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Статті в журналах з теми "Skeletal muscle satellite cells"
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Yablonka-Reuveni, Zipora. "The Skeletal Muscle Satellite Cell." Journal of Histochemistry & Cytochemistry 59, no. 12 (December 2011): 1041–59. http://dx.doi.org/10.1369/0022155411426780.
Повний текст джерелаАнотація:
The skeletal muscle satellite cell was first described and named based on its anatomic location between the myofiber plasma and basement membranes. In 1961, two independent studies by Alexander Mauro and Bernard Katz provided the first electron microscopic descriptions of satellite cells in frog and rat muscles. These cells were soon detected in other vertebrates and acquired candidacy as the source of myogenic cells needed for myofiber growth and repair throughout life. Cultures of isolated myofibers and, subsequently, transplantation of single myofibers demonstrated that satellite cells were myogenic progenitors. More recently, satellite cells were redefined as myogenic stem cells given their ability to self-renew in addition to producing differentiated progeny. Identification of distinctively expressed molecular markers, in particular Pax7, has facilitated detection of satellite cells using light microscopy. Notwithstanding the remarkable progress made since the discovery of satellite cells, researchers have looked for alternative cells with myogenic capacity that can potentially be used for whole body cell-based therapy of skeletal muscle. Yet, new studies show that inducible ablation of satellite cells in adult muscle impairs myofiber regeneration. Thus, on the 50th anniversary since its discovery, the satellite cell’s indispensable role in muscle repair has been reaffirmed.
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Azab, Azab. "Skeletal Muscles: Insight into Embryonic Development, Satellite Cells, Histology, Ultrastructure, Innervation, Contraction and Relaxation, Causes, Pathophysiology, and Treatment of Volumetric Muscle I." Biotechnology and Bioprocessing 2, no. 4 (May 28, 2021): 01–17. http://dx.doi.org/10.31579/2766-2314/038.
Повний текст джерелаАнотація:
Background: Skeletal muscles are attached to bone and are responsible for the axial and appendicular movement of the skeleton and for maintenance of body position and posture. Objectives: The present review aimed to high light on embryonic development of skeletal muscles, histological and ultrastructure, innervation, contraction and relaxation, causes, pathophysiology, and treatment of volumetric muscle injury. The heterogeneity of the muscle fibers is the base of the flexibility which allows the same muscle to be used for various tasks from continuous low-intensity activity, to repeated submaximal contractions, and to fast and strong maximal contractions. The formation of skeletal muscle begins during the fourth week of embryonic development as specialized mesodermal cells, termed myoblasts. As growth of the muscle fibers continues, aggregation into bundles occurs, and by birth, myoblast activity has ceased. Satellite cells (SCs), have single nuclei and act as regenerative cells. Satellite cells are the resident stem cells of skeletal muscle; they are considered to be self-renewing and serve to generate a population of differentiation-competent myoblasts that will participate as needed in muscle growth, repair, and regeneration. Based on various structural and functional characteristics, skeletal muscle fibres are classified into three types: Type I fibres, Type II-B fibres, and type II-A fibres. Skeletal muscle fibres vary in colour depending on their content of myoglobin. Each myofibril exhibits a repeating pattern of cross-striations which is a product of the highly ordered arrangement of the contractile proteins within it. The parallel myofibrils are arranged with their cross-striations in the register, giving rise to the regular striations seen with light microscopy in longitudinal sections of skeletal muscle. Each skeletal muscle receives at least two types of nerve fibers: motor and sensory. Striated muscles and myotendinous junctions contain sensory receptors that are encapsulated proprioceptors. The process of contraction, usually triggered by neural impulses, obeys the all-or-none law. During muscle contraction, the thin filaments slide past the thick filaments, as proposed by Huxley's sliding filament theory. In response to a muscle injury, SCs are activated and start to proliferate; at this stage, they are often referred to as either myogenic precursor cells (MPC) or myoblasts. In vitro, evidence has been presented that satellite cells can be pushed towards the adipogenic and osteogenic lineages, but contamination of such cultures from non-myogenic cells is sometimes hard to dismiss as the underlying cause of this observed multipotency. There are, however, other populations of progenitors isolated from skeletal muscle, including endothelial cells and muscle-derived stem cells (MDSCs), blood-vessel-associated mesoangioblasts, muscle side-population cells, CD133+ve cells, myoendothelial cells, and pericytes. Volumetric muscle loss (VML) is defined as the traumatic or surgical loss of skeletal muscle with resultant functional impairment. It represents a challenging clinical problem for both military and civilian medicine. VML results in severe cosmetic deformities and debilitating functional loss. In response to damage, skeletal muscle goes through a well-defined series of events including; degeneration (1 to 3days), inflammation, and regeneration (3 to 4 weeks), fibrosis, and extracellular matrix remodeling (3 to 6 months).. Mammalian skeletal muscle has an impressive ability to regenerate itself in response to injury. During muscle tissue repair following damage, the degree of damage and the interactions between muscle and the infiltrating inflammatory cells appear to affect the successful outcome of the muscle repair process. The transplantation of stem cells into aberrant or injured tissue has long been a central goal of regenerative medicine and tissue engineering. Conclusion: It can be concluded that the formation of skeletal muscle begins during the fourth week of embryonic development as specialized mesodermal cells, termed myoblasts, by birth myoblast activity has ceased. Satellite cells are considered to be self-renewing, and serve to generate a population of differentiation-competent myoblasts. Skeletal muscle fibres are classified into three types. The process of contraction, usually triggered by neural impulses, obeys the all-or-none law. VML results in severe cosmetic deformities and debilitating functional loss. Mammalian skeletal muscle has an impressive ability to regenerate itself in response to injury. The transplantation of stem cells into aberrant or injured tissue has long been a central goal of regenerative medicine and tissue engineering.
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Shadrach, Jennifer L., and Amy J. Wagers. "Stem cells for skeletal muscle repair." Philosophical Transactions of the Royal Society B: Biological Sciences 366, no. 1575 (August 12, 2011): 2297–306. http://dx.doi.org/10.1098/rstb.2011.0027.
Повний текст джерелаАнотація:
Skeletal muscle is a highly specialized tissue composed of non-dividing, multi-nucleated muscle fibres that contract to generate force in a controlled and directed manner. Skeletal muscle is formed during embryogenesis from a subset of muscle precursor cells, which generate both differentiated muscle fibres and specialized muscle-forming stem cells known as satellite cells. Satellite cells remain associated with muscle fibres after birth and are responsible for muscle growth and repair throughout life. Failure in satellite cell function can lead to delayed, impaired or failed recovery after muscle injury, and such failures become increasingly prominent in cases of progressive muscle disease and in old age. Recent progress in the isolation of muscle satellite cells and elucidation of the cellular and molecular mediators controlling their activity indicate that these cells represent promising therapeutic targets. Such satellite cell-based therapies may involve either direct cell replacement or development of drugs that enhance endogenous muscle repair mechanisms. Here, we discuss recent breakthroughs in understanding both the cell intrinsic and extrinsic regulators that determine the formation and function of muscle satellite cells, as well as promising paths forward to realizing their full therapeutic potential.
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Eržen, Ida. "PLASTICITY OF SKELETAL MUSCLE STUDIED BY STEREOLOGY." Image Analysis & Stereology 23, no. 3 (May 3, 2011): 143. http://dx.doi.org/10.5566/ias.v23.p143-152.
