Growth Factor And Steroid Regulation Of Skeletal Muscle Growth And Development
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Growth Factors and Cytokines in Skeletal Muscle Development, Growth, Regeneration and Disease
| Author | : Jason White |
| Publisher | : Springer |
| Total Pages | : 197 |
| Release | : 2016-03-22 |
| Genre | : Science |
| ISBN | : 3319275119 |
This book describes the diverse roles that growth factors and cytokines play in skeletal muscle. The extracellular environment has profound effects on the biology of skeletal muscle. The soluble portion of this environment includes a rich milieu of growth factors and cytokines which have been shown to regulate virtually all facets of the response of skeletal muscle to external stimuli, whether it be exercise induced metabolic shifts, remodeling in response to trauma or loading of the ongoing pathology associated with neuromuscular disease. The chapters included in this work illustrate growth factors that directly affect skeletal muscle cells and those which influence non-muscle cells that contribute to the biology of skeletal muscle as a whole tissue. The current state of the art, with the advent of systems biology, allows for the delineation of signaling networks which are regulated by suites of growth factors. This is in stark contrast to early more traditional studies, which only examined the effects of isolated growth factors on the activity of skeletal muscle precursor cells in tissue culture. The work presented in this volume ranges from reviewing and analyzing the roles of individual growth factors in detail, to the complex interplay of multiple soluble factors in the control of muscle functional, and dysfunctional states. The material covered in this volume will particularly suit readers from a range of research fields spanning general muscle biology and physiology, and those working on diseases and conditions affecting skeletal muscle both directly and indirectly.
Regulation of Skeletal Muscle Growth by Polypeptide Growth Factors
| Author | : Vickie Elaine Baracos |
| Publisher | : |
| Total Pages | : 39 |
| Release | : 1992 |
| Genre | : Growth factors |
| ISBN | : |
Designing Foods
| Author | : National Research Council |
| Publisher | : National Academies Press |
| Total Pages | : 384 |
| Release | : 1988-02-01 |
| Genre | : Medical |
| ISBN | : 0309037956 |
This lively book examines recent trends in animal product consumption and diet; reviews industry efforts, policies, and programs aimed at improving the nutritional attributes of animal products; and offers suggestions for further research. In addition, the volume reviews dietary and health recommendations from major health organizations and notes specific target levels for nutrients.
The Role of Transforming Growth Factor Beta-extracellular Matrix Signaling in Skeletal Muscle Growth and Development
| Author | : Xuehui Li |
| Publisher | : |
| Total Pages | : 320 |
| Release | : 2008 |
| Genre | : Extracellular matrix |
| ISBN | : |
Abstract: Muscle development is a highly organized process, regulated by interactions between muscle cells and their extracellular matrix (ECM) environment. The ECM through its regulation of growth factors plays a pivotal role in muscle growth and development. Transforming growth factor-[beta]1 (TGF-[beta]1) is a potent inhibitor of muscle cell proliferation and differentiation. Decorin, one of components in the ECM, binds to TGF-[beta]1 and modulates muscle cell responsiveness to TGF-[beta]1. The TGF-[beta]1 signal is carried by Smad proteins into the cell nucleus, resulting in an inhibition of the expression of certain myogenic regulatory factors. In addition, TGF-[beta]1 affects expression of cell [beta]1 integrin adhesion receptor that is involved in cell adhesion and survival. However, the mechanism by which these factors interact and the signaling pathway is largely unknown. To address this mechanism, both in vitro and in vivo studies were preformed. In vitro studies showed that TGF-[beta]1 reduced both decorin and [beta]1 integrin expression, and altered the localization of [beta]1 integrin in satellite cells. Decorin plays a negative role in the TGF-[beta]1-dependent signaling pathway in terms of inhibiting satellite cell responsiveness to TGF-[beta]1, resulting in enhanced cell proliferation and differentiation. Decreased expression of [beta]1 integrin is likely involved in the programmed cell death or apoptotic effect of TGF-[beta]1 on muscle cells through regulating focal adhesion kinase signaling pathway. The expression of myogenic regulatory factors, MyoD and myogenin, was inhibited by TGF-[beta]1 through Smad3-mediated pathway, resulting in decreased satellite cell proliferation and differentiation. In vivo studies investigated the function of TGF-[beta]1 on the expression and localization of [beta]1 integrin and decorin during muscle formation by injection of TGF-[beta]1 into the developing chicken embryo. In addition, the muscle cells from Low Score Normal (LSN) chicken, genetic muscle weakness, showed a different cellular responsiveness to TGF-[beta]1 compared to the normal, which suggests a complex mechanism involved in the LSN condition. This study provides new information on the role of the TGF-[beta]1-ECM signaling pathway in muscle growth and development, which will not only be critical to the domestic animal industries, but also benefit human health in terms of the repair and regeneration of muscle with age.
