The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
NO production results in suspension-induced muscle atrophy through dislocation of neuronal NOS
Open accessAbstract
Forkhead box O (Foxo) transcription factors induce muscle atrophy by upregulating the muscle-specific E3 ubiquitin ligases MuRF-1 and atrogin-1/MAFbx, but other than Akt, the upstream regulators of Foxos during muscle atrophy are largely unknown. To examine the involvement of the dystrophin glycoprotein complex (DGC) in regulation of Foxo activities and muscle atrophy, we analyzed the expression of DGC members during tail suspension, a model of unloading-induced muscle atrophy. Among several DGC members, only neuronal NOS (nNOS) quickly dislocated from the sarcolemma to the cytoplasm during tail suspension. Electron paramagnetic resonance spectrometry revealed production of NO in atrophying muscle. nNOS-null mice showed much milder muscle atrophy after tail suspension than did wild-type mice. Importantly, nuclear accumulation of dephosphorylated Foxo3a was not evident in nNOS-null muscle, and neither MuRF-1 nor atrogin-1/MAFbx were upregulated during tail suspension. Furthermore, an nNOS-specific inhibitor, 7-nitroindazole, significantly prevented suspension-induced muscle atrophy. The NF-kappaB pathway was activated in both wild-type and nNOS-null muscle during tail suspension. We also show that nNOS was involved in the mechanism of denervation-induced atrophy. We conclude that nNOS/NO mediates muscle atrophy via regulation of Foxo transcription factors and is a new therapeutic target for disuse-induced muscle atrophy.
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“Sarcolemmal nNOS is reported to be a versatile molecule that modulates satellite cell activation (34), formation of neuromuscular junction (35), glucose uptake (36), muscle contraction, and vasodilation (37).”
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Mechanisms regulating skeletal muscle growth and atrophy
Schiaffino, S., Dyar, K. A., Ciciliot, S., Blaauw, B., & Sandri, M. (2013) · The FEBS Journal · doi:10.1111/febs.12253 · Cited by 1,492
Cellular and molecular mechanisms of muscle atrophy
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FoxO transcription factors in the maintenance of cellular homeostasis during aging
Salih, D. A., & Brunet, A. (2008) · Current Opinion in Cell Biology · doi:10.1016/j.ceb.2008.02.005 · Cited by 604
Frailty and sarcopenia: The potential role of an aged immune system
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Crosstalk between Glucocorticoid Receptor and Nutritional Sensor mTOR in Skeletal Muscle
Shimizu, N., Yoshikawa, N., Ito, N., Maruyama, T., Suzuki, Y., Takeda, S.-I., Nakae, J., Tagata, Y., Nishitani, S., Takehana, K., et al. (2011) · Cell Metabolism · doi:10.1016/j.cmet.2011.01.001 · Cited by 498
Self-citation
Metadata
- Authors
- Suzuki, N., Motohashi, N., Uezumi, A., Fukada, S.-I., Yoshimura, T., Itoyama, Y., Aoki, M., Miyagoe-Suzuki, Y., & Takeda, S.
- Venue
- Journal of Clinical Investigation
- Published
- 2007-09-04
- Volume
- 117
- Issue
- 9
- Pages
- 2468-2476
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2035088786
- Cited by
- 188
- References
- 8
- FWCI
- 3.71
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Suzuki, N., Motohashi, N., Uezumi, A., Fukada, S.-I., Yoshimura, T., Itoyama, Y., Aoki, M., Miyagoe-Suzuki, Y., & Takeda, S. (2007). NO production results in suspension-induced muscle atrophy through dislocation of neuronal NOS. Journal of Clinical Investigation. https://doi.org/10.1172/jci30654
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