Повний текст джерелаАнотація:
The present contribution provides an overview of stereological methods applied in the skeletal muscle research at the Institute of Anatomy of the Medical Faculty in Ljubljana. Interested in skeletal muscle plasticity we studied three different topics: (i) expression of myosin heavy chain isoforms in slow and fast muscles under experimental conditions, (ii) frequency of satellite cells in young and old human and rat muscles and (iii) capillary supply of rat fast and slow muscles. We analysed the expression of myosin heavy chain isoforms within slow rat soleus and fast extensor digitorum longus muscles after (i) homotopic and heterotopic transplantation of both muscles, (ii) low frequency electrical stimulation of the fast muscle and (iii) transposition of the fast nerve to the slow muscle. The models applied were able to turn the fast muscle into a completely slow muscle, but not vice versa. One of the indicators for the regenerative potential of skeletal muscles is its satellite cell pool. The estimated parameters, number of satellite cells per unit fibre length, corrected to the reference sarcomere length (Nsc/Lfib) and number of satellite cells per number of nuclei (myonuclei and satellite cell nuclei) (Nsc/Nnucl) indicated that the frequency of M-cadherin stained satellite cells declines in healthy old human and rat muscles compared to young muscles. To access differences in capillary densities among slow and fast muscles and slow and fast muscle fibres, we have introduced Slicer and Fakir methods, and tested them on predominantly slow and fast rat muscles. Discussing three different topics that require different approach, the present paper reflects the three decades of the development of stereological methods: 2D analysis by simple point counting in the 70's, the disector in the 80's and virtual spatial probes in the 90's. In all methods the interactive computer assisted approach was utilised.
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CIECIERSKA, ANNA, TOMASZ SADKOWSKI, and TOMASZ MOTYL. "Role of satellite cells in growth and regeneration of skeletal muscles." Medycyna Weterynaryjna 75, no. 11 (2019): 6349–2019. http://dx.doi.org/10.21521/mw.6349.
Повний текст джерелаАнотація:
Postnatal growth and regeneration capacity of skeletal muscles is dependent mainly on adult muscle stem cells called satellite cells. Satellite cells are quiescent mononucleated cells that are normally located outside the sarcolemma within the basal lamina of the muscle fiber. Their activation, which results from injury, is manifested by mobilization, proliferation, differentiation and, ultimately, fusion into new muscle fibers. The satellite cell pool is responsible for the remarkable regenerative capacity of skeletal muscles. Moreover, these cells are capable of self-renewal and can give rise to myogenic progeny.
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Bischoff, Richard. "Chemotaxis of skeletal muscle satellite cells." Developmental Dynamics 208, no. 4 (April 1997): 505–15. http://dx.doi.org/10.1002/(sici)1097-0177(199704)208:4<505::aid-aja6>3.0.co;2-m.
Повний текст джерела
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Jurdana, Mihaela. "EXERCISE EFFECTS ON MUSCLE STEM CELLS." Annales Kinesiologiae 8, no. 2 (January 26, 2018): 125–35. http://dx.doi.org/10.35469/ak.2017.134.
Повний текст джерелаАнотація:
Satellite cells are skeletal muscle stem cells that facilitate muscle repair and regeneration after “damage” which occurs after physiological stimuli: exercise, post-training micro-injuries and electrical stimulation. Exercise stimuli lead to activation and proliferation of these cells from their quiescent state, therefore, increasing cell numbers having the potential to provide additional myonuclei to their parent muscle fibre or return to a quiescent state. Different exercise modalities are the focus of numerous studies on satellite cells activation. An increase in muscle activity augments satellite cells proliferation as well as skeletal muscle mass and function, both in young and elderly.
This review provides an updated view of the contribution of skeletal muscle satellite cells in regulating skeletal muscle mass and the efficiency of the exercise intervention to attenuate the decline in muscle mass.
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Yin, Hang, Feodor Price, and Michael A. Rudnicki. "Satellite Cells and the Muscle Stem Cell Niche." Physiological Reviews 93, no. 1 (January 2013): 23–67. http://dx.doi.org/10.1152/physrev.00043.2011.
Повний текст джерелаАнотація:
Adult skeletal muscle in mammals is a stable tissue under normal circumstances but has remarkable ability to repair after injury. Skeletal muscle regeneration is a highly orchestrated process involving the activation of various cellular and molecular responses. As skeletal muscle stem cells, satellite cells play an indispensible role in this process. The self-renewing proliferation of satellite cells not only maintains the stem cell population but also provides numerous myogenic cells, which proliferate, differentiate, fuse, and lead to new myofiber formation and reconstitution of a functional contractile apparatus. The complex behavior of satellite cells during skeletal muscle regeneration is tightly regulated through the dynamic interplay between intrinsic factors within satellite cells and extrinsic factors constituting the muscle stem cell niche/microenvironment. For the last half century, the advance of molecular biology, cell biology, and genetics has greatly improved our understanding of skeletal muscle biology. Here, we review some recent advances, with focuses on functions of satellite cells and their niche during the process of skeletal muscle regeneration.
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Englund, Davis A., Bailey D. Peck, Kevin A. Murach, Ally C. Neal, Hannah A. Caldwell, John J. McCarthy, Charlotte A. Peterson, and Esther E. Dupont-Versteegden. "Resident muscle stem cells are not required for testosterone-induced skeletal muscle hypertrophy." American Journal of Physiology-Cell Physiology 317, no. 4 (October 1, 2019): C719—C724. http://dx.doi.org/10.1152/ajpcell.00260.2019.
Повний текст джерелаАнотація:
It is postulated that testosterone-induced skeletal muscle hypertrophy is driven by myonuclear accretion as the result of satellite cell fusion. To directly test this hypothesis, we utilized the Pax7-DTA mouse model to deplete satellite cells in skeletal muscle followed by testosterone administration. Pax7-DTA mice (6 mo of age) were treated for 5 days with either vehicle [satellite cell replete (SC+)] or tamoxifen [satellite cell depleted (SC-)]. Following a washout period, a testosterone propionate or sham pellet was implanted for 21 days. Testosterone administration caused a significant increase in muscle fiber cross-sectional area in SC+ and SC- mice in both oxidative (soleus) and glycolytic (plantaris and extensor digitorum longus) muscles. In SC+ mice treated with testosterone, there was a significant increase in both satellite cell abundance and myonuclei that was completely absent in testosterone-treated SC- mice. These findings provide direct evidence that testosterone-induced muscle fiber hypertrophy does not require an increase in satellite cell abundance or myonuclear accretion. Listen to a podcast about this Rapid Report with senior author E. E. Dupont-Versteegden ( https://ajpcell.podbean.com/e/podcast-on-paper-that-shows-testosterone-induced-skeletal-muscle-hypertrophy-does-not-need-muscle-stem-cells /).
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Adams, Gregory R. "Satellite cell proliferation and skeletal muscle hypertrophy." Applied Physiology, Nutrition, and Metabolism 31, no. 6 (December 2006): 782–90. http://dx.doi.org/10.1139/h06-053.
Повний текст джерелаАнотація:
Satellite cells are small, mononuclear cells found in close association with striated skeletal muscles cells (myofibers). These cells appear to function as reserve myoblasts. A critical role for these cells in the process of muscle regeneration following injury has been clearly established. In that role, satellite cells have been shown to proliferate extensively. Some of the progeny of these cells then fuse with each other to form replacement myofibers, whereas others return to quiescence, thereby maintaining this reserve population. In response to injury, activated satellite cells can also fuse with damaged but viable myofibers to promote repair and regeneration. It has also been observed that satellite cells are activated during periods of significantly increased muscle loading and that some of these cells fuse with apparently undamaged myofibers as part of the hypertrophy process. The observation that the inactivation of satellite cell proliferation prevents most of the hypertrophy response to chronic increases in loading has lead to the hypothesis that a limitation to the expansion of myofiber size is imposed by the number of myonuclei present. Recent evidence suggests that a potential limitation to muscle hypertrophy, in the absence of a reserve supply of myonuclei, may be the inability to sustain increases in ribosomes, thereby limiting translational capacity.
