TY - JOUR. T1 - Muscle-bone interactions in dystrophin-deficient and myostatin-deficient mice. AU - Montgomery, Eric. AU - Pennington, Catherine. AU - Isales, Carlos M.. AU - Hamrick, Mark W.. PY - 2005/9/1. Y1 - 2005/9/1. N2 - We have investigated muscle-bone interactions using two mouse mutants that are known to differ from normal mice in skeletal muscle growth and development: mice lacking myostatin (GDF8) and mice lacking dystrophin (mdx). Myostatin-deficient mice show increased muscle size and strength compared to normal mice, whereas the mdx mouse is a well-established animal model for Duchenne muscular dystrophy. The mdx mice have significantly larger hindlimb muscles than controls, and histological sections of the quadriceps muscles show dystrophic changes with extensive fibrosis. Femoral bone mineral density (BMD) and fracture strength (Fu) are significantly greater in mdx mice than controls, and these variables are more strongly correlated with quadriceps muscle mass than with body ...

Myostatin inhibits myogenesis and there is reduced abundance of the mature protein in skeletal muscles of adult male compared with female mice. This reduction probably occurs after translation, which suggests that it is a regulated mechanism to reduce the availability of myostatin in males. Reduced myostatin may, thereby, contribute to the development of sexually dimorphic growth of skeletal muscle. Our first objective was to determine if the decrease in mature myostatin protein occurs before the linear growth phase to aid growth, or afterwards to maintain the mass of adult muscle. Mice were killed from 2 to 32 weeks and the gastrocnemius muscle was excised. Myostatin mRNA increased from 2 to 32 weeks and was higher in males than females (P , 0.001). In contrast, mature protein decreased in males after 6 weeks (P , 0.001). Our second objective was to determine if growth hormone (GH) induces the decrease in mature myostatin protein. GH increased myostatin mRNA and decreased the abundance of ...

Myostatin (MSTN) is a secreted protein that acts as a negative regulator of skeletal muscle growth. Deficiencies in this protein have been shown to increase muscle mass in a variety of animal models. Consequently, clinical suppression of myostatin is now being pursued as a therapeutic strategy to counteract the muscle wasting that occurs in patients with degenerative neuromuscular diseases such as Duchenne Muscular Dystrophy (DMD). Although research supports the use of myostatin suppression therapy to increase muscle mass, investigation into the effects of myostatin on tendon is limited. The aim of this study was to investigate the effects of myostatin deficiency by characterizing the structural, material and compositional properties of the Achilles tendons from mature (16 week old) male myostatin deficient (MSTN-/-), wild type (MSTN+/+), and heterozygous (MSTN+/-) mice. Specifically, we tested the hypothesis that myostatin deficiency is associated with stiffer and stronger tendons, that these effects

Myostatin (GDF8, MSTN) belongs to the transforming growth factor β (TGFBs) superfamily, which includes: TGF-βs, the bone morphogenetic proteins (BMPs), growth differentiation factors (GDFs), activins and inhibins. As other members of this superfamily, it is synthesized and secreted as a homodimeric prepropeptide that is cleaved by proprotein convertases such as furin to generate the dimeric N- terminal propeptide and the dimeric C-terminal mature active protein. Myostatin is one of the most important proteins that controls myoblast proliferation and it is a potent negative regulator of skeletal muscle mass in a number of animal species. Several studies have shown that Myostatin could play an important role in cardiac development and physiology. Genetic deletion of Myostatin or in vivo administration of the Myostatin propeptide induces muscle hypertrophy as well as enhanced glucose utilization and insulin sensitivity and a reduction in overall fat mass. Recombinant human Myostatin is a ...

Myostatin (also known as growth differentiation factor 8, abbreviated GDF-8) is a myokine. A myokine is a protein produced and released by myocytes that acts on the autocrine function of muscle cells to inhibit myogenesis: muscle cell growth and differentiation. In humans it is encoded by the MSTN gene. Myostatin is a secreted growth differentiation factor that is a member of the TGF beta protein family. Myostatin also inhibits Akt, a kinase that causes muscle hypertrophy, in part through the activation of protein synthesis. Further research into myostatin and the myostatin gene may lead to therapies for muscular dystrophy.. *This description is meant for informational purposes only and is publicly available. ...

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TY - JOUR. T1 - Bone architecture and disc degeneration in the lumbar spine of mice lacking GDF-8 (myostatin). AU - Hamrick, Mark W.. AU - Pennington, Catherine. AU - Byron, Craig D.. PY - 2003/1/1. Y1 - 2003/1/1. N2 - GDF-8, also known as myostatin, is a member of the transforming growth factor-β superfamily of secreted growth and differentiation factors that is expressed in vertebrate skeletal muscle. Myostatin functions as a negative regulator of skeletal muscle growth and myostatin null mice show a doubling of muscle mass compared to normal mice. We describe here morphology of the lumbar spine in myostatin knockout (Mstn-/-) mice using histological and densitometric techniques. The Mstn-/- mice examined in this study weigh approximately 10% more than controls (p , 0.001) but the iliopsoas muscle is over 50% larger in the knockout mice than in wild-type mice (p , 0.001). Peripheral quantitative computed tomography (pQCT) data from the fifth lumbar vertebra show that mice lacking myostatin ...

