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Relevant bibliographies by topics / Muscle cells

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Academic literature on the topic 'Muscle cells'

Author: Grafiati

Published: 4 June 2021

Last updated: 30 July 2024

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Journal articles on the topic "Muscle cells"

1

Griffin, D. M., H. M. Hudson, A. Belhaj-Saïf, B. J. McKiernan, and P. D. Cheney. "Do Corticomotoneuronal Cells Predict Target Muscle EMG Activity?" Journal of Neurophysiology 99, no. 3 (March 2008): 1169–986. http://dx.doi.org/10.1152/jn.00906.2007.

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Data from two rhesus macaques were used to investigate the pattern of cortical cell activation during reach-to-grasp movements in relation to the corresponding activation pattern of the cell's facilitated target muscles. The presence of postspike facilitation (PSpF) in spike-triggered averages (SpTAs) of electromyographic (EMG) activity was used to identify cortical neurons with excitatory synaptic linkages with motoneurons. EMG activity from 22 to 24 muscles of the forelimb was recorded together with the activity of M1 cortical neurons. The extent of covariation was characterized by 1) identifying the task segment containing the cell and target muscle activity peaks, 2) quantifying the timing and overlap between corticomotoneuronal (CM) cell and EMG peaks, and 3) applying Pearson correlation analysis to plots of CM cell firing rate versus EMG activity of the cell's facilitated muscles. At least one firing rate peak, for nearly all (95%) CM cells tested, matched a corresponding peak in the EMG activity of the cell's target muscles. Although some individual CM cells had very strong correlations with target muscles, overall, substantial disparities were common. We also investigated correlations for ensembles of CM cells sharing the same target muscle. The ensemble population activity of even a small number of CM cells influencing the same target muscle produced a relatively good match ( r ≥ 0.8) to target muscle EMG activity. Our results provide evidence in support of the notion that corticomotoneuronal output from primary motor cortex encodes movement in a framework of muscle-based parameters, specifically muscle-activation patterns as reflected in EMG activity.

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Reyes, Morayma, and Jeffrey S. Chamberlain. "Perivascular CD45−:Sca-1+:CD34− Cells Are Derived from Bone Marrow Cells and Participate in Dystrophic Skeletal Muscle Regeneration." Blood 106, no. 11 (November 16, 2005): 394. http://dx.doi.org/10.1182/blood.v106.11.394.394.

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Abstract Multiple mechanisms may account for bone marrow (BM) cell incorporation into myofibers following muscle damage. Here, we demonstrated that CD45−:Sca-1+:CD34− cells may play a role in the regeneration of mdx4cv skeletal muscles, an animal model for Duchenne muscular dystrophy. To understand the origin of CD45−:Sca-1+:CD34− cells in skeletal muscle, we reconstituted lethally irradiated wild type (wt) or mdx4cv mice with unfractionated BM cells from transgenic mice ubiquitously expressing green fluorescence protein (GFP). 1, 2, and 6 months post-transplantation, we analyzed the skeletal muscle mononuclear cells from the recipients by flow cytometry for GFP, CD45-PerCP, Sca-1-PE, and CD34-APC. To our surprise, we found a small percentage of BM-derived (GFP+) CD45−:Sca-1+:CD34− cells in the skeletal muscles of these GFP+ BM transplant recipients. These BM-derived cells are localized in the perivascular tissue by immunostaining and their frequency increases with time. We were interested in the potential of these cells for clinical application for muscle diseases. Thus, we FACS-sorted CD45−:Sca-1+:CD34− cells from GFP transgenic mouse skeletal muscles and transplanted them in the tibialis anterior (TA) muscle of mdx4cv mice. In ten days we found significant muscle engraftment. In addition, we studied the response of this population upon acute muscle injury. For this, we injected cardiotoxin in the right TA muscle of mdx4cv and wt mice, followed by BrdU administration in drinking water for three days. After 3.5 days, mice were sacrificed and the right and left (control) TA muscles were harvested and muscle CD45−:Sca-1+:CD34− cells were FACS-sorted, fixed and stained for BrdU and Myf-5. In the injured muscle (right TA), more than 70% of these cells were BrdU+ and more than 50% were Myf-5+, compared to baseline levels (close to zero) in the left TA. This indicates that this population can undergo proliferation and myogenic commitment upon muscle injury. To understand how these BM cells migrate to the muscle and once in the muscle how they mobilize, we investigated the in vitro chemotatic response of GFP+ (BM derived) CD45−:Sca-1+ cells isolated from muscles of GFP+ BM transplant recipients. We found that these cells were highly chemoattrated to stroma derived factor, SDF-1, a chemo-attractant for cells expressing CXCR4. We also observed higher frequency of BM-derived CD45−:Sca-1+:CD34− cells in dystrophic muscle than wt muscle, which may be explained by higher expression levels of SDF-1 in dystrophic muscles. In an effort to determine the identity of these cells when ex vivo cultured, we cultured them in several stem cell media, including a low-serum medium containing specific cytokines for the isolation and expansion of multipotent adult progenitor cells (MAPCs). MAPCs can be isolated from skeletal muscle and BM and can differentiate into multiple tissue cells. Strikingly, we found that MAPCs were enriched up to 40 folds by sorting this population from skeletal muscle. The frequency of BM-derived muscle MAPCs also increases with time post-transplantation in dystrophic muscles. These BM-derived muscle MAPCs displayed the typical MAPC immunophenotypes, displayed a normal diploid karyotype and were capable to differentiate into endothelial cells, hepatocytes and neurons. Taken together, our results suggest that dystrophic muscles recruit BM cells that localize in perivascular tissues and can be defined as CD45-:Sca-1+:CD34-. This population when cultured enriches for MAPCs and can participate in muscle regeneration in dystrophic muscles.