Дисертації з теми "Skeletal muscle satellite cells"
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Blackwell, Danielle. "The role of Talpid3 in skeletal muscle satellite cells and skeletal muscle regeneration." Thesis, University of East Anglia, 2017. https://ueaeprints.uea.ac.uk/66948/.
Повний текст джерелаАнотація:
The primary cilium has recently been recognised as an essential regulator of the Sonic hedgehog (Shh) signalling pathway. Mutations that disrupt cilia function in humans can cause conditions known as ciliopathies. A wide range of phenotypes is observed in chick and mouse ciliopathy models,including polydactyly, craniofacial defects and polycystic kidneys. The Shh pathway and therefore primary cilia are vital for many developmental processes, including embryonic muscle development, with recent evidence suggesting they may also play a role in adult muscle regeneration. Our studies focus on the Talpid3 gene, which encodes a centrosomal protein required for primary cilia formation and Shh signalling. The Talpid3 loss-of-function mutant has perturbed ciliogenesis and displays many of the phenotypes that are typically associated with developmental Shh mutants and with ciliopathies. Talpid3 mutants have defects in Shh signalling, and processing of Gli transcription factors is affected in structures such as the developing limb buds and the neural tube. However, the role of Talpid3 in muscle development and regeneration remains unknown. The role of Talpid3 in adult muscle regeneration was investigated using a tamoxifen inducible, satellite cell specific knock-out of Talpid3 in mice. This mouse model was generated by crossing Talpid3 floxed mice to a mouse carrying an inducible Pax7-CreERT2 allele. To determine whether loss of Talpid3 affects muscle regeneration a cardiotoxin injury model was used. This showed that loss of Talpid3 in satellite cells results in a regeneration defect as fibres were smaller after 5, 10, 15 and 25 days of regeneration compared to control mice. This defect may be due to a reduced ability of Talpid3 mutant satellite cells to differentiate. We also show that Talpid3 plays a role in satellite cell self-renewal as we observe a complete loss of regeneration in some areas of the muscle following repeat injuries. We provide the first evidence that Talpid3 is critical for the regeneration of skeletal muscle following injury.
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Thompson, Steven Howard 1958. "The effect of trenbolone on skeletal muscle satellite cells." Thesis, The University of Arizona, 1987. http://hdl.handle.net/10150/276633.
Повний текст джерелаАнотація:
Young female rats treated with trenbolone demonstrated an increase in weight gain per day and overall weight increase during the treatment period. Trenbolone treated rats also experienced improved feed efficiency. Muscles removed from the lower hind limb of trenbolone treated rats had a greater DNA to protein ratio than muscles from control animals. However, there was no significant difference in wet muscle weight between trenbolone treated and control muscles. Satellite cells from untreated female rats were not responsive to trenbolone added in vitro. In studies utilizing serum free medium, trenbolone alone, and in the presence of growth factors, could not stimulate proliferation above controls. In similar serum free medium studies, satellite cells from trenbolone treated rats were more responsive to growth factors than cells from control rats.
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Rathbone, Christopher R. "Mechanisms regulating skeletal muscle satellite cell cycle progression." Diss., Columbia, Mo. : University of Missouri-Columbia, 2006. http://hdl.handle.net/10355/5866.
Повний текст джерелаАнотація:
Thesis (Ph. D.)--University of Missouri-Columbia, 2006.The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. "December 2006" Includes bibliographical references.
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Collins, Charlotte Anne. "An investigation of the stem cell potential of skeletal muscle satellite cells." Thesis, University College London (University of London), 2004. http://discovery.ucl.ac.uk/1446604/.
Повний текст джерелаАнотація:
Satellite cells are defined by their position beneath the basal lamina of myofibres, and are a source of new myonuclei in adult skeletal muscles. However, other phenotypes also contribute to muscle regeneration, and the relative importance of satellite cells is not known. This work aimed to analyse the stem cell potential of satellite cells by formally investigating their contribution to muscle regeneration. Myofibres isolated from extensor digitorum longus, soleus, and tibialis anterior muscles were found to have respective means of 7,22 and 10 associated satellite cells. When a single myofibre was grafted into an irradiated dystrophic mouse muscle, the associated satellite cells underwent extensive, stem cell-like proliferation, generating progeny which sometimes gave rise to a cluster of more than 100 new myofibres. Cluster size varied according to the muscle group from which the graft was derived, but was not proportional to satellite cell number. Primary myoblasts derived from equivalent muscle groups did not undergo such extensive proliferation, or show inter-muscle variability, suggesting that stem cell activity is critically dependent on a component of the satellite cell niche. Single myofibres isolated from irradiated muscles were non-myogenic after grafting. Satellite cells associated with single myofibres were found to generate new satellite cells in engrafted muscles, demonstrating that satellite cell compartment is maintained by self-renewal. When single myofibre-engrafted muscles were damaged with myotoxin, graft-derived cells underwent rapid clonal expansion to regenerate compact clusters of donor-derived myofibres. The percentage of engrafted muscles containing identifiable donor-derived nuclei was increased after damage, showing that previously inactive cells had been recruited into an active myogenic program. Without experimentally-induced damage, frequency of muscle formation and cluster size were spontaneously augmented over time. These findings demonstrate that satellite cells have several stem cell-like qualities, and thus constitute a self-sufficient and sustainable source of regeneration in adult muscles.
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Morisi, F. "AUTOPHAGY AND SKELETAL MUSCLE WASTING: EFFECTS ON SATELLITE CELLS POPULATION." Doctoral thesis, Università degli Studi di Milano, 2016. http://hdl.handle.net/2434/347854.
Повний текст джерелаАнотація:
The project is divided in two sections: the formeris focused on the study of the relationship between the NO system, mitochondrial structure/activity and skeletal muscle wasting, paying attention on the role of autophagy and using a mouse model in which NOS1 (nNOSμ) is absent. My data demonstrate that an altered NO signaling leads to mitochondrial dysfunction resulting in enhanced autophagy and reduced muscle growth, however not associated with atrophy induction. Furthermore autophagy is essential to maintain muscle mass, but its role on regenerating population and its impact on muscle growth and development has not been evaluated yet. Starting form conclusion in the second part of my PhD project i focalized my attention on the role of autophagy specifically on satellite cells population, generating a transgenic mice in which autophagy is selectively inhibited in satellite cells and studying their impact on muscle growth. My data suggest that autophagy is involved in the controlling of satellite cells functions. Autophagy loss of function in satellite cells impairs their proliferation rate as well as their capability to fuse and differentiate.
The study of these two different transgenic mice reveals as in muscle, unbalanced autophagy from the early phase of growth affects satellite cells population causing muscle wasting and suggests how during skeletal muscle development is important to have appropriate levels of autophagy.
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Judson, Robert Neil. "The role of Yes-associated protein (YAP) in skeletal muscle satellite cells and myofibres." Thesis, University of Aberdeen, 2012. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=189444.
