AI Article Synopsis
- Nitric oxide (NO) plays a crucial role in regulating functions in skeletal muscle, with a specific focus on its relationship to Duchenne muscular dystrophy (DMD).
- Contrary to earlier beliefs that only the neuronal isoform (NOS1) was lost in DMD, recent studies show that all three NOS isoforms (NOS1, NOS2, NOS3) are present in the muscle tissue of both healthy and DMD-affected individuals.
- This research indicates that the muscle degeneration in DMD may stem from a deficiency of NO due to superoxides interfering with its action, rather than a decrease in NOS production itself.
Article Abstract
Nitric oxide (NO) mediates fundamental physiological actions on skeletal muscle. The neuronal NO synthase isoform (NOS1) was reported to be located exclusively in the sarcolemma. Its loss from the sarcolemma was associated with development of Duchenne muscular dystrophy (DMD). However, new studies evidence that all three NOS isoforms-NOS1, NOS2, and NOS3-are co-expressed in the sarcoplasm both in normal and in DMD skeletal muscles. To address this controversy, we assayed NOS expression in DMD myofibers in situ cytophotometrically and found NOS expression in DMD myofibers up-regulated. These results support the hypothesis that NO deficiency with consequent muscle degeneration in DMD results from NO scavenging by superoxides rather than from reduced NOS expression.
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| http://dx.doi.org/10.1016/j.bbrc.2006.07.056 | DOI Listing |
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