In mammals, reduced levels of myostatin or increased levels of follistatin, which acts to inhibit myostatin production, can be achieved by a variety of methods ranging from gene therapy to RNA interference, the standard panoply of technologies used to adjust the amounts of a particular protein in animal studies. Suitably altered levels of myostatin or follistatin result in greatly increased muscle growth, lower amounts of body fat, and in mice at least a possible but disputed modest life extension to go along with it. The most direct methodology is knockout of the myostatin gene, and this is the path chosen of late by Chinese researchers in their work on dogs, using CRISPR, one of the latest advances in genetic editing technology.. The creation of genetically altered, heavily muscled dogs is not an isolated line of research. There is at least one dog breed in which a myostatin mutation has occurred naturally, and the same goes for cows, another species heavily influenced by centuries of quite ...

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Author SummaryAn individuals genetic profile can play a role in defining their natural skills and talents. The canine species presents an excellent system in which to find such associative genes. The purebred dog has a long history of selective breeding, which has produced specific breeds of extraordinary strength, intelligence, and speed. We have discovered a mutation in the canine myostatin gene, a negative regulator of muscle mass, which affects muscle composition, and hence racing speed, in whippets. Dogs that possess a single copy of this mutation are more muscled than normal and are among the fastest dogs in competitive racing events. However, dogs with two copies of the same mutation are grossly overmuscled, superficially resembling double-muscled cattle known to possess similar mutations. This result is the first to quantitatively link a mutation in the myostatin gene to athletic performance. Further, it emphasizes what is sure to be a growing area of research for performance-enhancing

Extreme heat and cold events can create deleterious physiological changes in cattle as they attempt to cope. The genetic background of animals can influence their response to these events. The objective of the current study was to determine the impact of myostatin genotype (MG) on body temperature during periods of heat and cold stress. Two groups of crossbred steers and heifers of unknown pedigree and breed fraction with varying percentages of Angus, Simmental, and Piedmontese were placed in a feedlot over 2 summers and 2 winters. Before arrival, animals were genotyped for the Piedmontese-derived myostatin mutation (C313Y) to determine their MG as either homozygous normal (0 copy; n = 84), heterozygous (1 copy; n = 96), or homozygous for inactive myostatin (2 copy; n = 59). Hourly tympanic and vaginal temperature measurements were collected for steers and heifers, respectively, for 5 d during times of anticipated heat and cold stress. Mean (±SD) ambient temperature for summer and winter stress events

We cloned and characterized a 3.3-kb fragment containing the 5-regulatory region of the human myostatin gene. The promoter sequence contains putative muscle growth response elements for glucocorticoid, androgen, thyroid hormone, myogenic differentiation factor 1, myocyte enhancer factor 2, peroxiso …

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When John Knopf co-founded Acceleron Pharma in the spring of 2003, a muscle protein called myostatin had been on his and other researchers radar for several years. The protein had been identified as a negative regulator (limiter) of muscle growth and regeneration back in 1997. And, since that time, myostatin-deficient mice and cattle had been shown to have large, strong muscles without... ...

The effects of resistance training on serum levels of myostatin and GASP-1, may explain the increased muscle mass that is amplified by creatine supplementation. Myostatin is a catabolic regulator of skeletal muscle mass. The purpose of this study was to determine the effect of resistance training for 8 weeks in conjunction with creatine supplementation on muscle strength, lean body mass, and serum levels of myostatin and growth and differentiation factor-associated serum protein-1 (GASP-1). In a double-blinded design 27 healthy male subjects (23.42+/-2.2 years) were assigned to control (CON), resistance training+placebo (RT+PL) and resistance training+creatine supplementation (RT+CR) groups. The protocol consisted of 3 days per week of training for 8 weeks, each session including three sets of 8-10 repetitions at 60-70% of 1 RM for whole-body exercise. Blood sampling, muscular strength testing and body composition analysis (full body DEXA) were performed at 0, 4th and 8th weeks. Myostatin and GASP-1 was

Myostatin or growth and differentiation factor 8 (GDF8), is a skeletal muscle regulator factor that determines muscle mass in animals including human beings. Mutation in the myostatin gene sequence controls its regulating function and results in growth via hypertrophy of muscles. Mutation in myostatin gene has been found in various species of animals and has three exons and two introns in all species. Considering the MSTN gene as a candidate gene for gene assisted selection for growth traits, the present study was aimed to study its polymorphism and its association in Boer and Bakerwal goats in Kashmir valley. We screened polymorphism of the myostatin gene in 600 goats from two goat populations (Boer and Bakerwal) and applied PCR and DNA sequencing analysis to reveal single nucleotide polymorphisms (g.368A|C (p.Lys to Thr). At g.368A|C locus, the frequencies of g.368A allele were 0.70-0.80, and the frequencies of g.368C allele were 0.20-0.30 in Boer goats. And at g.368A|C locus, the frequencies