Повний текст джерелаАнотація:
In spite of its post mitotic nature, skeletal muscle maintains remarkable plasticity. Muscle fibres (myofibres) are capable of large alterations in their size as well as an enormous ability to regenerate following injury – thanks to a potent population of resident stem cells (satellite cells). Deciphering the molecular signalling networks responsible for skeletal muscle growth and regeneration is of key scientific interest – not least because of the therapeutic potential these pathways may hold for the treatment of diseases such as muscular dystrophy. In this thesis, the transcriptional co-factor Yes-Associated protein (Yap), the downstream effector of the Hippo Pathway, was investigated in skeletal muscle. Using gain and loss of function approaches within in vitro, ex vivo and in vivo models, the contribution of Yap in regulating both satellite cell behaviour and myofibre growth was investigated. Yap expression and activity are dynamically regulated during satellite cell activation, proliferation and differentiation ex vivo. Overexpression of Yap increased satellite cell proliferation and maintained cells in a ‘naive’, ‘activated’ state by inhibiting myogenic commitment. Knock-down of Yap impaired satellite cell expansion, but did not influence myogenic differentiation. Yap interacts with Tead transcription factors in myoblasts to upregulate genes such as CyclinD1 and Myf5. Forced expression of Yap eventually led to the oncogenic transformation of myoblasts in vitro. Contrary to predictions, constitutive expression of Yap under an inducible muscle-specific promoter in adult mice failed to induce growth and instead led to muscle wasting, atrophy and degeneration – providing evidence against the notion that Yap represents a universal regulator of tissue growth. These data provide the first insight into the function of Yap in skeletal muscle. Results highlight a novel role for Yap in regulating myogenic progression in satellite cells, as well as its propensity to induce oncogenic transformation. The precise function of Yap in adult myofibres remains unclear however, data presented here demonstrates clear cell-type specific roles for Yap compared to observations made in other tissues.
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Lindström, Mona. "Satellite cells in human skeletal muscle : molecular identification quantification and function." Doctoral thesis, Umeå universitet, Anatomi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-29817.
Повний текст джерелаАнотація:
Skeletal muscle satellite cells located between the plasma membrane and the basal lamina of muscle fibres, could for many years, only be studied in situ by electron microscopy. The introduction of immunohistochemistry and the discovery of molecular markers of satellite cells then made them accessible for light microscopic studies and a wealth of information is today available. Satellite cells are myogenic stem cells that can be activated from a quiescent state to proliferate for self-renewal or differentiate into myogenic cells. The satellite cells are involved in muscle growth during fetal and postnatal development and play a key role in repair and regeneration of damaged muscle fibres. The satellite cells are also essential for muscle fibre hypertrophy and maintenance of muscle mass in the adult. When the present thesis was initiated, studies on satellite cells in human skeletal muscle relied on the neuronal cell adhesion molecule (NCAM) as a marker for satellite cell identification. The results from different studies varied markedly. Therefore the aims of the present thesis were i) to develop a highly reliable method using light microscopy for satellite cell identification and quantification in biopsies of human skeletal muscle in normal and pathological conditions. A molecular marker for the myofibre basal lamina or plasma membrane to enhance the reliability of myonuclei and satellite cell identification were to be included. Furthermore unbiased morphometric methods should be used in the quantification process. ii) to evaluate which molecular markers which had been described for satellite cell and stem cell identification in different cell states (quiescence, activated or differentiated) are the most useful for studies on human skeletal muscle. iii) to further explore the function and heterogeneity of satellite cells with respect to different markers in human skeletal muscle by studying the effects of strength-training, intake of anabolic substances and pathological conditions. A new immunofluorescence method was developed where in the same tissue section, two satellite cell markers, the basal lamina and nuclei were monitored. From the evaluation of different markers it was found that both NCAM and Pax7 identified the majority of satellite cells but that both markers were needed for reliable identification. The members of the myogenic regulatory family were evaluated and by using the new method MyoD and myogenin were found to be useful markers to identify activated and differentiated satellite cells. Upon re-examination of biopsies from power-lifters, power-lifters using anabolic substances and untrained subjects it was observed that the new results on satellite cell frequency were significantly different from those obtained when using staining for NCAM and nuclei alone. In addition three subtypes of satellite cells (94.4% NCAM+/Pax7+, 4.2% NCAM+/Pax7– and 1.4% NCAM–/Pax7+) were observed. Thus the multiple marker method gave more information about satellite cells heterogeneity in human muscle and we propose that this is more reliable than previous methods. Low numbers of MyoD or myogenin stained satellite cells were observed in both untrained and strength trained subjects. Other markers such as DLK1/FA1, a member of the EGF-like family and c-Met, the receptor for hepatocyte growth factor showed that satellite cell heterogeneity in human muscle is far greater than previously shown. Furthermore, new evidence is presented for so called fibre splitting observed in hypertrophic muscle fibres to be due to defect regeneration of partially damaged fibres.
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Brandt, Amanda Maverick. "Regulation of satellite cells by extrinsic factors during recovery from exercise in horses." Diss., Virginia Tech, 2019. http://hdl.handle.net/10919/89089.
Повний текст джерелаАнотація:
The vast majority of horses engage in some form of exercise, whether it be for leisure or competition. Despite almost half of the approximately 7.2 million horses engaging in structured athletic work, very little is known about one of the most critical facets of recovery: satellite cells (SCs). Satellite cells lie adjacent to the myofiber of skeletal muscle, poised to enter the myogenic program and fuse to the nearby muscle after a damaging event. Hepatocyte growth factor (HGF) and insulin-like growth factor-1 (IGF-1) transcript abundance increased after an exhaustive bout of endurance exercise in concert with myogenic regulator factors and preceding increased SC abundance in a previous study. This suggests that SCs may participate in repair of exercise-induced muscle damage. To assess the role of HGF in this process, equine SCs (eqSCs) were isolated from the gluteus medius of mature thoroughbred geldings for activation, proliferation and differentiation assays. Activation was not accelerated by 1, 5, 10, or 25 ng/mL HGF. Instead, 25 ng/mL HGF increased the proliferation rate of eqSC via protein kinase C δ and decreased differentiation. The influence of dietary L-citrulline, an amino acid that has the potential to influence SC activity and nutrient availability by its metabolism to L-arginine, was assessed during recovery from exercise in unfit adult horses. To model submaximal exercise, horses were exercised for 1 h at an average heart rate of 116 bpm, suggested to be typical of a heavy exercise session by the National Research Council. L-citrulline decreased myogenin mRNA abundance compared to controls while exercise increased peroxisome proliferator-activated receptor gamma coactivator 1- α (PGC1α) mRNA abundance, a master regulator of energy metabolism, at 1 d post-exercise. Although SCs were not activated in response to a single bout of submaximal exercise, metabolic regulators increased in the early period of recovery. Through these studies eqSC dynamics during exercise are better defined.Doctor of Philosophy
The horse is well-known as an athletic creature and is often used in amateur and professional athletic events. Despite its popularity as a pastime in low and high-stakes competition, certain facets directly related to performance during exercise remain relatively unstudied. One crucial component of recovery from exercise is the intrinsic ability of skeletal muscle to repair exercise-induced muscle damage. This is accomplished largely through the incorporation of new nuclei, which originate from a position orbiting the muscle, hence the name satellite cells. This cell is essential to muscle regeneration from injury as often demonstrated in rodent models, but the role of satellite cells in recovery from exercise remains elusive in all species, but particularly so in horses. For instance, whether satellite cells only contribute nuclei after exercise to stimulate gains in muscle mass or whether they may also play a role in the process of adaptation to exercise is not clearly understood. The purpose of my work was to define the response of satellite cells to hepatocyte growth factor, a factor present in skeletal muscle during exercise that is already well-studied in rodent models. Additionally, to determine whether the addition of the non-essential amino acid, citrulline, would influence satellite cells and nutrient reserves after a session of submaximal exercise. I found that hepatocyte growth factor does not influence satellite cells isolated from horses in the same way it influences those from rodents, nor through the same mechanisms. Additionally, I found that satellite cells were not stimulated after a session of submaximal exercise, but a factor involved in regulation of genetic expression that is associated with satellite cells and skeletal muscle was downregulated with the addition of citrulline. Together, these results suggest that satellite cells may behave like other species in some ways, such as some responses to hepatocyte growth factor and the lack of response to a submaximal bout of exercise, but that there is still much to be learned in order to begin to influence management and training decisions as regards skeletal muscle recovery.