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Becker, S., G. Pasca, D. Strumpf, L. Min, and T. Volk. "Reciprocal signaling between Drosophila epidermal muscle attachment cells and their corresponding muscles." Development 124, no. 13 (July 1, 1997): 2615–22. http://dx.doi.org/10.1242/dev.124.13.2615.

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Directed intercellular interactions between distinct cell types underlie the basis for organogenesis during embryonic development. This paper focuses on the establishment of the final somatic muscle pattern in Drosophila, and on the possible cross-talk between the myotubes and the epidermal muscle attachment cells, occurring while both cell types undergo distinct developmental programs. Our findings suggest that the stripe gene is necessary and sufficient to initiate the developmental program of epidermal muscle attachment cells. In stripe mutant embryos, these cells do not differentiate correctly. Ectopic expression of Stripe in various epidermal cells transforms these cells into muscle-attachment cells expressing an array of epidermal muscle attachment cell-specific markers. Moreover, these ectopic epidermal muscle attachment cells are capable of attracting somatic myotubes from a limited distance, providing that the myotube has not yet been attached to or been influenced by a closer wild-type attachment cell. Analysis of the relationships between muscle binding and differentiation of the epidermal muscle attachment cell was performed in mutant embryos in which loss of muscles, or ectopic muscles were induced. This analysis indicated that, although the initial expression of epidermal muscle-attachment cell-specific genes including stripe and groovin is muscle independent, their continuous expression is maintained only in epidermal muscle attachment cells that are connected to muscles. These results suggest that the binding of a somatic muscle to an epidermal muscle attachment cell triggers a signal affecting gene expression in the attachment cell. Taken together, our results suggest the presence of a reciprocal signaling mechanism between the approaching muscles and the epidermal muscle attachment cells. First the epidermal muscle attachment cells signal the myotubes and induce myotube attraction and adhesion to their target cells. Following this binding, the muscle cells send a reciprocal signal to the epidermal muscle attachment cells inducing their terminal differentiation into tendon-like cells.

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Yoshimoto, Momoko, Toshio Heike, Mitsutaka Shiota, Hirohiko Kobayashi, Katsutsugu Umeda, and Tatsutoshi Nakahata. "Hematopoietic Stem Cells Can Give Rise to Satellite-Like Cells in Skeletal Muscles." Blood 104, no. 11 (November 16, 2004): 2690. http://dx.doi.org/10.1182/blood.v104.11.2690.2690.