eng] Increasing size and strength of skeletal muscle represents a promising therapeutic strategy for muscular disorders. One possible new tool is Myostatin (Mstn) because it plays a crucial role in regulating skeletal muscle mass. The first goal of our work was to determine whether Mstn inhibition could prevent muscle atrophy in catabolic states. As glucocorticoids play a major role in most muscle atrophy models, we assessed whether muscle atrophy caused by glucocorticoids in excess could be prevented by Mstn inhibition. This hypothesis was suggested by the fact that glucocorticoids increase muscle Mstn expression and that Mstn muscle overexpression is sufficient to cause muscle atrophy. Our work showed that deletion of Mstn gene protects skeletal muscle from glucocorticoid-induced atrophy, partially through inhibition of proteolysis. The identification of Mstn binding proteins able to inhibit Mstn activity has led to potential new approaches for postdevelopmental muscle mass enhancement. These ...

The main finding in the current study was that chronic elevations in the GH/IGF axis regulate critical signaling pathways involved in both skeletal muscle protein synthesis and atrophy. Transgenic bGH mice have elevations in Akt1 expression and increased phosphorylation of downstream targets responsible for muscle hypertrophy. However, these mice also show increased intramuscular signaling typically associated with skeletal muscle atrophy. We provide novel evidence that MuRF1 is upregulated in a muscle group-dependent manner in bGH mice. We also demonstrate for the first time that myostatin, its receptor (AcvR2B), and part of its canonical pathway (Smad2) are upregulated in the skeletal muscle of mice overexpressing GH. Taken together, our findings suggest that in environments of chronic GH and/or IGF-1 excess, MuRF1 and myostatin may act to inhibit excess muscle growth, especially in skeletal muscle containing a high proportion of fast twitch fibers.. To our knowledge, this is the first study ...

Myostatin (Mstn) is a negative regulator of skeletal muscle fibre size and satellite cell proliferation whose role in mature fibre compensatory growth has not been fully characterized. Myostatin knockout (Mstn-/-) mice display consistently larger skeletal muscle masses, as well as an overall increase in size and number of myofibres within the muscle, compared to the wild-type mice. Previous research has shown that Mstn plays a major role in the attenuation of both the hypertrophic and hyperplasic pathways of myofibre growth. Immunohistochemical staining of overloaded plantaris muscles was performed to analyze phenotypic and morphological changes in wild-type and Mstn-/- muscles. Preliminary results of these analyses indicated a tendency for muscles from Mstn-/- mice to express an increased number of myofibres, whereas muscles from Mstn+/+ mice tended to display hypertrophied pre-existing mature myofibres as a response to the overload stimulus. Additionally, using semi-quantitative PCR and ...

North American Piedmontese cattle are a breed of domestic beef cattle originating from an imported herd of select Italian purebred Piedmontese cattle (Piemontese or razza bovina Piemontese). The foundation line of breeding stock was first imported from Italy into Canada in 1979, and into the United States in the early 1980s. Piedmontese cattle are distinguished by a unique, naturally occurring gene identified as the myostatin allele mutation, or inactive myostatin gene. Myostatin prohibits muscle growth whereas an inactive gene has the opposite effect. Purebred Piedmontese are homozygous, (2 copy), which means they have two identical alleles present for this unique gene. Research indicates the presence of the myostatin allele mutation produces morphological characteristics unique to the breed, such as double-muscling, beef tenderness, reduced fat content and high yield. According to the North American Piedmontese Association (NAPA), they are the first breed registry to base animal registration ...

The Belgian Blue has a natural mutation in the myostatin gene which codes for the protein, myostatin (myo meaning muscle and statin meaning stop).[5] Myostatin is a protein that inhibits muscle development. This mutation also interferes with fat deposition, resulting in very lean meat.[5] The truncated myostatin gene is unable to function in its normal capacity, resulting in accelerated lean muscle growth. Muscle growth is due primarily to physiological changes in the animals muscle cells (fibers) from hypertrophy to a hyperplasia mode of growth. This particular type of growth is seen early in the fetus of a pregnant dam, which results in a calf that is born with two times the number of muscle fibers at birth than a calf with no myostatin gene mutation.[5] In addition, a newborn double-muscled calfs birth weight is significantly greater than that of a normal calf.[4] Belgian Blue cattle have improved feed conversion ratio (FCR) due to lower feed intake compared to weight gain[4] due to an ...

Myostatin, a member of the transforming growth factor-β (TGF-β) superfamily of secreted proteins, is a potent negative regulator of myogenesis. Free myostatin induces the phosphorylation of the Smad family of transcription factors, which, in turn, regulates gene expression, via the canonical TGF-β signaling pathway. There is, however, emerging evidence that myostatin can regulate gene expression independent of Smad signaling.. As such, researchers at the University of Calgary, Canada acquired global gene expression data from the gastrocnemius muscle of C57BL/6 mice following a 6-day treatment with recombinant myostatin compared with vehicle-treated animals. Of the many differentially expressed genes, the myostatin-associated decrease (-11.20-fold; P , 0.05) in the noncoding metastasis-associated lung adenocarcinoma transcript 1 (Malat1) was the most significant and the most intriguing because of numerous reports describing its novel role in regulating cell growth.. ...