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Mofarrahi, Mahroo. "Regulation of skeletal muscle satellite cell proliferation by NADPH oxidase." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111521.
Повний текст джерелаАнотація:
Skeletal satellite cells are adult stem cells located among muscle fibers. Proliferation, migration and subsequent differentiation of these cells are critical steps in the repair of muscle injury. We document in this study the roles and mechanisms through which the NAPDH oxidase complex regulates skeletal satellite cell proliferation. The NADPH oxidase subunits Nox2, Nox4, p22phox, p47phox and p67 phox were detected in primary human and murine skeletal muscle satellite cells. In human satellite cells, NADPH oxidase-fusion proteins were localized in the cytosolic and membrane compartments of the cell, except for p47 phox, which was detected in the nucleus. In proliferating subconfluent satellite cells, both Nox2 and Nox4 contributed to O2- production. However, Nox4 expression was significantly attenuated in confluent cells and in differentiated myotubes. Proliferation of satellite cells was significantly reduced by antioxidants (N-acetylcysteine and apocynin), inhibition of p22phox expression using siRNA oligonucleotides, and reduction of Nox4 and p47phox activities with dominant-negative vectors resulted in attenuation of activities of the Erk1/2, PI-3 kinase/AKT and NFkappaB pathways and significant reduction in cyclin D1 levels. We conclude that NADPH oxidase is expressed in skeletal satellite cells and that its activity plays an important role in promoting proliferation of these cells.
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Correra, Rosa Maria. "Pw1/Peg3 regulates skeletal muscle growth and satellite cell self-renewal." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066339.
Повний текст джерелаАнотація:
Pw1/Peg3 est un gène d’empreinte parental exprimé par l’allèle paternel. Il est exprimé dans l’ensemble des populations de cellules souches, y compris les cellules satellites du tissu musculaire. Nous avons découvert que la perte constitutive de Pw1/Peg3 entraîne une perte de la masse musculaire, résultat d’une diminution du nombre de fibres musculaires. Le nombre de fibres réduit est présent dès la naissance. De plus, les souris double KO ont un nombre de fibres encore inférieur, suggérant que l’allèle maternel est fonctionnel pendant le développement pré-natal, et des analyses de souris hybrides C57BL6J/CAST/Ei révèlent une expression bi-allélique de Pw1/Peg3 d’environ 10%. Pw1/Peg3 est également fortement exprimé après blessure du muscle squelettique. Chez les souris Pw1/Peg3 KO, nous avons observé que les cellules satellites montrent une réduction de leur capacité d’auto-renouvèlement à la suite d’une blessure. Pw1/Peg3 est également exprimé dans une sous-population de cellules souches interstitielles, les PICS. Afin de déterminer le rôle spécifique de Pw1/Peg3 dans les cellules satellites nous avons croisé notre allèle conditionnel Pw1/Peg3 avec la lignée Pax7-Cre-ER. Ces souris ont un phénotype présentant un défaut de régénération prononcé, montrant ainsi un rôle clair et direct de Pw1/Peg3 dans la fonction régénératrice des cellules satellites. En résumé, l’ensemble de ces données montre un rôle de Pw1/Peg3 dans le développement fœtal et la détermination du nombre de fibres musculaires par son action dans l’auto-renouvellement des cellules satellites du tissu musculairePw1/Peg3 is a parentally imprinted gene expressed from the paternal allele. It is expressed in all adult progenitor/stem cell populations examined to date including muscle satellite cells. We examined the impact of loss-of-function of Pw1/Peg3 in skeletal muscle, a tissue that greatly contributes to body mass. We found that constitutive loss of Pw1/Peg3 results in reduced muscle mass resulting from a decrease in muscle fiber number. The reduced fiber number is present at birth. Mice lacking both the paternal and maternal alleles display a lower fiber number as compared to mice carrying the paternal deletion, suggesting that the maternal allele is functional during prenatal development. Hybrid analyses (C57BL6J and Cast/Ei) of muscle tissue reveal a bi-allelic expression of Pw1/Peg3 around 10%. Pw1/Peg3 is strongly up-regulated in response to muscle injury. Using the constitutive Pw1/Peg3 knock out mouse, we observed that satellite cells display a reduced self-renewal capacity following muscle injury. Pw1/Peg3 is expressed in satellite cells as well as a subset of muscle interstitial cells (PICs). To determine the specific role of Pw1/Peg3 in satellite cells, we crossed our conditional Pw1/Peg3 allele with the Pax7-CreER line. Interestingly, these mice displayed a more pronounced phenotype of impaired regeneration revealing a clear and direct role for Pw1/Peg3 in satellite cells. Taken together, our data show that Pw1/Peg3 plays a role during fetal development in the determination of muscle fiber number that is gene-dosage dependent and plays a specific role in muscle satellite cell self-renewal
Книги з теми "Skeletal muscle satellite cells"
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Greg, Molnar, and United States. National Aeronautics and Space Administration., eds. Skeletal muscle satellite cells cultured in simulated microgravity. [Washington, DC: National Aeronautics and Space Administration, 1993.
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Vandenburgh, Herman H. Computer aided mechanogenesis of skeletal muscle organs from single cells in vitro. [Washington, DC]: National Aeronautics and Space Administration, 1990.
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3
Herman, Vandenburgh, and United States. National Aeronautics and Space Administration., eds. Tissue-engineered skeletal muscle organoids for reversible gene therapy: Brief report. [Washington, DC: National Aeronautics and Space Administration, 1996.
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Sarabia, Vivian E. Calcium homeostasis and regulation of glucose uptake in human skeletal muscle cells in culture. Ottawa: National Library of Canada, 1990.
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5
Prud'homme, Renée. The Role of calmodulin and nuclear factor of activated T-cells in growth of mature skeletal muscle after injury or overload. Sudbury, Ont: Laurentian University, 2002.
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Skeletal muscle satellite cells cultured in simulated microgravity. [Washington, DC: National Aeronautics and Space Administration, 1993.
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Molnar, Greg. Properties of satellite cells isolated from sheep skeletal muscle. 1993.
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8
Skeletal Muscle Muscular Dystrophy A Visual Approach. Morgan & Claypool Publishers, 2011.
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Pinheiro, Carlos Hermano J., and Lucas Guimarães-Ferreira, eds. Frontiers in Skeletal Muscle Wasting, Regeneration and Stem Cells. Frontiers Media SA, 2016. http://dx.doi.org/10.3389/978-2-88919-832-0.
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Fibre Types in Skeletal Muscles (Advances in Anatomy, Embryology and Cell Biology). Springer, 2002.
Знайти повний текст джерелаЧастини книг з теми "Skeletal muscle satellite cells"
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Schultz, Edward, and Kathleen M. McCormick. "Skeletal muscle satellite cells." In Reviews of Physiology, Biochemistry and Pharmacology, 213–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/bfb0030904.