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Abstract Recent studies have indicated that bone marrow cells can regenerate damaged muscles, but also that they can adopt phenotype of other cells by cell fusion. It has also been reported that single hematopoietic stem cells (HSCs) can regenerate skeletal muscle although it is still controversial whether HSCs differentiate into satellite cells in muscle or not. In order to investigate the roles of HSCs in muscle regeneration and whether they can generate satellite cells or not, we purified and injected CD45+Lin−Sca-1+c-kit+(CD45+KSL) HSCs labeled by green fluorescent protein (GFP) into mice with or without irradiation. We examined time-course behavior of HSCs in recipient muscles with a fluorescent stereomicroscope and then immunohitochemical staining during the early and late phase after transplantation. Our direct visualization system gave evidence of massive GFP signals in all the muscles of only irradiated mice in early phase after transplantation. Transverse cryostat sections showed GFP+ Myosin+ muscle fibers along with numerous GFP+ hematopoietic cells in damaged muscle. We also found myogenin+GFP+ cells like myoblasts in very low number. These phenomena were temporal and GFP signals had dramatically reduced 30 days after transplantation. FISH analysis confirmed the GFP-DNAs in the nuclei of muscle fibers. These results suggested that most of GFP+HSCs fused with myofibers and participated in regeneration of damaged muscles, and a very few HSCs can differentiate into myoblast like cells expressing myogenin. After 6 months, GFP+ fibers could be hardly detected but GFP+c-Met+ mononuclear cells were located beneath the laminin+ basal lamina. Single fiber cultures from these mice showed proliferation of GFP+ fibers. These results suggested that HSC-derived cells settled beneath the basal lamina like satellite cells and might acquired the satellite cell activity.

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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.

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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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Mitchell, Patrick O., and Grace K. Pavlath. "Skeletal muscle atrophy leads to loss and dysfunction of muscle precursor cells." American Journal of Physiology-Cell Physiology 287, no. 6 (December 2004): C1753—C1762. http://dx.doi.org/10.1152/ajpcell.00292.2004.

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Atrophy of skeletal muscle leads to decreases in myofiber size and nuclear number; however, the effects of atrophic conditions on muscle precursor cells (MPC) are largely unknown. MPC lie outside myofibers and represent the main source of additional myonuclei necessary for muscle growth and repair. In the present study, we examined the properties of MPC after hindlimb suspension (HS)-induced atrophy and subsequent recovery of the mouse hindlimb muscles. We demonstrated that the number of MPC in atrophied muscles was decreased. RT-PCR analysis of cells isolated from atrophied muscles indicated that several mRNA characteristic of the myogenic program in MPC were absent. Cells isolated from atrophied muscles failed to properly proliferate and undergo differentiation into multinucleated myotubes. Thus atrophy led to a decrease in MPC and caused dysfunction in those MPC that remained. Upon regrowth of the atrophied muscles, these deleterious effects were reversed. Our data suggest that preventing loss or dysfunction of MPC may be a new pharmacological target during muscle atrophy.

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Zhao, Shudong, Jishizhan Chen, Lei Wu, Xin Tao, Naheem Yaqub, and Jinke Chang. "Induced Pluripotent Stem Cells for Tissue-Engineered Skeletal Muscles." International Journal of Molecular Sciences 24, no. 14 (July 15, 2023): 11520. http://dx.doi.org/10.3390/ijms241411520.

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Skeletal muscle, which comprises a significant portion of the body, is responsible for vital functions such as movement, metabolism, and overall health. However, severe injuries often result in volumetric muscle loss (VML) and compromise the regenerative capacity of the muscle. Tissue-engineered muscles offer a potential solution to address lost or damaged muscle tissue, thereby restoring muscle function and improving patients’ quality of life. Induced pluripotent stem cells (iPSCs) have emerged as a valuable cell source for muscle tissue engineering due to their pluripotency and self-renewal capacity, enabling the construction of tissue-engineered artificial skeletal muscles with applications in transplantation, disease modelling, and bio-hybrid robots. Next-generation iPSC-based models have the potential to revolutionize drug discovery by offering personalized muscle cells for testing, reducing reliance on animal models. This review provides a comprehensive overview of iPSCs in tissue-engineered artificial skeletal muscles, highlighting the advancements, applications, advantages, and challenges for clinical translation. We also discussed overcoming limitations and considerations in differentiation protocols, characterization methods, large-scale production, and translational regulations. By tackling these challenges, iPSCs can unlock transformative advancements in muscle tissue engineering and therapeutic interventions for the future.

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Challa, Stalin Reddy, and Swathi Goli. "Differentiation of Human Embryonic Stem Cells into Engrafting Myogenic Precursor Cells." Stem cell Research and Therapeutics International 1, no. 1 (April 16, 2019): 01–05. http://dx.doi.org/10.31579/2643-1912/002.

