scholarly journals miRNA Transcriptome of Hypertrophic Skeletal Muscle with Overexpressed Myostatin Propeptide

2014 ◽  
Vol 2014 ◽  
pp. 1-19 ◽  
Author(s):  
Ruheena Javed ◽  
Lu Jing ◽  
Jinzeng Yang ◽  
Xinyun Li ◽  
Jianhua Cao ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Transgenic Mice ◽  
Muscle Hypertrophy ◽  
Cell Metabolism ◽  
Regulation Of Gene Expression ◽  
Vital Role ◽  
Differentially Expressed ◽  
Mirna Targets ◽  
Skeletal Muscle Hypertrophy ◽  
Solexa Deep Sequencing

MicroRNAs (miRNAs) play an imperative role in cell proliferation, differentiation, and cell metabolism through regulation of gene expression. Skeletal muscle hypertrophy that results from myostatin depression by its propeptide provides an interesting model to understand how miRNA transcriptome is involved in myostatin-based fiber hypertrophy. This study employed Solexa deep sequencing followed by Q-PCR methods to analyze miRNA transcriptome of skeletal muscle of myostatin propeptide transgenic mice in comparison with their littermate controls. A total of 461 mature known and 69 novel miRNAs were reported from this study. Fifty-seven miRNAs were expressed differentially between transgenic and littermate controls, of which most abundant miRNAs, miR-133a and 378a, were significantly differentially expressed. Expression profiling was validated on 8 known and 2 novel miRNAs. The miRNA targets prediction and pathway analysis showed that FST, SMAD3, TGFBR1, and AcvR1a genes play a vital role in skeletal muscle hypertrophy in the myostatin propeptide transgenic mice. It is predicted that miR-101 targeted to TGFBR1 and SMAD3, miR-425 to TGFBR2 and FST, and miR-199a to AcvR2a and TGF-βgenes. In conclusion, the study offers initial miRNA profiling and methodology of miRNA targets prediction for myostatin-based hypertrophy. These differentially expressed miRNAs are proposed as candidate miRNAs for skeletal muscle hypertrophy.

Reduced protein degradation rates and low expression of proteolytic systems support skeletal muscle hypertrophy in transgenic mice overexpressing the c-ski oncogene

2003 ◽  
Vol 200 (2) ◽  
pp. 153-160 ◽  
Author(s):  
Paola Costelli ◽  
Neus Carbó ◽  
Sı́lvia Busquets ◽  
Francisco J López-Soriano ◽  
Francesco M Baccino ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Transgenic Mice ◽  
Protein Degradation ◽  
Muscle Hypertrophy ◽  
Skeletal Muscle Hypertrophy ◽  
Degradation Rates ◽  
Low Expression

scholarly journals Hypertrophy of Rat Skeletal Muscle Is Associated with Increased SIRT1/Akt/mTOR/S6 and Suppressed Sestrin2/SIRT3/FOXO1 Levels

2021 ◽  
Vol 22 (14) ◽  
pp. 7588
Author(s):  
Zoltan Gombos ◽  
Erika Koltai ◽  
Ferenc Torma ◽  
Peter Bakonyi ◽  
Attila Kolonics ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Hypertrophy ◽  
Male Rats ◽  
Cellular Interactions ◽  
Molecular Signaling ◽  
Protein Breakdown ◽  
Rat Skeletal Muscle ◽  
Plantaris Muscle ◽  
Skeletal Muscle Hypertrophy ◽  
Intensive Investigation

Despite the intensive investigation of the molecular mechanism of skeletal muscle hypertrophy, the underlying signaling processes are not completely understood. Therefore, we used an overload model, in which the main synergist muscles (gastrocnemius, soleus) of the plantaris muscle were surgically removed, to cause a significant overload in the remaining plantaris muscle of 8-month-old Wistar male rats. SIRT1-associated pro-anabolic, pro-catabolic molecular signaling pathways, NAD and H2S levels of this overload-induced hypertrophy were studied. Fourteen days of overload resulted in a significant 43% (p < 0.01) increase in the mass of plantaris muscle compared to sham operated animals. Cystathionine-β-synthase (CBS) activities and bioavailable H2S levels were not modified by overload. On the other hand, overload-induced hypertrophy of skeletal muscle was associated with increased SIRT1 (p < 0.01), Akt (p < 0.01), mTOR, S6 (p < 0.01) and suppressed sestrin 2 levels (p < 0.01), which are mostly responsible for anabolic signaling. Decreased FOXO1 and SIRT3 signaling (p < 0.01) suggest downregulation of protein breakdown and mitophagy. Decreased levels of NAD+, sestrin2, OGG1 (p < 0.01) indicate that the redox milieu of skeletal muscle after 14 days of overloading is reduced. The present investigation revealed novel cellular interactions that regulate anabolic and catabolic processes in the hypertrophy of skeletal muscle.

