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• W2783163763 abstract "New Findings What is the central question of this study ? Translocation of nNOSμ initiates catabolic signalling via FoxO3a and skeletal muscle atrophy during mechanical unloading. Recent evidence suggests that unloading‐induced muscle atrophy and FoxO3a activation are redox sensitive. Will a mimetic of superoxide dismutase and catalase (i.e. Eukarion‐134) also mitigate suppression of the Akt–mTOR pathway? What is the main finding and its importance? Eukarion‐134 rescued Akt–mTOR signalling and sarcolemmal nNOSμ, which were linked to protection against the unloading phenotype, muscle fibre atrophy and partial fibre‐type shift from slow to fast twitch. The loss of nNOSμ from the sarcolemma appears crucial to Akt phosphorylation and is redox sensitive, although the mechanisms remain unresolved. Abstract Mechanical unloading stimulates rapid changes in skeletal muscle morphology, characterized by atrophy of muscle fibre cross‐sectional area and a partial fibre‐type shift from slow to fast twitch. Recent studies revealed that oxidative stress contributes to activation of forkhead box O3a (FoxO3a), proteolytic signalling and unloading‐induced muscle atrophy via translocation of the μ‐splice variant of neuronal nitric oxide synthase (nNOSμ) and activation of FoxO3a. There is limited understanding of the role of reactive oxygen species in the Akt–mammalian target of rapamycin (mTOR) pathway signalling during unloading. We hypothesized that Eukarion‐134 (EUK‐134), a mimetic of the antioxidant enzymes superoxide dismutase and catalase, would protect Akt–mTOR signalling in the unloaded rat soleus. Male Fischer 344 rats were separated into the following three study groups: ambulatory control ( n = 11); 7 days of hindlimb unloading + saline injections (HU, n = 11); or 7 days of HU + EUK‐134; (HU + EUK‐134, n = 9). EUK‐134 mitigated unloading‐induced dephosphorylation of Akt, as well as FoxO3a, in the soleus. Phosphorylation of mTOR in the EUK‐treated HU rats was not different from that in control animals. However, EUK‐134 did not significantly rescue p70S6K phosphorylation. EUK‐134 attenuated translocation of nNOSμ from the membrane to the cytosol, reduced nitration of tyrosine residues and suppressed upregulation of caveolin‐3 and dysferlin. EUK‐134 ameliorated HU‐induced remodelling, atrophy of muscle fibres and the 12% increase in type II myosin heavy chain‐positive fibres. Attenuation of the unloaded muscle phenotype was associated with decreased reactive oxygen species, as assessed by ethidium‐positive nuclei. We conclude that oxidative stress affects Akt–mTOR signalling in unloaded skeletal muscle. Direct linkage of abrogation of nNOSμ translocation with Akt–mTOR signalling during unloading is the subject of future investigation." @default.
• W2783163763 created "2018-01-26" @default.
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• W2783163763 date "2018-02-28" @default.
• W2783163763 modified "2023-09-30" @default.
• W2783163763 title "Effect of Eukarion‐134 on Akt–mTOR signalling in the rat soleus during 7 days of mechanical unloading" @default.
• W2783163763 cites W1545904013 @default.
• W2783163763 cites W1549689418 @default.
• W2783163763 cites W1558821075 @default.
• W2783163763 cites W1575314596 @default.
• W2783163763 cites W1586159393 @default.
• W2783163763 cites W1606604744 @default.
• W2783163763 cites W1893400247 @default.
• W2783163763 cites W1912057247 @default.
• W2783163763 cites W1952466414 @default.
• W2783163763 cites W1968746864 @default.
• W2783163763 cites W196896886 @default.
• W2783163763 cites W1971857747 @default.
• W2783163763 cites W1973434197 @default.
• W2783163763 cites W1973595217 @default.
• W2783163763 cites W1976040089 @default.
• W2783163763 cites W1977724043 @default.
• W2783163763 cites W1986218642 @default.
• W2783163763 cites W1995775121 @default.
• W2783163763 cites W1996868097 @default.
• W2783163763 cites W1997009529 @default.
• W2783163763 cites W1997591046 @default.
• W2783163763 cites W2014329618 @default.
• W2783163763 cites W2023079710 @default.
• W2783163763 cites W2023470228 @default.
• W2783163763 cites W2024411090 @default.
• W2783163763 cites W2029604265 @default.
• W2783163763 cites W2031928067 @default.
• W2783163763 cites W2035088786 @default.
• W2783163763 cites W2053768799 @default.
• W2783163763 cites W2067087675 @default.
• W2783163763 cites W2073719262 @default.
• W2783163763 cites W2074128329 @default.
• W2783163763 cites W2074595210 @default.
• W2783163763 cites W2086493132 @default.
• W2783163763 cites W2090224335 @default.
• W2783163763 cites W2100036657 @default.
• W2783163763 cites W2122524549 @default.
• W2783163763 cites W2124474450 @default.
• W2783163763 cites W2133664160 @default.
• W2783163763 cites W2134811841 @default.
• W2783163763 cites W2144577761 @default.
• W2783163763 cites W2145208853 @default.
• W2783163763 cites W2149012512 @default.
• W2783163763 cites W2150766174 @default.
• W2783163763 cites W2152535965 @default.
• W2783163763 cites W2154042628 @default.
• W2783163763 cites W2159234192 @default.
• W2783163763 cites W2159802435 @default.
• W2783163763 cites W2160605920 @default.
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• W2783163763 cites W2167759935 @default.
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• W2783163763 cites W2206766868 @default.
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• W2783163763 doi "https://doi.org/10.1113/ep086649" @default.
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