Transcriptional Regulation of Skeletal Muscle Development
| Author | : Analeah B. Heidt |
| Publisher | : |
| Total Pages | : 326 |
| Release | : 2006 |
| Genre | : |
| ISBN | : |
A critical MyoD target during skeletal muscle development is the mef2c gene. MEF2 transcription factors are known to be critical regulators of muscle differentiation. We sought to determine the function of MEF2C in skeletal muscle development and function. Mice lacking mef2c die at midgestation, too soon to analyze skeletal muscle development, we therefore used a conditional inactivation approach. Mice lacking MEF2C function in skeletal muscle have a decrease in overall body size, decreased exercise endurance and defects in mitochondrial morphology. In addition, these mice accumulate abnormal amounts of glycogen in their skeletal muscle. We hypothesize that MEF2C is a critical regulator of energy metabolism in skeletal muscle, and that an inefficiency of energy usage in skeletal muscle causes a negative energy balance in the organism, and therefore a smaller overall body size.
Effects of Steroid Hormones on Skeletal Muscle
| Author | : |
| Publisher | : |
| Total Pages | : 273 |
| Release | : 2008 |
| Genre | : |
| ISBN | : |
Steroid hormones are small lipophilic compounds synthesized from cholesterol and are important for numerous physiological and hormonal functions. This dissertation is focused on the effects of two types of steroid hormones, estrogens and glucocorticoids, on skeletal muscle. The first part of this dissertation investigates estrogen effects on skeletal muscle growth at the molecular level. Previous work suggested estrogen limits skeletal muscle growth in ovariectomized (OVX) rats. The underlying mechanisms were further investigated by monitoring specific muscle growth factors, myostatin and insulin-like growth factor-1 (IGF-1), following estrogen administration in the OVX rats. The mRNA and protein expression of both growth factors were measured at the end of 1 week or 5 weeks of treatments. Myostatin protein was found to increase with 1-week estrogen treatment only in the slow muscle (soleus, SOL), while IGF-1 protein was universally down-regulated by estrogen in the fast (extensor digitorum longus, EDL), slow, and mixed (gastrocnemius, GAS) muscles. Discordance between the mRNA and protein of both growth factors was observed. There was no treatment effect on IGF-1 and myostatin expression in the 5 week study suggesting a transient estrogen effect or up-regulation of a compensatory mechanism to counteract the estrogen effect observed at the earlier time point (1 week). The second part was to elucidate a better understanding of the potential underlying mechanism(s) of glucocorticoid-induced muscle atrophy. Gene array technology (Affymetrix) was employed to study multiple genes simultaneously. Glucocorticoid treatment was found to affect some of the ubiquitin-conjugases (E2 enzymes) and the ubiquitin-ligases (E3 enzymes) in the UPS pathway. A mechanism-based PK/PD modeling on the E3 enzymes, namely MuRF-1 and Atrogin-1, was conducted. The proposed model captured the acute data well; however, the model predicted an elevated expression throughout the chronic study and as such, did not capture the last time point (168 hour) where the gene expression had returned to the baseline. The results suggested the current understanding of the glucocorticoid receptor mechanism is not sufficient in describing the genomic response in skeletal muscle. A compensatory mechanism in addition to the down-regulation of the glucocorticoid receptor may exist and together they govern glucocorticoid resistance.
Examining the Negative Regulation of Skeletal Muscle Growth
| Author | : Mitchell Todd Sitnick |
| Publisher | : |
| Total Pages | : |
| Release | : 2009 |
| Genre | : |
| ISBN | : |
Skeletal Muscle is a dynamic tissue that plays an integral role in locomotion, respiration and balance through its unique ability to produce force. Skeletal muscle also serves as the major metabolic engine in the human system. As such, it is of critical importance to maintain healthy muscle tissue. Due to the high variability in its roles, skeletal muscle has evolved into a highly dynamic tissue changing both it genotype and phenotype in response to alterations is loading and other environmental conditions. In healthy individuals skeletal muscle mass will atrophy with unloading/disuse and will recover following normal loading through manipulation of the protein synthetic pathways. Likewise through similar mechanisms, in times of increased loading, skeletal muscle will hypertrophy resulting in the capacity for increased force production. The ability to increase muscle mass in response to loading either following atrophy or in response to increased mechanical loading is severely blunted under several conditions, most notably with aging. This is largely due to severe deficits in the activation of protein synthesis pathways in response to loading as well as changes in the growth factor status. Ultimately, the exact mechanism regulating the failed growth of aged muscle is still unknown. The purpose of these studies was to elucidate several key mechanisms that underlay the reduced capacity for skeletal muscle growth in the elderly population. Two separate conditions associated with aging were isolated and tested whether there was a significant effect on the capacity for muscle growth. The first investigated whether circulating estrogen levels played a role in the ability to recover atrophied muscle mass with reloading. The second study examined whether diet-induced obesity attenuated the ability to increased muscle mass in response to functional overload. It was determined that for both models of skeletal muscle growth, both removal of circulating estrogens and the increased adiposity of diet-induce obesity resulted in the failure in the typical growth response concurrent with the failed activation of the protein synthetic pathways, specifically the Akt/mTOR signaling pathway. Taken together, these results shed some light on possible mechanisms for the attenuated growth of skeletal muscle seen with aging.
