABSTRACT FROM AUTHOR]

Published
2022
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13. Role of miR-200c in Myogenic Differentiation Impairment via p66Shc: Implication in Skeletal Muscle Regeneration of Dystrophic mdx Mice

Author

D’Agostino, Marco, primary, Torcinaro, Alessio, additional, Madaro, Luca, additional, Marchetti, Lorenza, additional, Sileno, Sara, additional, Beji, Sara, additional, Salis, Chiara, additional, Proietti, Daisy, additional, Imeneo, Giulia, additional, C. Capogrossi, Maurizio, additional, De Santa, Francesca, additional, and Magenta, Alessandra, additional

Published
2018
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15. Oxidative Stress-Induced miR-200c Disrupts the Regulatory Loop Among SIRT1, FOXO1, and eNOS

Author

Carlomosti, Fabrizio, primary, D'Agostino, Marco, additional, Beji, Sara, additional, Torcinaro, Alessio, additional, Rizzi, Roberto, additional, Zaccagnini, Germana, additional, Maimone, Biagina, additional, Di Stefano, Valeria, additional, De Santa, Francesca, additional, Cordisco, Sonia, additional, Antonini, Annalisa, additional, Ciarapica, Roberta, additional, Dellambra, Elena, additional, Martelli, Fabio, additional, Avitabile, Daniele, additional, Capogrossi, Maurizio Colognesi, additional, and Magenta, Alessandra, additional

Published
2017
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17. Ranolazine Counteracts Strength Impairment and Oxidative Stress in Aged Sarcopenic Mice

Author

Alessio Torcinaro, Donato Cappetta, Francesca De Santa, Marialucia Telesca, Massimiliano Leigheb, Liberato Berrino, Konrad Urbanek, Antonella De Angelis, Elisabetta Ferraro, Torcinaro, A, Cappetta, D, De Santa, F, Telesca, M, Leigheb, M, Berrino, L, Urbanek, K, De Angelis, A, Ferraro, E, Torcinaro, Alessio, Cappetta, Donato, De Santa, Francesca, Telesca, Marialucia, Leigheb, Massimiliano, Berrino, Liberato, Urbanek, Konrad, De Angelis, Antonella, and Ferraro, Elisabetta

Subjects
sarcopenia, Endocrinology, Diabetes and Metabolism, aging, metabolic reprogramming, ranolazine, skeletal muscle, Molecular Biology, Biochemistry
Abstract

Sarcopenia is defined as the loss of muscle mass associated with reduced strength leading to poor quality of life in elderly people. The decline of skeletal muscle performance is characterized by bioenergetic impairment and severe oxidative stress, and does not always strictly correlate with muscle mass loss. We chose to investigate the ability of the metabolic modulator Ranolazine to counteract skeletal muscle dysfunctions that occur with aging. For this purpose, we treated aged C57BL/6 mice with Ranolazine/vehicle for 14 days and collected the tibialis anterior and gastrocnemius muscles for histological and gene expression analyses, respectively. We found that Ranolazine treatment significantly increased the muscle strength of aged mice. At the histological level, we found an increase in centrally nucleated fibers associated with an up-regulation of genes encoding MyoD, Periostin and Osteopontin, thus suggesting a remodeling of the muscle even in the absence of physical exercise. Notably, these beneficial effects of Ranolazine were also accompanied by an up-regulation of antioxidant and mitochondrial genes as well as of NADH-dehydrogenase activity, together with a more efficient protection from oxidative damage in the skeletal muscle. These data indicate that the protection of muscle from oxidative stress by Ranolazine might represent a valuable approach to increase skeletal muscle strength in elderly populations.

Published
2022

18. Role of miR-200c in Myogenic Differentiation Impairment via p66Shc: Implication in Skeletal Muscle Regeneration of Dystrophic mdx Mice.

Author

D'Agostino M, Torcinaro A, Madaro L, Marchetti L, Sileno S, Beji S, Salis C, Proietti D, Imeneo G, C Capogrossi M, De Santa F, and Magenta A

Subjects
Animals, Cell Line, Mice, Inbred C57BL, Mice, Inbred mdx, MicroRNAs genetics, Muscle Fibers, Skeletal metabolism, Phosphorylation, Phosphoserine metabolism, Cell Differentiation genetics, MicroRNAs metabolism, Muscle Development genetics, Muscle, Skeletal physiopathology, Muscular Dystrophy, Animal physiopathology, Regeneration, Src Homology 2 Domain-Containing, Transforming Protein 1 metabolism
Abstract

Duchenne muscular dystrophy (DMD) is a genetic disease associated with mutations of Dystrophin gene that regulate myofiber integrity and muscle degeneration, characterized by oxidative stress increase. We previously published that reactive oxygen species (ROS) induce miR-200c that is responsible for apoptosis and senescence. Moreover, we demonstrated that miR-200c increases ROS production and phosphorylates p66Shc in Ser-36. p66Shc plays an important role in muscle differentiation; we previously showed that p66Shc -/- muscle satellite cells display lower oxidative stress levels and higher proliferation rate and differentiated faster than wild-type ( wt ) cells. Moreover, myogenic conversion, induced by MyoD overexpression, is more efficient in p66Shc -/- fibroblasts compared to wt cells. Herein, we report that miR-200c overexpression in cultured myoblasts impairs skeletal muscle differentiation. Further, its overexpression in differentiated myotubes decreases differentiation indexes. Moreover, anti-miR-200c treatment ameliorates myogenic differentiation. In keeping, we found that miR-200c and p66Shc Ser-36 phosphorylation increase in mdx muscles. In conclusion, miR-200c inhibits muscle differentiation, whereas its inhibition ameliorates differentiation and its expression levels are increased in mdx mice and in differentiated human myoblasts of DMD. Therefore, miR-200c might be responsible for muscle wasting and myotube loss, most probably via a p66Shc-dependent mechanism in a pathological disease such as DMD.

Published
2018
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