TY - JOUR. T1 - Myostatin inhibition prevents skeletal muscle pathophysiology in Huntingtons disease mice. AU - Bondulich, Marie K.. AU - Jolinon, Nelly. AU - Osborne, Georgina F.. AU - Smith, Edward J.. AU - Rattray, Ivan. AU - Neueder, Andreas. AU - Sathasivam, Kirupa. AU - Ahmed, Mhoriam. AU - Ali, Nadira. AU - Benjamin, Agnesska C.. AU - Chang, Xiaoli. AU - DIck, James R.T.. AU - Ellis, Matthew. AU - Franklin, Sophie A.. AU - Goodwin, Daniel. AU - Inuabasi, Linda. AU - Lazell, Hayley. AU - Lehar, Adam. AU - Richard-Londt, Angela. AU - Rosinski, Jim. AU - Smith, Donna L.. AU - Wood, Tobias. AU - Tabrizi, Sarah J.. AU - Brandner, Sebastian. AU - Greensmith, Linda. AU - Howland, David. AU - Munoz-Sanjuan, Ignacio. AU - Lee, Se Jin. AU - Bates, Gillian P.. N1 - Funding Information: We wish to thank Rainer Kuhn, Andreas Weiss and Michal Mielcarek for helpful discussions and Michal Mielcarek for experimental work. This work was supported by the CHDI Foundation, the Medical Research Council ...

So heres whats in Hyper Gain Black and why its so effective:. Kre-Alkalyn®: We couldnt call it Hyper Gain without including the original ingredient that started it all! Still heralded as the King of Creatine with its patented pH-buffered profile, Kre-Alkalyn is up to 10x more potent than regular creatine monohydrate because it doesnt convert to the toxic byproduct creatinine. This means more creatine in your cells for more power, more pumps, and more endurance - leading to greater muscle growth!. Creatine has also recently been shown to be a myostatin inhibitor, meaning it temporarily prevents the myostatin protein from being synthesized by your skeletal muscle. If youre not familiar, myostatin is the major governor on your overall muscle-growth potential. Less myostatin means more muscle - and supplementing with creatine has shown to do exactly that!. Creatine MagnaPower®: A newcomer to the buffered creatine market, CMP is another impressive, patented buffered creatine that actually ...

Amthor H, Nicholas G, McKinnell I, Kemp CF, et al. (2004). Follistatin complexes Myostatin and antagonises Myostatin-mediated inhibition of myogenesis. Dev. Biol. 270: 19-30. http://dx.doi.org/10.1016/j.ydbio.2004.01.046 PMid:15136138 Diel P, Schiffer T, Geisler S, Hertrampf T, et al. (2010). Analysis of the effects of androgens and training on myostatin propeptide and follistatin concentrations in blood and skeletal muscle using highly sensitive immuno PCR. Mol. Cell Endocrinol. 330: 1-9. http://dx.doi.org/10.1016/j.mce.2010.08.015 PMid:20801187 Dinh P, Hazel A, Palispis W, Suryadevara S, et al. (2009). Functional assessment after sciatic nerve injury in a rat model. Microsurgery 29: 644-649. http://dx.doi.org/10.1002/micr.20685 PMid:19653327 Gilson H, Schakman O, Kalista S, Lause P, et al. (2009). Follistatin induces muscle hypertrophy through satellite cell proliferation and inhibition of both myostatin and activin. Am. J. Physiol. Endocrinol. Metab. 297: E157-E164. ...

Obese adults are prone to develop metabolic and cardiovascular diseases. Furthermore, over-weight expectant mothers give birth to large babies who also have increased likelihood of developing metabolic and cardiovascular diseases. Fundamental advancements to better understand the pathophysiology of obesity are critical in the development of anti-obesity therapies not only for this but also future generations. Skeletal muscle plays a major role in fat metabolism and much work has focused in promoting this activity in order to control the development of obesity. Research has evaluated myostatin inhibition as a strategy to prevent the development of obesity and concluded in some cases that it offers a protective mechanism against a high-fat diet. Pregnant as well as virgin myostatin null mice and age matched wild type animals were raised on a high fat diet for up to 10 weeks. The effect of the diet was tested on skeletal muscle, liver and fat. Quantitate PCR, Western blotting, immunohistochemistry, in-vivo

Smad7 is an intracellular antagonist of transforming growth factor-β signalling pathways and modulates muscle growth in vivo. Loss of Smad7 results in decreased muscle mass, reduced force generation, fibre type switching from glycolytic towards oxidative type and delayed recovery from injury. Upregulated Smad2/3 signalling in Smad7(-/-) muscle results in reduced myoblast proliferation and differentiation. Smad7 is an important regulator of muscle growth and may be a potential intracellular therapeutic target for muscle disorders.The transforming growth factor-β (TGF-β) family of growth factors plays an essential role in mediating cellular growth and differentiation. Myostatin is a muscle-specific member of the TGF-β superfamily and a negative regulator of muscle growth. Myostatin inhibitors are currently being pursued as therapeutic options for muscle disorders. Smad7 inhibits intracellular myostatin signalling via Smad2/3, and thus presents a means of regulating myostatin and potentiating ...

