scholarly journals Epac2a-knockout mice are resistant to dexamethasone-induced skeletal muscle atrophy and short-term cold stress

BMB Reports ◽  
2018 ◽  
Vol 51 (1) ◽  
pp. 39-44 ◽  
Author(s):  
Seung-Eun Song ◽  
Su-Kyung Shin ◽  
So-Young Park ◽  
Il-Seon Hwang ◽  
Seung-Soon Im ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cold Stress ◽  
Muscle Atrophy ◽  
Knockout Mice ◽  
Skeletal Muscle Atrophy ◽  
Short Term

scholarly journals Effect of short-term hindlimb immobilization on skeletal muscle atrophy and the transcriptome in a low compared with high responder to endurance training model

PLoS ONE ◽  
2022 ◽  
Vol 17 (1) ◽  
pp. e0261723
Author(s):  
Jamie-Lee M. Thompson ◽  
Daniel W. D. West ◽  
Thomas M. Doering ◽  
Boris P. Budiono ◽  
Sarah J. Lessard ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endurance Training ◽  
Muscle Atrophy ◽  
Female Rats ◽  
Skeletal Muscle Atrophy ◽  
Biological Processes ◽  
Short Term ◽  
Cast Immobilization ◽  
Protein Ubiquitination ◽  
Differential Gene

Skeletal muscle atrophy is a physiological response to disuse, aging, and disease. We compared changes in muscle mass and the transcriptome profile after short-term immobilization in a divergent model of high and low responders to endurance training to identify biological processes associated with the early atrophy response. Female rats selectively bred for high response to endurance training (HRT) and low response to endurance training (LRT; n = 6/group; generation 19) underwent 3 day hindlimb cast immobilization to compare atrophy of plantaris and soleus muscles with line-matched controls (n = 6/group). RNA sequencing was utilized to identify Gene Ontology Biological Processes with differential gene set enrichment. Aerobic training performed prior to the intervention showed HRT improved running distance (+60.6 ± 29.6%), while LRT were unchanged (-0.3 ± 13.3%). Soleus atrophy was greater in LRT vs. HRT (-9.0 ±8.8 vs. 6.2 ±8.2%; P<0.05) and there was a similar trend in plantaris (-16.4 ±5.6% vs. -8.5 ±7.4%; P = 0.064). A total of 140 and 118 biological processes were differentially enriched in plantaris and soleus muscles, respectively. Soleus muscle exhibited divergent LRT and HRT responses in processes including autophagy and immune response. In plantaris, processes associated with protein ubiquitination, as well as the atrogenes (Trim63 and Fbxo32), were more positively enriched in LRT. Overall, LRT demonstrate exacerbated atrophy compared to HRT, associated with differential gene enrichments of biological processes. This indicates that genetic factors that result in divergent adaptations to endurance exercise, may also regulate biological processes associated with short-term muscle unloading.

scholarly journals Exercise preconditioning diminishes skeletal muscle atrophy after hindlimb suspension in mice

2018 ◽  
Vol 125 (4) ◽  
pp. 999-1010 ◽  
Author(s):  
Nicholas T. Theilen ◽  
Nevena Jeremic ◽  
Gregory J. Weber ◽  
Suresh C. Tyagi
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Muscle Atrophy ◽  
Mitochondrial Biogenesis ◽  
Weight Ratio ◽  
Hindlimb Suspension ◽  
Skeletal Muscle Atrophy ◽  
Short Term ◽  
Concurrent Exercise ◽  
And Function

The aim of the present study was to investigate whether short-term, concurrent exercise training before hindlimb suspension (HLS) prevents or diminishes both soleus and gastrocnemius atrophy and to analyze whether changes in mitochondrial molecular markers were associated. Male C57BL/6 mice were assigned to control at 13 ± 1 wk of age, 7-day HLS at 12 ± 1 wk of age (HLS), 2 wk of exercise training before 7-day HLS at 10 ± 1 wk of age (Ex+HLS), and 2 wk of exercise training at 11 ± 1 wk of age (Ex) groups. HLS resulted in a 27.1% and 21.5% decrease in soleus and gastrocnemius muscle weight-to-body weight ratio, respectively. Exercise training before HLS resulted in a 5.6% and 8.1% decrease in soleus and gastrocnemius weight-to-body weight ratio, respectively. Exercise increased mitochondrial biogenesis- and function-associated markers and slow myosin heavy chain (SMHC) expression, and reduced fiber-type transitioning marker myosin heavy chain 4 (Myh4). Ex+HLS revealed decreased reactive oxygen species (ROS) and oxidative stress compared with HLS. Our data indicated the time before an atrophic setting, particularly caused by muscle unloading, may be a useful period to intervene short-term, progressive exercise training to prevent skeletal muscle atrophy and is associated with mitochondrial biogenesis, function, and redox balance. NEW & NOTEWORTHY Mitochondrial dysfunction is associated with disuse-induced skeletal muscle atrophy, whereas exercise is known to increase mitochondrial biogenesis and function. Here we provide evidence of short-term concurrent exercise training before an atrophic event protecting skeletal muscle from atrophy in two separate muscles with different, dominant fiber-types, and we reveal an association with the adaptive changes of mitochondrial molecular markers to exercise.