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Magovern, G. J. "Myocardial Regeneration with Skeletal Muscle Satellite Cells." In The Transplantation and Replacement of Thoracic Organs, 785–87. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-0-585-34287-0_88.
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Musarò, Antonio, and Silvia Carosio. "Isolation and Culture of Satellite Cells from Mouse Skeletal Muscle." In Adult Stem Cells, 155–67. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6756-8_12.
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Yablonka-Reuveni, Zipora, and Kenneth Day. "Skeletal Muscle Stem Cells in the Spotlight: The Satellite Cell." In Regenerating the Heart, 173–200. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-021-8_11.
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von Maltzahn, Julia, C. Florian Bentzinger, and Michael A. Rudnicki. "Characteristics of Satellite Cells and Multipotent Adult Stem Cells in the Skeletal Muscle." In Stem Cells and Cancer Stem Cells, Volume 12, 63–73. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-017-8032-2_6.
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Dumont, Nicolas A., and Michael A. Rudnicki. "Characterizing Satellite Cells and Myogenic Progenitors During Skeletal Muscle Regeneration." In Methods in Molecular Biology, 179–88. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6788-9_12.
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Krstić, Radivoj V. "Skeletal Musculature. White Muscle Fiber and Satellite Cell." In General Histology of the Mammal, 260–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70420-8_127.
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Tedesco, Francesco Saverio, Louise A. Moyle, and Eusebio Perdiguero. "Muscle Interstitial Cells: A Brief Field Guide to Non-satellite Cell Populations in Skeletal Muscle." In Methods in Molecular Biology, 129–47. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6771-1_7.
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Alameddine, Hala S., and Michel Fardeau. "Regeneration of Skeletal Muscle Induced by Satellite Cell Grafts." In Myoblast Transfer Therapy, 159–66. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5865-7_18.
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Alameddine, Hala. "Regeneration of Skeletal Muscle Fibers by In Vitro Multiplied Autologous Satellite Cells." In Recent Trends in Regeneration Research, 169–71. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-9057-2_18.
Повний текст джерелаТези доповідей конференцій з теми "Skeletal muscle satellite cells"
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Hoque, Sanzana, Krzysztof Kucharz, Marie Sjögren, Andreas Neueder, Michael Orth, Maria Björkqvist, and Rana Soylu Kucharz. "A21 Assessment of satellite progenitor cell differentiation in hd skeletal muscle in vitro." In EHDN Abstracts 2021. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/jnnp-2021-ehdn.20.
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Lee, Raphael C., Stephanie M. Hammer, and Daniel J. Canaday. "Transient electropore lifetimes in skeletal muscle cells." In 1992 14th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.5760977.
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Lee, Hammer, and Canaday. "Transient Electropore Lifetimes In Skeletal Muscle Cells." In Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.589732.
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Höckele, S., P. Huypens, C. Hoffmann, T. Jeske, M. Hastreiter, A. Böhm, J. Beckers, HU Häring, M. Hrabe de Angelis, and C. Weigert. "TGFß regulates metabolism of human skeletal muscle cells by miRNAs." In Diabetes Kongress 2018 – 53. Jahrestagung der DDG. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1641809.
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Kogure, Tsukasa, Yoshitake Akiyama, Takayuki Hoshino, and Keisuke Morishima. "Fabrication of a controllable bio-micropump driven by skeletal muscle cells." In TRANSDUCERS 2009 - 2009 International Solid-State Sensors, Actuators and Microsystems Conference. IEEE, 2009. http://dx.doi.org/10.1109/sensor.2009.5285549.
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Garcia, F., AM Jank, and TJ Schulz. "Age-related impairment of muscle resident progenitor cells affect the metabolic homeostasis of skeletal muscle." In Late Breaking Abstracts: – Diabetes Kongress 2017 – 52. Jahrestagung der DDG. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1603536.
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McKeon-Fischer, K. D., D. H. Flagg, J. H. Rossmeisl, A. R. Whittington, and J. W. Freeman. "Electroactive, Multi-Component Scaffolds for Skeletal Muscle Regeneration." In ASME 2013 2nd Global Congress on NanoEngineering for Medicine and Biology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/nemb2013-93197.
Повний текст джерелаАнотація:
After loss of skeletal muscle function due to traumatic injuries, muscle healing may result in scar tissue formation and reduced function. A restoration method is needed to create a bioartificial muscle that supports cell growth. An electroactive, coaxial electrospun scaffold was created using PCL, MWCNT, and a PAA/PVA hydrogel. This scaffold was conductive and displayed an actuation response when electrically stimulated. Rat primary skeletal muscle cells were biocompatible with the scaffold and displayed multi-nucleated constructs with actin interaction. MWCNT toxicity was tested using a single exposure method on rat primary skeletal muscle cells. A decrease in cellular activity was found on day 14, but a recovering trend was observed on days 21 and 28. Scaffolds were implanted in the quadriceps muscle of rats for in vivo biocompatibility investigation. Muscle cells were found to have attached and infiltrated the PCL-MWCNT-PAA/PVA scaffolds over the 28 day period. Further development of this scaffold would lead to a viable option for a bioartificial muscle as it is biocompatible and may provide some functional movement to the patient.
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Gokalp, G., D. Zhao, R. C. Atalay, Y. Tian, R. B. Hamanaka, and G. M. Mutlu. "Glutamine Is Required for Mitochondrial Respiration and Differentiation of Skeletal Muscle Cells." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5595.
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Qin, Zhongya, Yanyang Long, Qiqi Sun, Zhenguo Wu, Jianan Y. Qu, Sicong He, Xuesong Li, and Congping Chen. "In vivo two-photon imaging of macrophage activities in skeletal muscle regeneration." In Imaging, Manipulation, and Analysis of Biomolecules, Cells, and Tissues XVI, edited by Daniel L. Farkas, Dan V. Nicolau, and Robert C. Leif. SPIE, 2018. http://dx.doi.org/10.1117/12.2286834.
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Jiao, Yang, Hananeh Derakhshan, Barbara St Pierre Schneider, Emma Regentova, and Mei Yang. "Automated quantification of white blood cells in light microscopic images of injured skeletal muscle." In 2018 IEEE 8th Annual Computing and Communication Workshop and Conference (CCWC). IEEE, 2018. http://dx.doi.org/10.1109/ccwc.2018.8301750.
Повний текст джерелаЗвіти організацій з теми "Skeletal muscle satellite cells"
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Halevy, Orna, Sandra Velleman, and Shlomo Yahav. Early post-hatch thermal stress effects on broiler muscle development and performance. United States Department of Agriculture, January 2013. http://dx.doi.org/10.32747/2013.7597933.bard.