The bodys remarkable ability to repair itself from damage is both very useful and extremely complex. The wound healing system is characterised by four overlapping phases: hemostasis, inflammation, proliferation, and remodelling. It is designed to heal rapidly and efficiently any breach in the protective barrier we call skin, in order to restore normal body function in the quickest possible time. However, pathological conditions such as keloids or hypertrophic scar may arise if events in the wound healing cascade are not coordinated properly, which can lead to loss of skin function and disfigurement. The purpose of this study was to determine whether myostatin plays a role in the healing of burn wounds in skin. Myostatin is best known for its powerful negative regulation of muscle development. Absence of myostatin results in a heavy muscling phenotype, whereas over-expression is associated with muscle wasting conditions. Recently, myostatin has been shown to be involved in muscle wound healing, ...

Myostatin, a member of the TGF- family, has been identified as a powerful inhibitor of muscle growth. the absence of myostatin involves little or no input from satellite cells. Hypertrophic fibers contain no more myonuclei or satellite cells and myostatin had no significant effect on satellite cell proliferation in vitro, while expression of myostatin receptors dropped to Amonafide (AS1413) IC50 the limits of detectability in postnatal satellite cells. Moreover, hypertrophy of dystrophic muscle arising from myostatin blockade was achieved without any apparent enhancement of contribution of myonuclei from satellite cells. These findings contradict the accepted model of myostatin-based Amonafide (AS1413) IC50 control of size of postnatal muscle and reorient fundamental investigations away from the mechanisms that control satellite cell proliferation and toward those that increase myonuclear domain, by modulating synthesis and turnover of structural muscle fiber proteins. It predicts too that any ...

The truth is, your muscle size has a limit. Sure it may seem obvious when you hear it, but your muscles are under the strict control of a protein called Myostatin, which determines exactly how large a muscle can become. And this limit is different for everyone depending on their myostatin levels. As a muscle reaches this limit, myostatin prevents any further growth. But if the myostatin itself is limited or absent, this muscle limit suddenly goes away. This phenomenon was first noticed in Belgian Blue Cattle. These cows developed 2-3 times more muscle mass than a normal cow, and it was later discovered that they had a deletion of the gene GDF-8, which just so happens to create myostatin. As a result, without any exercise or special diet, these cows have incredible muscles mass. Similar cases have been documented in dogs, mice, and even a few cases of human babies lacking the GDF-8 gene. These finding have helped scientists understand why some people bulk up easily, while others struggle to. ...

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Background: Myostatin (MSTN) is a member of the transforming growth factor-β superfamily that negatively regulates growth of skeletal muscle tissue. The gene encoding for the MSTN peptide is a consolidate candidate for the enhancement of productivity in terrestrial livestock. This gene potentially represents an important target for growth improvement of cultured finfish.. Results: Here we report molecular characterization, tissue expression and sequence variability of the barramundi (Lates calcarifer) MSTN-1 gene. The barramundi MSTN-1 was encoded by three exons 379, 371 and 381 bp in length and translated into a 376-amino acid peptide. Intron 1 and 2 were 412 and 819 bp in length and presented typical GT...AG splicing sites. The upstream region contained cis-regulatory elements such as TATA-box and E-boxes. A first assessment of sequence variability suggested that higher mutation rates are found in the 5 flanking region with several SNPs present in this species. A putative micro RNA target ...

Kocsis T, Trencsenyi G, Szabo K, Baan JA, Muller G, Mendler L, Garai I, Reinauer H, Deak F, Dux L, Keller-Pinter A: Myostatin propeptide mutation of the hypermuscular Compact mice decreases the formation of myostatin and improves insulin sensitivity., AMERICAN JOURNAL OF PHYSIOLOGY: ENDOCRINOLOGY AND METABOLISM 312: (3) pp. E150-E160 ...

MSTN: This gene codes for the myostatin protein which is involved in muscle development. A German boy, nicknamed Popeye, was born with a non-functional myostatin protein; at the age of 7 months his muscles were already twice as big as those of other children his age.. ...

Myostatin Myostatin Other names:GDF-8, Myostatin Genetic data Locus: Chr. 2 q32.2 Gene code: HUGO: GDF8 Protein Structure/Function Protein type: TGF beta

Mice with the myostatin gene removed grow more muscle, and researchers have been looking into therapies for muscle wasting based on this mechanism for a number of years. Here is another confirmation that myostatin is involved in age-related changes in muscle mass and strength via its effect on stem cells: Human aging is accompanied by a progressive loss of muscle mass (sarcopenia). We tested the hypothesis that older males (OMs, 70±4 yr, n=9) would have a blunted myogenic response to a physiological stimulus compared to younger controls (21±3 yr, n=9). Subjects completed an acute bout of intense unilateral muscle loading. Young healthy males matched for body mass and activity level served as the control group. Muscle biopsies and blood were obtained before and at 3, 24, and 48 h after muscle loading. The muscle stem cell response was analyzed ... OMs had 35% fewer basal stem cells and a type II fiber-specific impairment in stem cell content and proliferation. Myogenic determination factor ...