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Degenerative muscle diseases affect muscle tissue integrity and function. Human embryonic stem cells (hESC) are an attractive source of cells to use in regenerative therapies due to their unlimited capacity to divide and ability to specialize into a wide variety of cell types. A practical way to derive therapeutic myogenic stem cells from hESC is lacking. In this study, we demonstrate the development of two serum-free conditions to direct the differentiation of hESC towards a myogenic precursor state. Using TGFß and PI3Kinase inhibitors in combination with bFGF we showed that one week of differentiation is sufficient for hESC to specialize into PAX3+/PAX7+ myogenic precursor cells. These cells also possess the capacity to further differentiate in vitro into more specialized myogenic cells that express MYOD, Myogenin, Desmin and MYHC, and showed engraftment in vivo upon transplantation in immunodeficient mice. Ex vivo myomechanical studies of dystrophic mouse hindlimb muscle showed functional improvement one month post-transplantation. In summary, this study describes a promising system to derive engrafting muscle precursor cells solely using chemical substances in serum-free conditions and without genetic manipulation.

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Heslop, L., J. E. Morgan, and T. A. Partridge. "Evidence for a myogenic stem cell that is exhausted in dystrophic muscle." Journal of Cell Science 113, no. 12 (June 15, 2000): 2299–308. http://dx.doi.org/10.1242/jcs.113.12.2299.

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Injection of the myotoxin notexin, was found to induce regeneration in muscles that had been subjected to 18 Gy of radiation. This finding was unexpected as irradiation doses of this magnitude are known to block regeneration in dystrophic (mdx) mouse muscle. To investigate this phenomenon further we subjected mdx and normal (C57Bl/10) muscle to irradiation and notexin treatment and analysed them in two ways. First by counting the number of newly regenerated myofibres expressing developmental myosin in cryosections of damaged muscles. Second, by isolating single myofibres from treated muscles and counting the number of muscle precursor cells issuing from these over 2 day and 5 day periods. After irradiation neither normal nor dystrophic muscles regenerate to any significant extent. Moreover, single myofibres cultured from such muscles produce very few muscle precursor cells and these undergo little or no proliferation. However, when irradiated normal and mdx muscles were subsequently treated with notexin, regeneration was observed. In addition, some of the single myofibres produced rapidly proliferative muscle precursor cells when cultured. This occurred more frequently, and the myogenic cells proliferated more extensively, with fibres cultured from normal compared with dystrophic muscles. Even after 25 Gy, notexin induced some regeneration but no proliferative myogenic cells remained associated with the muscle fibres. Thus, skeletal muscles contain a number of functionally distinct populations of myogenic cells. Most are radiation sensitive. However, some survive 18 Gy as proliferative myogenic cells that can be evoked by extreme conditions of muscle damage; this population is markedly diminished in muscles of the mdx mouse. A small third population survives 25 Gy and forms muscle but not proliferative myogenic cells.

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Balch, Ying. "Subculture human skeletal muscle cells to produce the cells with different Culture medium compositions." Clinical Research and Clinical Trials 3, no. 4 (April 30, 2021): 01–03. http://dx.doi.org/10.31579/2693-4779/036.

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This study aimed to subculture human skeletal muscle cells (HSkMC) using a culture medium with different compositions to determine the most efficient medium for the growth of the human skeletal muscle cells. The culture media was divided into three groups: Group1. An HSkMC growth medium. Group 2. An HSkMC growth medium + with 10% high glucose (GH). Group 3. An HSkMC growth medium + 10% fetal bovine serum (FBS). HSkMC from groups 1 to 3 gradually became round in shape and gathered in clusters. These changes differed between the groups. In group 3, the HSkMC clusters were more in numbers and gathered as significantly more prominent than in the other groups under the EVOS-Microscope shown. We concluded that by manipulating the composition of the culture medium, it is possible to induce HSkMC to promote the best growth.

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Dissertations / Theses on the topic "Muscle cells"

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Leskinen, Markus. "Mast cell-mediated apoptosis of smooth muscle cells and endothelial cells." Helsinki : University of Helsinki, 2003. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/leskinen/.

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Woodhouse, Samuel. "The role of Ezh2 in adult muscle stem cell fate." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610201.

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Tomc, Lyn Kathryn. "Role of MEF2 proteins in the activation of the c-jun and MCK genes in skeletal muscle /." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0018/MQ56210.pdf.

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PESSINA, PATRIZIA. "Necdin enhances muscle reconstitution of dystrophic muscle by mesoangioblast cells." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2009. http://hdl.handle.net/10281/7594.