scholarly journals Is an Energy Surplus Required to Maximize Skeletal Muscle Hypertrophy Associated With Resistance Training

2019 ◽  
Vol 6 ◽  
Author(s):  
Gary John Slater ◽  
Brad P. Dieter ◽  
Damian James Marsh ◽  
Eric Russell Helms ◽  
Gregory Shaw ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Resistance Training ◽  
Muscle Hypertrophy ◽  
Skeletal Muscle Hypertrophy ◽  
Energy Surplus

scholarly journals Skeletal muscle hypertrophy and structure and function of skeletal muscle fibres in male body builders

2006 ◽  
Vol 570 (3) ◽  
pp. 611-627 ◽  
Author(s):  
Giuseppe D'Antona ◽  
Francesca Lanfranconi ◽  
Maria Antonietta Pellegrino ◽  
Lorenza Brocca ◽  
Raffaella Adami ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Hypertrophy ◽  
Structure And Function ◽  
Muscle Fibres ◽  
Male Body ◽  
Skeletal Muscle Hypertrophy ◽  
And Function ◽  
Skeletal Muscle Fibres

scholarly journals Pericytes Contribute to Exercise‐Induced Skeletal Muscle Hypertrophy

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Kai Zou ◽  
Heather D. Huntsman ◽  
Carmen Valero ◽  
John T. Skelton ◽  
Joseph T. Adams ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Hypertrophy ◽  
Skeletal Muscle Hypertrophy ◽  
Exercise Induced

scholarly journals The ROS scavenger PDTC affects adaptation to treadmill running in mice: distinct effects on murine body mass, resting heart rate and skeletal muscle fiber type composition

2021 ◽  
Vol 224 (6) ◽  
pp. jeb234237
Author(s):  
Franziska Röchner ◽  
Angelika Schmitt ◽  
Anne-Lena Brändle ◽  
Annunziata Fragasso ◽  
Barbara Munz
Keyword(s):  
Skeletal Muscle ◽  
Heart Rate ◽  
Muscle Hypertrophy ◽  
Muscle Fibers ◽  
Treadmill Running ◽  
Moderate Intensity ◽  
Resting Heart Rate ◽  
Skeletal Muscle Hypertrophy ◽  
Skeletal Muscle Fibers ◽  
Ros Scavenger

ABSTRACTRegular exercise induces a broad spectrum of adaptation reactions in a variety of tissues and organs. However, the respective mechanisms are incompletely understood. In the context of their analysis, animal model systems, specifically rodent treadmill running protocols, play an important role. However, few researchers have studied different aspects of adaptation, such as cardiorespiratory and skeletal muscle training effects, within one set of experiments. Here, we analyzed physiological adaptation to 10 weeks of regular, moderate-intensity, uphill treadmill running in mice, a widely used model for endurance exercise training. To study the effects of reactive oxygen species (ROS), which have been suggested to be major regulators of training adaptation, a subgroup of mice was treated with the ROS scavenger PDTC (pyrrolidine dithiocarbamate). We found that mass gain in mice that exercised under PDTC treatment lagged behind that of all other experimental groups. In addition, both exercise and PDTC significantly and additively decreased resting heart rate. Furthermore, there was a trend towards an enhanced proportion of type 2A skeletal muscle fibers and differential expression of metabolism-associated genes, indicating metabolic and functional adaptation of skeletal muscle fibers. By contrast, there were no effects on grip strength and relative mass of individual muscles, suggesting that our protocol of uphill running did not increase skeletal muscle hypertrophy and strength. Taken together, our data suggest that a standard protocol of moderate-intensity uphill running induces adaptation reactions at multiple levels, part of which might be modulated by ROS, but does not enhance skeletal muscle hypertrophy and force.

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