Muscular dystrophies comprise a large group of inherited disorders that lead to progressive muscle wasting. We wanted to investigate if targeting satellite cells can enhance muscle regeneration and thus increase muscle mass. We treated mice with hepatocyte growth factor and leukemia inhibitory factor under three conditions: normoxia, hypoxia and during myostatin deficiency. We found that hepatocyte growth factor treatment led to activation of the Akt/mTOR/p70S6K protein synthesis pathway, up-regulation of the myognic transcription factors MyoD and myogenin, and subsequently the negative growth control factor, myostatin and atrophy markers MAFbx and MuRF1. Hypoxia-induced atrophy was partially restored by hepatocyte growth factor combined with leukemia inhibitory factor treatment. Dividing satellite cells were three-fold increased in the treatment group compared to control. Finally, we demonstrated that myostatin regulates satellite cell activation and myogenesis in vivo following treatment, ...

Mstn+/- and Mstn-/- mice were protected from age-related decline in muscle mass and contractility. MSTN+/- mice demonstrated a 15% increase in maximal lifespan when compared to Mstn+/+ and Mstn-/- mice ...

Myostatin is a potent negative regulator of muscle mass, i.e. high levels of myostatin induce loss of muscle. Surprisingly, severely obese humans and obese mice have elevated levels of serum myostatin, but the role of ...

In addition to increasing energy, creatine accelerates recovery in your muscles and even increases muscle mass. How does creatine do these things? It allows your body to endure through longer periods of extreme exercise which helps your muscle grow. It also increases cell signaling that helps with muscle growth and more importantly muscle recovery. Finally, creatine elevates water levels in the cells, which not only helps with the function but also plumps the muscle up.. Taking creatine is shown to significantly reduce the breakdown of proteins that comprise our muscles. It encourages the growth of the muscle by lowering myostatin levels, the protein that can prevent muscle growth. Additional studies have found that the increase of phosphocreatine in the brain enhances function and can prevent neurological malfunctions.. Creatine can have other benefits, too, says Dr. Niket Sonpal, a doctor based in New York City.. Sleep deprivation has a negative effect on mental performance and mood. This can ...

Muscular dystrophies are characterized by weakness and wasting of skeletal muscle tissues. Several drugs targeting the myostatin pathway have been used in clinical trials to increase muscle mass and function but most showed limited efficacy. Here we show that the expression of components of the myostatin signaling pathway is downregulated in muscle wasting or atrophying diseases, with a decrease of myostatin and activin receptor, and an increase of the myostatin antagonist, follistatin. We also provide in vivo evidence in the congenital myotubular myopathy mouse model (knock-out for the myotubularin coding gene Mtm1) that a down-regulated myostatin pathway can be reactivated by correcting the underlying gene defect ...

AsapScience shows us the effects of myostatin on muscle development. They analyze how big muscles can really get and what stops you from getting those nice biceps at the gym.

Poster (2013, February). The Belgian Blue beef cattle is well known for its double muscling phenotype resulting from fixation of a deletion in the myostatin gene. Since this fixation, further intensive selection for muscular ... [more ▼]. The Belgian Blue beef cattle is well known for its double muscling phenotype resulting from fixation of a deletion in the myostatin gene. Since this fixation, further intensive selection for muscular development has been particularly succesful. This response to selection might be due to fixation of more genetic variants increasing muscular development. In the present study, we search for selective sweeps in the Belgian Blue genome which might result from the fixation of such variants. To that end we used data from 593 sires genotyped with the BovineHD SNP array. In addition, we used the Belgian Blue dual purpose and the Holstein breeds as controls. We first performed scans for regions of complete homozygosity resulting from fixation. Large fixed regions were ...

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Simple way to increase muscle mass Everybody knows that one of the most important things you can do for your health as you get older is to maintain a healthy muscle mass. But thats not so easy. Its certainly not as easy as it was when we were younger. Studies have shown that older people lose the muscle mass they gain from exercise at an alarmingly fast rate. Stop for about two months and you are back to square one. But what if there was a pill you could take that could significantly increase your muscle mass in only months? Well, according to a recent experiment it looks like there is such a pill.

How to increase muscle mass?. Every man has a dream of making a strong body and females are more attracted to the masculine figure which reflect the real personality of a man. It is, therefore, obvious that men are always behind bodybuilding and use methods such as weight lifting, workouts at gym, consumption of protein supplements, and whatever they can do to make them stronger. But the question is best supplements for mass to become stronger. You can do it in natural ways or some drugs and supplements can do this job. Weight lifting is one of the old and proven methods that wrestlers and athletes use to increase their muscle mass. The heavier the weight you lift more the muscles grows. High intake of certain type of proteins, whey protein in particular, also accelerate muscle mass building. Some people believe in high rep isolation exercises, but these exercises are not too effective but can work in weight lifters who are already strong and make use of drugs.. Conclusion. The fact is that we ...

