5 results on '"Nicoletti, Carmine"'
Search Results
2. MicroRNAs Involved in Molecular Circuitries Relevant for the Duchenne Muscular Dystrophy Pathogenesis Are Controlled by the Dystrophin/nNOS Pathway.
- Author
-
Cacchiarelli, Davide, Martone, Julie, Girardi, Erika, Cesana, Marcella, Incitti, Tania, Morlando, Mariangela, Nicoletti, Carmine, Santini, Tiziana, Sthandier, Olga, Barberi, Laura, Auricchio, Alberto, Musarò, Antonio, and Bozzoni, Irene
- Subjects
NON-coding RNA ,DUCHENNE muscular dystrophy ,DYSTROPHIN ,NITRIC-oxide synthases ,SARCOLEMMA ,EXTRACELLULAR matrix proteins ,MUSCLE regeneration ,GENE expression - Abstract
Summary: In Duchenne muscular dystrophy (DMD) the absence of dystrophin at the sarcolemma delocalizes and downregulates nitric oxide synthase (nNOS); this alters S-nitrosylation of HDAC2 and its chromatin association. We show that the differential HDAC2 nitrosylation state in Duchenne versus wild-type conditions deregulates the expression of a specific subset of microRNA genes. Several circuitries controlled by the identified microRNAs, such as the one linking miR-1 to the G6PD enzyme and the redox state of cell, or miR-29 to extracellular proteins and the fibrotic process, explain some of the DMD pathogenetic traits. We also show that, at variance with other myomiRs, miR-206 escapes from the dystrophin-nNOS control being produced in activated satellite cells before dystrophin expression; in these cells, it contributes to muscle regeneration through repression of the satellite specific factor, Pax7. We conclude that the pathway activated by dystrophin/nNOS controls several important circuitries increasing the robustness of the muscle differentiation program. [ABSTRACT FROM AUTHOR]
- Published
- 2010
- Full Text
- View/download PDF
3. Accelerating the Mdx Heart Histo-Pathology through Physical Exercise.
- Author
-
Morroni, Jacopo, Schirone, Leonardo, Vecchio, Daniele, Nicoletti, Carmine, D'Ambrosio, Luca, Valenti, Valentina, Sciarretta, Sebastiano, Lozanoska-Ochser, Biliana, and Bouchè, Marina
- Subjects
MOLECULAR pathology ,MYOCARDIUM ,CAUSES of death ,DUCHENNE muscular dystrophy ,MYOSITIS ,HEART - Abstract
Chronic cardiac muscle inflammation and fibrosis are key features of Duchenne Muscular Dystrophy (DMD). Around 90% of 18-year-old patients already show signs of DMD-related cardiomyopathy, and cardiac failure is rising as the main cause of death among DMD patients. The evaluation of novel therapies for the treatment of dystrophic heart problems depends on the availability of animal models that closely mirror the human pathology. The widely used DMD animal model, the mdx mouse, presents a milder cardiac pathology compared to humans, with a late onset, which precludes large-scale and reliable studies. In this study, we used an exercise protocol to accelerate and worsen the cardiac pathology in mdx mice. The mice were subjected to a 1 h-long running session on a treadmill, at moderate speed, twice a week for 8 weeks. We demonstrate that subjecting young mdx mice (4-week-old) to "endurance" exercise accelerates heart pathology progression, as shown by early fibrosis deposition, increases necrosis and inflammation, and reduces heart function compared to controls. We believe that our exercised mdx model represents an easily reproducible and useful tool to study the molecular and cellular networks involved in dystrophic heart alterations, as well as to evaluate novel therapeutic strategies aimed at ameliorating dystrophic heart pathology. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF
4. Intraperitoneal injection of microencapsulated Sertoli cells restores muscle morphology and performance in dystrophic mice.