Повний текст джерелаАнотація:
In broilers, the immediate post-hatch handling period exposes chicks to cold or hot thermal stress, with potentially harmful consequences to product quantity and quality that could threaten poultry meat marketability as a healthy, low-fat food. This lower performance includes adverse effects on muscle growth and damage to muscle structure (e.g., less protein and more fat deposition). A leading candidate for mediating the effects of thermal stress on muscle growth and development is a unique group of skeletal muscle cells known as adult myoblasts (satellite cells). Satellite cells are multipotential stem cells that can be stimulated to follow other developmental pathways, especially adipogenesis in lieu of muscle formation. They are most active during the first week of age in broilers and have been shown to be sensitive to environmental conditions and nutritional status. The hypothesis of the present study was that immediate post-hatch thermal stress would harm broiler growth and performance. In particular, growth characteristics and gene expression of muscle progenitor cells (i.e., satellite cells) will be affected, leading to increased fat deposition, resulting in long-term changes in muscle structure and a reduction in meat yield. The in vitro studies on cultured satellite cells derived from different muscle, have demonstrated that, anaerobic pectoralis major satellite cells are more predisposed to adipogenic conversion and more sensitive during myogenic proliferation and differentiation than aerobic biceps femoris cells when challenged to both hot and cold thermal stress. These results corroborated the in vivo studies, establishing that chronic heat exposure of broiler chicks at their first two week of life leads to impaired myogenicity of the satellite cells, and increased fat deposition in the muscle. Moreover, chronic exposure of chicks to inaccurate temperature, in particular to heat vs. cold, during their early posthatch periods has long-term effects of BW, absolute muscle growth and muscle morphology and meat quality. The latter is manifested by higher lipid and collagen deposition and may lead to the white striping occurrence. The results of this study emphasize the high sensitivity of muscle progenitor cells in the early posthatch period at a time when they are highly active and therefore the importance of rearing broiler chicks under accurate ambient temperatures. From an agricultural point of view, this research clearly demonstrates the immediate and long-term adverse effects on broiler muscling and fat formation due to chronic exposure to hot stress vs. cold temperatures at early age posthatch. These findings will aid in developing management strategies to improve broiler performance in Israel and the USA. BARD Report - Project4592 Page 2 of 29
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Yahav, Shlomo, John Brake, and Orna Halevy. Pre-natal Epigenetic Adaptation to Improve Thermotolerance Acquisition and Performance of Fast-growing Meat-type Chickens. United States Department of Agriculture, September 2009. http://dx.doi.org/10.32747/2009.7592120.bard.
Повний текст джерелаАнотація:
: The necessity to improve broiler thermotolerance and performance led to the following hypothesis: (a) thethermoregulatory-response threshold for heat production can be altered by thermal manipulation (TM) during incubation so as to improve the acquisition of thermotolerance in the post-hatch broiler;and (b) TM during embryogenesis will improve myoblast proliferation during the embryonic and post-hatch periods with subsequent enhanced muscle growth and meat production. The original objectives of this study were as follow: 1. to assess the timing, temperature, duration, and turning frequency required for optimal TM during embryogenesis; 2. to evaluate the effect of TM during embryogenesis on thermoregulation (heat production and heat dissipation) during four phases: (1) embryogenesis, (2) at hatch, (3) during growth, and (4) during heat challenge near marketing age; 3. to investigate the stimulatory effect of thermotolerance on hormones that regulate thermogenesis and stress (T₄, T₃, corticosterone, glucagon); 4. to determine the effect of TM on performance (BW gain, feed intake, feed efficiency, carcass yield, breast muscle yield) of broiler chickens; and 5. to study the effect of TM during embryogenesis on skeletal muscle growth, including myoblast proliferation and fiber development, in the embryo and post-hatch chicks.This study has achieved all the original objectives. Only the plasma glucagon concentration (objective 3) was not measured as a result of technical obstacles. Background to the topic: Rapid growth rate has presented broiler chickens with seriousdifficulties when called upon to efficiently thermoregulate in hot environmental conditions. Being homeotherms, birds are able to maintain their body temperature (Tb) within a narrow range. An increase in Tb above the regulated range, as a result of exposure to environmental conditions and/or excessive metabolic heat production that often characterize broiler chickens, may lead to a potentially lethal cascade of irreversible thermoregulatory events. Exposure to temperature fluctuations during the perinatal period has been shown to lead to epigenetic temperature adaptation. The mechanism for this adaptation was based on the assumption that environmental factors, especially ambient temperature, have a strong influence on the determination of the “set-point” for physiological control systems during “critical developmental phases.” In order to sustain or even improve broiler performance, TM during the period of embryogenesis when satellite cell population normally expand should increase absolute pectoralis muscle weight in broilers post-hatch. Major conclusions: Intermittent TM (39.5°C for 12 h/day) during embryogenesis when the thyroid and adrenal axis was developing and maturing (E7 to E16 inclusive) had a long lasting thermoregulatory effect that improved thermotolerance of broiler chickens exposed to acute thermal stress at market age by lowering their functional Tb set point, thus lowering metabolic rate at hatch, improving sensible heat loss, and significantly decreasing the level of stress. Increased machine ventilation rate was required during TM so as to supply the oxygen required for the periods of increased embryonic development. Enhancing embryonic development was found to be accomplished by a combination of pre-incubation heating of embryos for 12 h at 30°C, followed by increasing incubation temperature to 38°C during the first 3 days of incubation. It was further facilitated by increasing turning frequency of the eggs to 48 or 96 times daily. TM during critical phases of muscle development in the late-term chick embryo (E16 to E18) for 3 or 6 hours (39.5°C) had an immediate stimulatory effect on myoblast proliferation that lasted for up to two weeks post-hatch; this was followed by increased hypertrophy at later ages. The various incubation temperatures and TM durations focused on the fine-tuning of muscle development and growth processes during late-term embryogenesis as well as in post-hatch chickens.
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Yahav, Shlomo, John McMurtry, and Isaac Plavnik. Thermotolerance Acquisition in Broiler Chickens by Temperature Conditioning Early in Life. United States Department of Agriculture, 1998. http://dx.doi.org/10.32747/1998.7580676.bard.
Повний текст джерелаАнотація:
The research on thermotolerance acquisition in broiler chickens by temperature conditioning early in life was focused on the following objectives: a. To determine the optimal timing and temperature for inducing the thermotolerance, conditioning processes and to define its duration during the first week of life in the broiler chick. b. To investigate the response of skeletal muscle tissue and the gastrointestinal tract to thermal conditioning. This objective was added during the research, to understand the mechanisms related to compensatory growth. c. To evaluate the effect of early thermo conditioning on thermoregulation (heat production and heat dissipation) during 3 phases: (1) conditioning, (2) compensatory growth, (3) heat challenge. d. To investigate how induction of improved thermotolerance impacts on metabolic fuel and the hormones regulating growth and metabolism. Recent decades have seen significant development in the genetic selection of the meat-type fowl (i.e., broiler chickens); leading to rapid growth and increased feed efficiency, providing the poultry industry with heavy chickens in relatively short growth periods. Such development necessitates parallel increases in the size of visceral systems such as the cardiovascular and the respiratory ones. However, inferior development of such major systems has led to a relatively low capability to balance energy expenditure under extreme conditions. Thus, acute exposure of chickens to extreme conditions (i.e., heat spells) has resulted in major economic losses. Birds are homeotherms, and as such, they are able to maintain their body temperature within a narrow range. To sustain thermal tolerance and avoid the deleterious consequences of thermal stresses, a direct response is elicited: the rapid thermal shock response - thermal conditioning. This technique of temperature conditioning takes advantage of the immaturity of the temperature regulation mechanism in young chicks during their first week of life. Development of this mechanism involves sympathetic neural activity, integration of thermal infom1ation in the hypothalamus, and buildup of the body-to-brain temperature difference, so that the potential for thermotolerance can be incorporated into the developing thermoregulation mechanisms. Thermal conditioning is a unique management tool, which most likely involves hypothalamic them1oregulatory threshold changes that enable chickens, within certain limits, to cope with acute exposure to unexpected hot spells. Short-tem1 exposure to heat stress during the first week of life (37.5+1°C; 70-80% rh; for 24 h at 3 days of age) resulted in growth retardation followed immediately by compensatory growth" which resulted in complete compensation for the loss of weight gain, so that the conditioned chickens achieved higher body weight than that of the controls at 42 days of age. The compensatory growth was partially explained by its dramatic positive effect on the proliferation of muscle satellite cells which are necessary for further muscle hypertrophy. By its significant effect of the morphology and functioning of the gastrointestinal tract during and after using thermal conditioning. The significant effect of thermal conditioning on the chicken thermoregulation was found to be associated with a reduction in heat production and evaporative heat loss, and with an increase in sensible heat loss. It was further accompanied by changes in hormones regulating growth and metabolism These physiological responses may result from possible alterations in PO/AH gene expression patterns (14-3-3e), suggesting a more efficient mechanism to cope with heat stress. Understanding the physiological mechanisms behind thermal conditioning step us forward to elucidate the molecular mechanism behind the PO/AH response, and response of other major organs. The thermal conditioning technique is used now in many countries including Israel, South Korea, Australia, France" Ecuador, China and some places in the USA. The improvement in growth perfom1ance (50-190 g/chicken) and thermotolerance as a result of postnatal thermal conditioning, may initiate a dramatic improvement in the economy of broiler's production.