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TY - JOUR. T1 - Left-right axis malformations associated with mutations in ACVR2B, the gene for human activin receptor type IIB. AU - Kosaki, Rika. AU - Gebbia, Marinella. AU - Kosaki, Kenjiro. AU - Lewin, Mark. AU - Bowers, Peter. AU - Towbin, Jeffry A.. AU - Casey, Brett. PY - 1999/1/1. Y1 - 1999/1/1. N2 - Targeted disruption of the mouse activin receptor type IIB gene (Acvr2b) results in abnormal left-right (LR) axis development among Acvr2b(-/-) homozygotes [Oh and Li, 1997: Genes Dev 11:1812,1826]. The resulting malformations include atrial and ventricular septal defects, right-sided morphology of the left atrium and left lung, and spleen hypoplasia. Based on these results, we hypothesized that mutations in the type IIB activin receptor gene are associated with some cases of LR axis malformations in humans. We report here characterization of the ACVR2B genomic structure, analysis of ACVR2B splice variants, and screening for ACVR2B mutations among 112 sporadic and 14 familial cases of LR ...

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Gene transfer of rAAV vectors to rodents has rarely been associated with elicitation of a cellular immune response against the AAV capsid proteins (Gregorevic et al. 2004a; Jooss and Chirmule 2003; Snyder et al. 1997; Xiao et al. 1996). In contrast, studies using IM injection of rAAV2 and 6 capsids in dogs elicited a strong cellmediated immune response against the vector (Wang et al. 2007a; Yuasa et al. 2007). However, a brief course of immune suppression was found sufficient to allow long-term expression of microdystrophin when delivered to the canine model of DMD using rAAV6 (Wang et al. 2007b). Several studies have used rAAV vectors for systemic gene transfer to muscles of dogs (Arruda et al. 2005; Greelish et al. 1999; Ohshima et al. 2009; Yue et al. 2008; Chamberlain et al. unpublished observations). A recent study used hydrodynamic limb vein injection of rAAV8 vectors to achieve widespread expression of the canine myostatin propeptide in limb musculature. Nevertheless, cardiomyocytes and ...

by Elzi Volk. Please send us your feedback on this article.. Super Cows and Mighty Mice. In 1997, scientists McPherron and Lee revealed to the public the secret of an anomaly that livestock breeders have capitalized since the late 1800 s: the gene responsible for big beefy cows (1). More than a century ago, livestock breeders in Europe observed that some of their cattle were more muscled than others. Being dabblers in genetics, they selectively bred these cattle to increase the progeny displaying this trait. Thus two breeds of cattle (Belgian Blue and Piedmontese) were developed that typically exhibit an increase in muscle mass relative to other conventional cattle breeds. Little did they know that many years later Mighty Mouse would be more than merely a cartoon.. A team of scientists led by McPherron and Lee at John Hopkins University was investigating a group of proteins that regulate cell growth and differentiation. During their investigations they discovered the gene that may be responsible ...

The purpose of this study was to examine if L-leucine (Leu), β-hydroxy-β-methylbutyrate (HMB), or creatine monohydrate (Crea) prevented potential atrophic effects of myostatin (MSTN) on differentiated C2C12 myotubes. After four days of differentiation, myotubes were treated with MSTN (10 ng/ml) for two additional days and four treatment groups were studied: 1) 3x per day 10 mM Leu, 2) 3x per day 10 mM HMB, 3) 3x per day 10 mM Crea, 4) DM only. Myotubes treated with DM without MSTN were analyzed as the control condition (DM/CTL). Following treatment, cells were analyzed for total protein, DNA content, RNA content, muscle protein synthesis (MPS, SUnSET method), and fiber diameter. Separate batch treatments were analyzed for mRNA expression patterns of myostatin-related genes (Akirin-1/Mighty, Notch-1, Ski, MyoD) as well as atrogenes (MuRF-1, and MAFbx/Atrogin-1). MSTN decreased fiber diameter approximately 30% compared to DM/CTL myotubes (p | 0.001). Leu, HMB and Crea prevented MSTN-induced atrophy.

Rad 140 Rad 140 has been shown to enhance speed, stamina and endurance during workouts as well as increase muscular gains within shorter periods of time.. MK EXTREME MK677 SARM acts as a potent, orally active growth hormone secretagogue, mimicking the GH stimulating action of the endogenous hormone ghrelin. A secretagogue is the term for a substance that chemically signals for the pituitary gland to secrete growth hormone.. Ostarine is a non-steroidal oral Selective Androgen Receptor Modulator (SARM) that has been used in clinical trials to attenuate muscle wasting and improve muscular hypertrophy. Alpha Form Labs Ostarine is the most anabolic of any SARMS and is perfect for people whose primary goal is gaining lean muscle.. YK11 is possibly the strongest of all the SARMs and does its job in a very unique way, When YK11 starts to effect the androgen receptor in your body it causes the production of follistatin, which is a powerful myostatin inhibitor this allows your muscular cells to grow ...

