nNOS/GSNOR interaction contributes to skeletal muscle differentiation and homeostasis

Costanza Montagna, Salvatore Rizza, Claudia Cirotti, Emiliano Maiani, Maurizio Muscaritoli, Antonio Musarò, Maria Teresa Carrí, Elisabetta Ferraro, Francesco Cecconi, Giuseppe Filomeni

Research output: Contribution to journalArticlepeer-review

Abstract

Neuronal nitric oxide synthase (nNOS) plays a crucial role in the maintenance of correct skeletal muscle function due, at least in part, to S-nitrosylation of specific protein targets. Similarly, we recently provided evidence for a muscular phenotype in mice lacking the denitrosylase S-nitrosoglutathione reductase (GSNOR). Here, we demonstrate that nNOS and GSNOR are concomitantly expressed during differentiation of C2C12. They colocalizes at the sarcolemma and co-immunoprecipitate in cells and in myofibers. We also provide evidence that GSNOR expression decreases in mouse models of muscular dystrophies and of muscle atrophy and wasting, i.e., aging and amyotrophic lateral sclerosis, suggesting a more general regulatory role of GSNOR in skeletal muscle homeostasis.

Original languageEnglish
Pages (from-to)354
JournalCell death & disease
Volume10
Issue number5
DOIs
Publication statusPublished - May 1 2019

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