- Author
-
Chiappalupi, Sara, Luca, Giovanni, Mancuso, Francesca, Madaro, Luca, Fallarino, Francesca, Nicoletti, Carmine, Calvitti, Mario, Arato, Iva, Falabella, Giulia, Salvadori, Laura, Di Meo, Antonio, Bufalari, Antonello, Giovagnoli, Stefano, Calafiore, Riccardo, Donato, Rosario, and Sorci, Guglielmo
- Subjects
- *
TREATMENT of Duchenne muscular dystrophy , *MICROENCAPSULATION , *INTRAPERITONEAL injections , *IMMUNOSUPPRESSIVE agents , *DRUG delivery systems - Abstract
Duchenne muscular dystrophy (DMD) is a genetic disease characterized by progressive muscle degeneration leading to impaired locomotion, respiratory failure and premature death. In DMD patients, inflammatory events secondary to dystrophin mutation play a major role in the progression of the pathology. Sertoli cells (SeC) have been largely used to protect xenogeneic engraftments or induce trophic effects thanks to their ability to secrete trophic, antiinflammatory, and immunomodulatory factors. Here we have purified SeC from specific pathogen-free (SPF)-certified neonatal pigs, and embedded them into clinical grade alginate microcapsules. We show that a single intraperitoneal injection of microencapsulated SPF SeC (SeC-MC) in an experimental model of DMD can rescue muscle morphology and performance in the absence of pharmacologic immunosuppressive treatments. Once i.p. injected, SeC-MC act as a drug delivery system that modulates the inflammatory response in muscle tissue, and upregulates the expression of the dystrophin paralogue, utrophin in muscles through systemic release of heregulin-β1, thus promoting sarcolemma stability. Analyses performed five months after single injection show high biocompatibility and long-term efficacy of SeC-MC. Our results might open new avenues for the treatment of patients with DMD and related diseases. [ABSTRACT FROM AUTHOR]
- Published
- 2016
- Full Text
- View/download PDF
5. MicroRNAs involved in molecular circuitries relevant for the duchenne muscular dystrophy pathogenesis are controlled by the dystrophin/nNOS pathway
- Author
-
Alberto Auricchio, Laura Barberi, Tiziana Santini, Mariangela Morlando, Olga Sthandier, Carmine Nicoletti, Tania Incitti, Erika Girardi, Julie Martone, Antonio Musarò, Irene Bozzoni, Marcella Cesana, Davide Cacchiarelli, Cacchiarelli, Davide, Martone, Julie, Girardi, Erika, Cesana, Marcella, Incitti, Tania, Morlando, Mariangela, Nicoletti, Carmine, Santini, Tiziana, Sthandier, Olga, Barberi, Laura, Auricchio, Alberto, Musar, Antonio, and Bozzoni, Irene
- Subjects
Physiology ,Duchenne muscular dystrophy ,HUMDISEASE ,Histone Deacetylase 2 ,DEVBIO ,Nitric Oxide Synthase Type I ,Dystrophin ,Mice ,0302 clinical medicine ,Muscular Dystrophy ,Muscular dystrophy ,Regulation of gene expression ,0303 health sciences ,Nitrosylation ,MicroRNA ,Skeletal ,musculoskeletal system ,Chromatin ,Cell biology ,Nitric oxide synthase ,Satellite Cells ,Muscle ,musculoskeletal diseases ,congenital, hereditary, and neonatal diseases and abnormalities ,Skeletal Muscle ,Satellite Cells, Skeletal Muscle ,DNA ,Animals ,Gene Expression Regulation ,Mice, Inbred mdx ,MicroRNAs ,Muscle, Skeletal ,Muscular Dystrophy, Animal ,Regeneration ,Biology ,03 medical and health sciences ,medicine ,devbio ,dna ,humdisease ,Molecular Biology ,030304 developmental biology ,Sarcolemma ,Animal ,Inbred mdx ,Cell Biology ,medicine.disease ,biology.protein ,Cancer research ,030217 neurology & neurosurgery - Abstract
SummaryIn Duchenne muscular dystrophy (DMD) the absence of dystrophin at the sarcolemma delocalizes and downregulates nitric oxide synthase (nNOS); this alters S-nitrosylation of HDAC2 and its chromatin association. We show that the differential HDAC2 nitrosylation state in Duchenne versus wild-type conditions deregulates the expression of a specific subset of microRNA genes. Several circuitries controlled by the identified microRNAs, such as the one linking miR-1 to the G6PD enzyme and the redox state of cell, or miR-29 to extracellular proteins and the fibrotic process, explain some of the DMD pathogenetic traits. We also show that, at variance with other myomiRs, miR-206 escapes from the dystrophin-nNOS control being produced in activated satellite cells before dystrophin expression; in these cells, it contributes to muscle regeneration through repression of the satellite specific factor, Pax7. We conclude that the pathway activated by dystrophin/nNOS controls several important circuitries increasing the robustness of the muscle differentiation program.
- Published
- 2010
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.