Skeletal muscle atrophy during short-term disuse: Implications for age-related sarcopenia

2013 ◽  
Vol 12 (4) ◽  
pp. 898-906 ◽  
Author(s):  
Benjamin T. Wall ◽  
Marlou L. Dirks ◽  
Luc J.C. van Loon
Keyword(s):  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Skeletal Muscle Atrophy ◽  
Short Term ◽  
Age Related

scholarly journals Skeletal muscle proteolysis in response to short-term unloading in humans

2008 ◽  
Vol 105 (3) ◽  
pp. 902-906 ◽  
Author(s):  
Per A. Tesch ◽  
Ferdinand von Walden ◽  
Thomas Gustafsson ◽  
Richard M. Linnehan ◽  
Todd A. Trappe
Keyword(s):  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Simulated Microgravity ◽  
Skeletal Muscle Atrophy ◽  
Muscle Loss ◽  
Short Term ◽  
Promising Tool ◽  
Muscle Disuse ◽  
Naturally Occurring ◽  
Muscle Contractile

Skeletal muscle atrophy is evident after muscle disuse, unloading, or spaceflight and results from decreased protein content as a consequence of decreased protein synthesis, increased protein breakdown or both. At this time, there are essentially no human data describing proteolysis in skeletal muscle undergoing atrophy on Earth or in space, primarily due to lack of valid and accurate methodology. This particular study aimed at assessing the effects of short-term unloading on the muscle contractile proteolysis rate. Eight men were subjected to 72-h unilateral lower limb suspension (ULLS) and intramuscular interstitial levels of the naturally occurring proteolytic tracer 3-methylhistidine (3MH) were measured by means of microdialysis before and on completion of this intervention. The 3MH concentration following 72-h ULLS (2.01 ± 0.22 nmol/ml) was 44% higher ( P < 0.05) than before ULLS (1.56 ± 0.20 nmol/ml). The present experimental model and the employed method determining 3MH in microdialysates present a promising tool for monitoring skeletal muscle proteolysis or metabolism of specific muscles during conditions resulting in atrophy caused by, e.g., disuse and real or simulated microgravity. This study provides evidence that the atrophic processes are evoked rapidly and within 72 h of unloading and suggests that countermeasures should be employed in the early stages of space missions to offset or prevent muscle loss during the period when the rate of muscle atrophy is the highest.

Absence of caspase-3 protects against denervation-induced skeletal muscle atrophy

2009 ◽  
Vol 107 (1) ◽  
pp. 224-234 ◽  
Author(s):  
Pamela J. Plant ◽  
James R. Bain ◽  
Judy E. Correa ◽  
Minna Woo ◽  
Jane Batt
Keyword(s):  
Skeletal Muscle ◽  
Muscle Atrophy ◽  
Knockout Mice ◽  
Caspase 3 ◽  
Skeletal Muscle Atrophy ◽  
Wild Type ◽  
Denervated Muscle ◽  
Apoptotic Signaling ◽  
Ubiquitin Proteasome ◽  
Denervated Muscles

The ubiquitin-proteasome system is a key proteolytic pathway activated during skeletal muscle atrophy. The proteasome, however, cannot degrade intact myofibrils or actinomyosin complexes. In rodent models of diabetes mellitus and uremia, caspase-3 is involved in actinomyosin cleavage, generating fragments that subsequently undergo ubiquitin-proteasome-mediated degradation. Here, we demonstrate that caspase-3 also mediates denervation-induced muscle atrophy. At 2 wk after tibial nerve transection, the denervated gastrocnemius of caspase-3-knockout mice weighed more and demonstrated larger fiber-type-specific cross-sectional area than the denervated gastrocnemius of wild-type mice. However, there was no difference between caspase-3-knockout and wild-type denervated muscles in the magnitude or pattern of actinomyosin degradation, as determined by Western blotting for actin and the 14-kDa actin fragment. Similarly, there was no difference between caspase-3-knockout and wild-type denervated muscles in the magnitude of increase in proteasome activity, total protein ubiquitination, or atrogin-1 and muscle-specific ring finger protein 1 transcript levels. In contrast, there was an increase in TdT-mediated dUTP nick end label-positive nuclei in the denervated muscle of wild-type compared with caspase-3-knockout mice. Apoptotic signaling upstream of caspase-3 remained intact, with equivalent mitochondrial Bax translocation and cytochrome c release and caspase-9 activation in the denervated gastrocnemius muscle of wild-type and caspase-3-knockout mice. In contrast, diminished poly(ADP-ribose) polymerase cleavage in the denervated muscle of caspase-3-knockout compared with wild-type mice revealed that apoptotic signaling downstream of caspase-3 was impaired, suggesting that the absence of caspase-3 protects against denervation-induced muscle atrophy by suppressing apoptosis as opposed to ubiquitin-proteasome-mediated protein degradation.

Sign in / Sign up

Export Citation Format

Share Document