ArticleAntioxidants & redox signaling2014
The stress protein/chaperone Grp94 counteracts muscle disuse atrophy by stabilizing subsarcolemmal neuronal nitric oxide synthase.
Article in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 27 citations in OpenAlex.
- DNA hypermethylation preceded by H3K27 trimethylation is linked to downregulation of gene expression in disuse muscle atrophy in male mice.Physiological reports · 2025Article
- Mechanotransduction and Skeletal Muscle Atrophy: The Interplay Between Focal Adhesions and Oxidative Stress.International journal of molecular sciences · 2025Review
- Chaperone Proteins: The Rising Players in Muscle Atrophy.Journal of cachexia, sarcopenia and muscle · 2025Review
- Article
- Role of Dietary Polyphenols in the Activity and Expression of Nitric Oxide Synthases: A Review.Antioxidants (Basel, Switzerland) · 2023Review
- CORP: Gene delivery into murine skeletal muscle using in vivo electroporation.Journal of applied physiology (Bethesda, Md. : 1985) · 2022Review
- Active nNOS Is Required for Grp94-Induced Antioxidant Cytoprotection: A Lesson from Myogenic to Cancer Cells.International journal of molecular sciences · 2022Article
- Nox2 Inhibition Regulates Stress Response and Mitigates Skeletal Muscle Fiber Atrophy during Simulated Microgravity.International journal of molecular sciences · 2021Article
- Review
- Nox2 signaling and muscle fiber remodeling are attenuated by losartan administration during skeletal muscle unloading.Physiological reports · 2021Article
- Perlecan Facilitates Neuronal Nitric Oxide Synthase Delocalization in Denervation-Induced Muscle Atrophy.Cells · 2020Article
- How Postural Muscle Senses Disuse? Early Signs and Signals.International journal of molecular sciences · 2020Review
- Loss of melusin is a novel, neuronal NO synthase/FoxO3-independent master switch of unloading-induced muscle atrophy.Journal of cachexia, sarcopenia and muscle · 2020Article
- Article
- Molecular regulation of skeletal muscle mass and the contribution of nitric oxide: A review.FASEB bioAdvances · 2019Article
- Exciting perspectives for Translational Myology in the Abstracts of the 2018Spring PaduaMuscleDays: Giovanni Salviati Memorial - Chapter II - Abstracts of March 15, 2018.European journal of translational myology · 2018Article
- Glucose-regulated protein 94 is a novel glioma biomarker and promotes the aggressiveness of glioma via Wnt/β-catenin signaling pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Skeletal muscle tissue engineering: methods to form skeletal myotubes and their applications.Tissue engineering. Part B, Reviews · 2014Review
- Time course analysis of mechanical ventilation-induced diaphragm contractile muscle dysfunction in the rat.The Journal of physiology · 2014Article
- Curcumin counteracts loss of force and atrophy of hindlimb unloaded rat soleus by hampering neuronal nitric oxide synthase untethering from sarcolemma.The Journal of physiology · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsRedox and growth-factor imbalance fosters muscle disuse atrophy. Since the endoplasmic-reticulum chaperone Grp94 is required for folding insulin-like growth factors (IGFs) and for antioxidant cytoprotection, we investigated its involvement in muscle mass loss due to inactivity.
resultsRat soleus muscles were transfected in vivo and analyzed after 7 days of hindlimb unloading, an experimental model of muscle disuse atrophy, or standard caging. Increased muscle protein carbonylation and decreased Grp94 protein levels (p<0.05) characterized atrophic unloaded solei. Recombinant Grp94 expression significantly reduced atrophy of transfected myofibers, compared with untransfected and empty-vector transfected ones (p<0.01), and decreased the percentage of carbonylated myofibers (p=0.001). Conversely, expression of two different N-terminal deleted Grp94 species did not attenuate myofiber atrophy. No change in myofiber trophism was detected in transfected ambulatory solei. The absence of effects on atrophic untransfected myofibers excluded a major role for IGFs folded by recombinant Grp94. Immunoprecipitation and confocal microscopy assays to investigate chaperone interaction with muscle atrophy regulators identified 160 kDa neuronal nitric oxide synthase (nNOS) as a new Grp94 partner. Unloading was demonstrated to untether nNOS from myofiber subsarcolemma; here, we show that such nNOS localization, revealed by means of NADPH-diaphorase histochemistry, appeared preserved in unloaded myofibers expressing recombinant Grp94, compared to those transfected with the empty vector or deleted Grp94 cDNA (p<0.02). INNOVATION: Grp94 interacts with nNOS and prevents its untethering from sarcolemma in unloaded myofibers.
conclusionMaintenance of Grp94 expression is sufficient to counter unloading atrophy and oxidative stress by mechanistically stabilizing nNOS-multiprotein complex at the myofiber sarcolemma.
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