2 research outputs found
nNOS/GSNOR interaction contributes to skeletal muscle differentiation and homeostasis
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