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Shani, Moshe, and C. P. Emerson. Genetic Manipulation of the Adipose Tissue via Transgenesis. United States Department of Agriculture, April 1995. http://dx.doi.org/10.32747/1995.7604929.bard.
Повний текст джерелаАнотація:
The long term goal of this study was to reduce caloric and fat content of beef and other red meats by means of genetic modification of the animal such that fat would not be accumulated. This was attempted by introducing into the germ line myogenic regulatory genes that would convert fat tissue to skeletal muscle. We first determined the consequences of ectopic expression of the myogenic regulatory gene MyoD1. It was found that deregulation of MyoD1 did not result in ectopic skeletal muscle formation but rather led to embryonic lethalities, probably due to its role in the control of the cell cycle. This indicated that MyoD1 should be placed under stringent control to allow survival. Embryonic lethalities were also observed when the regulatory elements of the adipose-specific gene adipsin directed the expression of MyoD1 or myogenin cDNAs, suggesting that these sequences are probably not strong enough to confer tissue specificity. To determine the specificity of the control elements of another fat specific gene (adipocyte protein 2-aP2), we fused them to the bacterial b-galactosidase reporter gene and established stable transgenic strains. The expression of the reporter gene in none of the strains was adipose specific. Each strain displayed a unique pattern of expression in various cell lineages. Most exciting results were obtained in a transgenic strain in which cells migrating from the ventro-lateral edge of the dermomyotome of developing somites to populate the limb buds with myoblasts were specifically stained for lacZ. Since the control sequences of the adipsin or aP2 genes did not confer fat specificity in transgenic mice we have taken both molecular and genetic approaches as an initial effort to identify genes important in the conversion of a multipotential cell such as C3H10T1/2 cell to adipoblast. Several novel adipocyte cell lines have been established that differ in the expression of transcription factors of the C/EBP family known to be markers for adipocyte differentiation. These studies revealed that one of the genetic programming changes which occur during 10T1/2 conversion from multipotential cell to a committed adipoblast is the ability to linduce C/EBPa gene expression. It is expected that further analysis of this gene would identify elements which regulate this lineage-specific expression. Such elements might be good candidates in future attempts to convert adipoblasts to skeletal muscle cells in vivo.
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Funkenstein, Bruria, and Shaojun (Jim) Du. Interactions Between the GH-IGF axis and Myostatin in Regulating Muscle Growth in Sparus aurata. United States Department of Agriculture, March 2009. http://dx.doi.org/10.32747/2009.7696530.bard.
Повний текст джерелаАнотація:
Growth rate of cultured fish from hatching to commercial size is a major factor in the success of aquaculture. The normal stimulus for muscle growth in growing fish is not well understood and understanding the regulation of muscle growth in fish is of particular importance for aquaculture. Fish meat constitutes mostly of skeletal muscles and provides high value proteins in most people's diet. Unlike mammals, fish continue to grow throughout their lives, although the size fish attain, as adults, is species specific. Evidence indicates that muscle growth is regulated positively and negatively by a variety of growth and transcription factors that control both muscle cell proliferation and differentiation. In particular, growth hormone (GH), fibroblast growth factors (FGFs), insulin-like growth factors (IGFs) and transforming growth factor-13 (TGF-13) play critical roles in myogenesis during animal growth. An important advance in our understanding of muscle growth was provided by the recent discovery of the crucial functions of myostatin (MSTN) in controlling muscle growth. MSTN is a member of the TGF-13 superfamily and functions as a negative regulator of skeletal muscle growth in mammals. Studies in mammals also provided evidence for possible interactions between GH, IGFs, MSTN and the musclespecific transcription factor My oD with regards to muscle development and growth. The goal of our project was to try to clarify the role of MSTNs in Sparus aurata muscle growth and in particular determine the possible interaction between the GH-IGFaxis and MSTN in regulating muscle growth in fish. The steps to achieve this goal included: i) Determining possible relationship between changes in the expression of growth-related genes, MSTN and MyoD in muscle from slow and fast growing sea bream progeny of full-sib families and that of growth rate; ii) Testing the possible effect of over-expressing GH, IGF-I and IGF-Il on the expression of MSTN and MyoD in skeletal muscle both in vivo and in vitro; iii) Studying the regulation of the two S. aurata MSTN promoters and investigating the possible role of MyoD in this regulation. The major findings of our research can be summarized as follows: 1) Two MSTN promoters (saMSTN-1 and saMSTN-2) were isolated and characterized from S. aurata and were found to direct reporter gene activity in A204 cells. Studies were initiated to decipher the regulation of fish MSTN expression in vitro using the cloned promoters; 2) The gene coding for saMSTN-2 was cloned. Both the promoter and the first intron were found to be polymorphic. The first intron zygosity appears to be associated with growth rate; 3) Full length cDNA coding for S. aurata growth differentiation factor-l I (GDF-II), a closely related growth factor to MSTN, was cloned from S. aurata brain, and the mature peptide (C-terminal) was found to be highly conserved throughout evolution. GDF-II transcript was detected by RT -PCR analysis throughout development in S. aurata embryos and larvae, suggesting that this mRNA is the product of the embryonic genome. Transcripts for GDF-Il were detected by RT-PCR in brain, eye and spleen with highest level found in brain; 4) A novel member of the TGF-Bsuperfamily was partially cloned from S. aurata. It is highly homologous to an unidentified protein (TGF-B-like) from Tetraodon nigroviridisand is expressed in various tissues, including muscle; 5) Recombinant S. aurata GH was produced in bacteria, refolded and purified and was used in in vitro and in vivo experiments. Generally, the results of gene expression in response to GH administration in vivo depended on the nutritional state (starvation or feeding) and the time at which the fish were sacrificed after GH administration. In vitro, recombinantsaGH activated signal transduction in two fish cell lines: RTHI49 and SAFI; 6) A fibroblastic-like cell line from S. aurata (SAF-I) was characterized for its gene expression and was found to be a suitable experimental system for studies on GH-IGF and MSTN interactions; 7) The gene of the muscle-specific transcription factor Myogenin was cloned from S. aurata, its expression and promoter activity were characterized; 8) Three genes important to myofibrillogenesis were cloned from zebrafish: SmyDl, Hsp90al and skNAC. Our data suggests the existence of an interaction between the GH-IGFaxis and MSTN. This project yielded a great number of experimental tools, both DNA constructs and in vitro systems that will enable further studies on the regulation of MSTN expression and on the interactions between members of the GHIGFaxis and MSTN in regulating muscle growth in S. aurata.