Atrophy responses to muscle inactivity. II. Molecular markers of protein deficits.

@article{Haddad2003AtrophyRT,
  title={Atrophy responses to muscle inactivity. II. Molecular markers of protein deficits.},
  author={F. Haddad and R. Roy and H. Zhong and V. Edgerton and K. Baldwin},
  journal={Journal of applied physiology},
  year={2003},
  volume={95 2},
  pages={
          791-802
        }
}
We examined the expression of several molecular markers of protein balance in response to skeletal muscle atrophy induced by spinal cord isolation (SI; i.e., a complete transection of the spinal cord at both a midthoracic and a high sacral level plus complete deafferentation between the two transection sites). This treatment nearly eliminates neuromuscular activity (activation and loading) of the hindlimb muscles while maintaining neuromuscular connectivity. SI was associated with a reduced… Expand
Atrophy responses to muscle inactivity. I. Cellular markers of protein deficits.
TLDR
A reduction in ribosomal RNA that is consistent with a reduction in protein translational capacity and an insufficient mRNA substrate for translating key sarcomeric proteins comprising the myofibril fraction, such as MHC and actin, are suggested. Expand
Gene expression during inactivity-induced muscle atrophy: effects of brief bouts of a forceful contraction countermeasure.
TLDR
It is demonstrated that upregulation of specific protein catabolic pathways plays a critical role in SI-induced atrophy, while this response was blunted by 4 min of daily high-resistance electromechanical stimulation and was able to preserve most of the muscle mass. Expand
Gene and protein expression associated with protein synthesis and breakdown in paraplegic skeletal muscle
TLDR
It is concluded that gene and protein expression of pathways associated with protein synthesis are reduced, whereas some markers of protein breakdown remain elevated following chronic paraplegia. Expand
Atrophy responses to muscle inactivity
Haddad, F., R. R. Roy, H. Zhong, V. R. Edgerton, and K. M. Baldwin. Atrophy responses to muscle inactivity. I. Cellular markers of protein deficits. J Appl Physiol 95: 781–790, 2003. First publishedExpand
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The purpose of this review is to synthesize the current understanding of the molecular regulation of muscle atrophy, and discusses how ongoing work should uncover more about the molecular underpinnings of muscle wasting, particularly that due to disuse. Expand
Rapid muscle atrophy response to unloading: pretranslational processes involving MHC and actin.
TLDR
The results show that after only 1 day of unloading, pre-mRNA and mRNA expression of muscle proteins and muscle-specific signaling factors are significantly reduced, suggesting that the downregulation of the synthesis side of the protein balance equation that occurs in atrophying muscle is initiated rapidly. Expand
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TLDR
The findings suggest that molecular markers of contractile protein gene expression serve as useful subcellular indicators for ascertaining the underlying mechanisms regulating alterations in muscle mass in human subjects in response to altered loading states. Expand
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This review examines the current understanding of the cellular and molecular events involved in the control of muscle mass under conditions of muscle use and disuse, with particular attention to the effects of resistance exercise/training. Expand
Inactivity‐induced modulation of Hsp20 and Hsp25 content in rat hindlimb muscles
TLDR
The data indicate that small heat shock protein levels are impacted to a greater degree in muscles that are predominantly slow or have an antigravity function than in flexor muscles, and this response is not influenced by neural activity–independent factors. Expand
Effects of inactivity on fiber size and myonuclear number in rat soleus muscle.
TLDR
The results indicate that a loss of myonuclei is not a prerequisite for sustained muscle fiber atrophy and indicates that chronic inactivity results in smaller, faster fibers that contain a higher than normal amount of DNA per unit of cytoplasm. Expand
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A reduction in ribosomal RNA that is consistent with a reduction in protein translational capacity and an insufficient mRNA substrate for translating key sarcomeric proteins comprising the myofibril fraction, such as MHC and actin, are suggested. Expand
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