scholarly journals Proteome Dynamics Rapidly Detect Protein Synthetic and Fibrogenic Changes Following Eccentric Contraction‐Induced Muscle Damage in mdx Mice

2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Stephen Stimpson ◽  
Fritz Kramer ◽  
Todd Shearer ◽  
Andrew Billin ◽  
Alan Russell ◽  
...  
1999 ◽  
Vol 31 (Supplement) ◽  
pp. S74
Author(s):  
V. M. Kovanen ◽  
D. Pottle ◽  
S. O.A. Koskinen ◽  
T. E.S. Takala ◽  
L. E. Gosselin

2016 ◽  
Vol 54 (1) ◽  
pp. 110-117 ◽  
Author(s):  
Kevin E. Schill ◽  
Alex. R. Altenberger ◽  
Jeovanna Lowe ◽  
Muthu Periasamy ◽  
Frederick A. Villamena ◽  
...  

2011 ◽  
Vol 111 (1) ◽  
pp. 200-205 ◽  
Author(s):  
Jarrod A. Call ◽  
James M. Ervasti ◽  
Dawn A. Lowe

Previously, we demonstrated functional substitution of dystrophin by TAT-μUtrophin (TAT-μUtr) in dystrophin-deficient mdx mice. Herein, we addressed whether TAT-μUtr could improve the phenotype of dystrophin and utrophin double-knockout ( mdx:utr−/−) mice. Specifically, we quantitatively compared survival and quality of life assessments in mdx:utr−/− mice receiving TAT-μUtr protein administration against placebo-treated mdx:utr−/− mice (PBS). Additionally, skeletal muscles from TAT-μUtr and PBS mice were tested in vivo and ex vivo for strength and susceptibility to eccentric contraction-induced injury. We found the TAT-μUtr treatment extended life span 45% compared with mice administered PBS. This was attributed to significantly increased food consumption (3.1 vs. 1.8 g/24 h) due to improved ability to search for food as daily cage activities were greater in TAT-μUtr mice (e.g., 364 vs. 201 m ambulation/24 h). The extensor digitorum longus muscles of TAT-μUtr-treated double-knockout mice also displayed increased force-generating capacity ex vivo (8.3 vs. 6.4 N/cm2) and decreased susceptibility to injury ex vivo and in vivo. These data indicate that the functional benefits of TAT-μUtr replacement treatment extend to the mdx:utr−/− double-knockout mouse and support its development as a therapy to mitigate muscle weakness in patients with Duchenne muscular dystrophy.


2013 ◽  
Vol 21 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Felipe Romano Damas Nogueira ◽  
Miguel Soares Conceição ◽  
Felipe Cassaro Vechin ◽  
Edson Manoel Mendes Junior ◽  
Guilherme Fernando Couto Rodrigues ◽  
...  

2017 ◽  
Vol 53 (4) ◽  
pp. 233
Author(s):  
Ahmad Abdullah ◽  
Herdianty Kusuma ◽  
Elyana Asnar ◽  
Bambang Purwanto

The eccentric contraction has been proven to improve Glut-1 expression in muscle and fasting glucose levels in mice. The same eccentric contraction occurs in human being when walking or running while wearing high heels. Innovation on the eccentric contraction with high heels can be done by using a specific shoe insole. The design of the rear insole is made thicker than the front. The purpose of this study was to determine the effects of insole use specified for eccentric activities on daily work shoes on the skeletal muscle damage after wearing the specified insole. Skeletal muscle damage was measured based on sTnI level. This was experimental study with pretest-posttest design. The subjects involved were non-diabetic woman workers in Faculty of Medicine of Universitas Airlangga, and were divided into two groups. Each group represented group members who wore 5-degree and 10-degree insoles respectively. The angle used for the shoe insoles were 5° and 10° respectively. These insoles were worn on weekdays for one week. Blood was taken one day after the subjects stop wearing the insoles. Data results showed that the levels of fasting blood glucose (FBG) of subjects who wore the 10-degree insole had a value of p<0.05. The use of insole lead to decreased levels of fasting blood glucose (FBG). This study found that the sTnI levels in the 5-degree and 10-degree insole groups had no significant effect on troponin I skeletal muscle levels before and after treatment.


2020 ◽  
Vol 105 (6) ◽  
pp. 989-999
Author(s):  
H. R. Spaulding ◽  
T. Quindry ◽  
J. C. Quindry ◽  
J. T. Selsby

2019 ◽  
Vol 30 (3) ◽  
pp. 462-471
Author(s):  
Eisuke Ochi ◽  
Hisashi Ueda ◽  
Yosuke Tsuchiya ◽  
Karina Kouzaki ◽  
Koichi Nakazato

2019 ◽  
Vol 126 (6) ◽  
pp. 1737-1745 ◽  
Author(s):  
Abhinandan Batra ◽  
Ravneet S. Vohra ◽  
Steve M. Chrzanowski ◽  
David W. Hammers ◽  
Donovan J. Lott ◽  
...  

Lack of sarcolemma-localized neuronal nitric oxide synthase mu (nNOSμ) contributes to muscle damage and fatigue in dystrophic muscle. In this study, we examined the effects of compensating for lack of nNOSμ with a phosphodiesterase type 5 (PDE5) inhibitor in mdx mice following downhill running and endurance training. Dystrophic mice ( mdx) were treated with sildenafil citrate and compared with untreated mdx and wild-type mice after an acute bout of downhill running and during a progressive low-intensity treadmill running program (5 days/wk, 4 wk). Magnetic resonance imaging (MRI) and spectroscopy (MRS) transverse relaxation time constant (T2) of hindlimb and forelimb muscles were measured as a marker of muscle damage after downhill running and throughout training. The MRI blood oxygenation level dependence (BOLD) response and 31phosphorus MRS (31P-MRS) data were acquired after stimulated muscle contractions. After downhill running, the increase in T2 was attenuated ( P < 0.05) in treated mdx and wild-type mice compared with untreated mdx. During training, resting T2 values did not change in wild-type and mdx mice from baseline values; however, the running distance completed during training was greater ( P < 0.05) in treated mdx (>90% of target distance) and wild-type (100%) than untreated mdx (60%). The post-contractile BOLD response was greater ( P < 0.05) in treated mdx that trained than untreated mdx, with no differences in muscle oxidative capacity, as measured by 31P-MRS. Our findings indicate that PDE5 inhibition reduces muscle damage after a single bout of downhill running and improves performance during endurance training in dystrophic mice, possibly because of enhanced microvascular function. NEW & NOTEWORTHY This study examined the combined effects of PDE5 inhibition and exercise in dystrophic muscle using high-resolution magnetic resonance imaging and spectroscopy. Our findings demonstrated that sildenafil citrate reduces muscle damage after a single bout of downhill running, improves endurance-training performance, and enhances microvascular function in dystrophic muscle. Collectively, the results support the combination of exercise and PDE5 inhibition as a therapeutic approach in muscular dystrophies lacking nNOSμ.


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