Terbutaline increases muscle mass at the expense of fitness Strength athletes who use terbutaline, a beta-2 agonist that resembles salbutamol, build up more muscles, but in the longer term may also become less fit and lose stamina. Researchers from the University of Copenhagen discovered this in a human study. The dosages they used used are permitted in sport. Study The Danes divided 46 healthy and active young men aged 18-36, who moved 2-5 hours a week, into 4 groups. The first

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DESCRIPTION provided by applicant Chronic kidney disease CKD is a major public health problem in the US with an estimated prevalence of million patients enter hemodialysis or peritoneal dialysis programs yearly A serious complication in of patients with CKD is cachexia or muscle wasting which decreases quality of life and increases morbidity and mortality Unfortunately there are no agents available in the clinic to treat CKD induced cachexia We determined that expression of myostatin a member of the TGF peptide hormone family and the major negative regulator of muscle mass is increased in the skeletal muscles of patients and mice with CKD Blocking myostatin in CKD mice with a humanized myostatin peptibody prevented CKD induced cachexia raising the possibility of using it to treat cachexia in CKD patients However a similar myostatin targeting strategy was halted in Phase I due to unexplained nose and gum bleeding We discovered that CKD in patients and mice activates signal transducer and ...

Caveolin-3, the muscle-specific isoform of caveolins, plays important roles in signal transduction. Dominant-negative mutations of the caveolin-3 gene cause autosomal dominant limb-girdle muscular dystrophy 1C (LGMD1C) with loss of caveolin-3. However, identification of the precise molecular mechanism leading to muscular atrophy in caveolin-3-deficient muscle has remained elusive. Myostatin, a member of the muscle-specific TGF-β superfamily, negatively regulates skeletal muscle volume. Here we report that caveolin-3 inhibited myostatin signaling by suppressing activation of its type I receptor; this was followed by hypophosphorylation of an intracellular effector, Mad homolog 2 (Smad2), and decreased downstream transcriptional activity. Loss of caveolin-3 in P104L mutant caveolin-3 transgenic mice caused muscular atrophy with increase in phosphorylated Smad2 (p-Smad2) as well as p21 (also known as Cdkn1a), a myostatin target gene. Introduction of the myostatin prodomain, an inhibitor of ...

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en] Two-dimensional electrophoresis was used to investigate the effects of a QTL for muscle hypertrophy on sarcoplasmic protein expression in ovine muscles. In the Belgian Texel breed, the QTL for muscle hypertrophy is localized in the myostatin-encoding gene. Based on microsatellite markers flanking the myostatin gene, we compared the hypertrophied genotype with the normal genotype. The average age of the sheep was 3 mo. Among the 4 muscles studied, in the hypertrophied genotype only the vastus medialis was normal, whereas the semimembranosus, tensor fasciae latae, and LM were hypertrophied. In the hypertrophied genotype, these muscles showed upregulation of enzymes involved in glycolytic metabolism together with oxidative metabolism in LM. Certain chaperone proteins, including glutathione S-transferase-Pi, heat shock protein-27, and heat shock cognate-70, were also more highly expressed, probably due to increased use of energetic pathways. Expression of the iron transport protein transferrin ...

View mouse Acvr2b Chr9:119402118-119434995 with: phenotypes, sequences, polymorphisms, proteins, references, function, expression

McPherron, Alexandra C., and Se-Jin Lee. Double muscling in cattle due to mutations in the myostatin gene. Proceedings of the National Academy of Sciences 94.23 (1997): 12457-12461. Web. 25 Oct. 2020. ...

Remember the Little Hercules with the myostatin mutation? His mother was very muscular, and reportedly there was a family history of mesomorphicity. One way population level quantitative trait mean value can shift through selection beyond the most extreme values of the original population without new mutation being necessary is simply to change the underlying allele frequencies enough so that originally unlikely combinations become common. Assortative mating is another variant of this dynamic, if people several sigmas from the mean mate, then new combinations are likely to emerge ...

CPB653Po21, OVA Conjugated Myostatin (MSTN), 肌肉生长抑制素(MSTN)卵白蛋白偶联物, GDF8; Growth Differentiation Factor 8 | 仅供体外研究使用，不用于临床诊断！请索取进口关税税单及报关单！

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Myostatin (MSTN) is an important member of the transforming growth factor-β (TGF-β) superfamily and is a muscle growth inhibitor. In the present study, we cloned the Chinese perch MSTN cDNA sequence and analyzed its expression patterns under various conditions. The MSTN full cDNA sequence was 3347 bp long, including an open-reading frame of 1131 bp, which encoded 376 amino acids. Sequence ... more ...

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At first glance, such a proposal looks like a mockery - why add a new item to the sports fitness schedule, which is already cracking with tension? Meanwhile, yoga is necessary as air! The fact is that strength and aerobic training is, after all, a kind of stress. Resisting stress, the body acquires new positive qualities - increases strength and endurance, gets rid of ballast - adipose tissue, and increases muscle mass. Continue reading →. ...

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