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Cacchiarelli, Davide; Martone, Julie; Girardi, Erika; Cesana, Marcella; Incitti, Tania; Morlando, Mariangela; Nicoletti, Carmine; Santini, Tiziana; Sthandier, Olga; Barberi, Laura; Auricchio, Alberto; Musarò, Antonio; Bozzoni, Irene
Cell metabolism, 10/2010, Letnik: 12, Številka: 4Journal Article
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. ► Dystrophin controls gene expression by nNOS relocalization and HDAC2 nitrosylation ► Epigenetic control of miRNA expression is involved in DMD pathogenesis ► miR-1 controls G6PD expression and the redox state of the cell ► miR-206 contributes to satellite cell differentiation by repressing Pax7
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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