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Improving stem cell therapy is a major goal for the treatment of muscle diseases, where physiological muscle regeneration is progressively exhausted. Mesoangioblasts are vessel-associated stem cells that appear to be the most promising cell type for the cell therapy for muscular dystrophies because of their significant contribution to restoration of muscle structure and function in different muscular dystrophy model. Here we report that MAGE protein Necdin enhances muscle differentiation and regeneration by mesoangioblasts. Indeed, when Necdin is constitutively overexpressed, it accelerates their differentiation and fusion in vitro and it increases their efficacy to restore dystrophic phenotype of α-sarcoglycan mutant mouse. Moreover, Necdin confers a enhanced survival ability when mesoangioblasts are exposed to cytotoxic stimuli that mimic inflammatory dystrophic environment. Taken together, these data demonstrate the pivotal role of Necdin in muscle reconstitution from which we could take advantage to boost therapeutic applications of mesoangioblasts.

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Peden, Ryan Stephen Medical Sciences Faculty of Medicine UNSW. "Activation of vascular smooth muscle cells." Awarded by:University of New South Wales. School of Medical Sciences, 2006. http://handle.unsw.edu.au/1959.4/24925.

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Vascular smooth muscle cells (VSMC) in the healthy adult arterial wall are a highlydifferentiated cell type with low levels of proliferation. However, when activated these cells can undergo a phenotypic change to become proliferative, migratory and excrete higher levels of extra-cellular matrix. While this cellular change is an essential element of the adaptable vasculature, excessive proliferation of VSMC underpins the development of a number of disease states, including atherosclerosis and restenosis after balloon angioplasty. The activation of VSMC is dependent on intracellular signalling pathways broadly altering gene expression. A key feature of this process is the initial potent regulation of transcription factors such as Egr-1, c-Jun and Ets-1, which then drive further transcriptional changes resulting in phenotypic change. The aim of this thesis was to discover novel genes, particularly transcription factors, regulated early upon stimulation and to characterise their contribution to the activation of VSMC. A key stimulus for activation of VSMC is the release of fibroblast growth factor 2 (FGF-2). A microarray used to explore the effects of FGF-2 exposure demonstrated the extensive nature of transcriptional modulation. In addition, it highlighted a number of transcription factors that were not previously described in VSMC: p8, ATF-4 and SHARP-2. In particular, SHARP-2 was potently upregulated and was reconfirmed in animal models of vascular injury. The subsequent contribution these factors make to VSMC activation was also demonstrated. p8 strongly induced VSMC proliferation, while ATF-4 contributed to cytokine production and SHARP-2 potently downregulated VSMC differentiation markers. A second area that was explored related to a gene known as YRDC, which was found to be upregulated upon stimulation of VSMC. YRDC is highly conserved across almost all cellular life, however its function remains unknown. A number of novel splice variants of YRDC were discovered and demonstrated to be differentially regulated in VSMC upon stimulation. Further work to commence characterising its function showed that it interacts with key ribosomal proteins and most likely plays a role in regulating translation. The discovery of the relevance of these genes to vascular biology in addition to their transcriptional regulation makes an important contribution to increasing our understanding of the molecular mechanisms behind vascular remodelling.

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Spendiff, Sally. "Mitochondrial myopathies and muscle stem cells." Thesis, University of Newcastle Upon Tyne, 2011. http://hdl.handle.net/10443/1530.

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Mitochondrial myopathies are a group of progressive muscle disorders caused by mutations in the mitochondrial genome (mtDNA) for which there is no effective treatment. Culturing of myoblasts from patients with sporadically occurring mitochondrial diseases has suggested that mtDNA mutations may be lower or absent in muscle stem cells (satellite cells). The activation of muscle satellite cells and subsequent repair of muscle fibres may favourably shift the balance of delete to wild-type (WT) mtDNA, thereby decreasing mtDNA mutation load in affected muscle. This research has investigated muscle precursor cells from patients with mitochondrial myopathy due to sporadically occurring mtDNA deletions. This was to determine if they will benefit from attempts to “gene shift” the balance of WT and mutated mtDNA in their muscles using high intensity resistance training. Fluorescently Activated Cell Sorting (FACS) on the basis of CD56 (NCam) was used to isolate satellite cells and real time PCR to analyse them. In all eight patients investigated mtDNA deletions were detected in satellite cells at levels similar to mature muscle. In most of these patients the mtDNA deletions were lost during the culturing of their myoblasts. In some patients, however, the mutation was maintained, although there was a gradual decline in mutation load as the myoblasts headed towards differentiation. It was hypothesised that this difference between patients in the maintenance or loss of mutations in their myoblasts was attributable to an mtDNA bottleneck effect at the point of satellite cell activation. A second selection point occurred during the process of myoblast proliferation, possibly mediated by segregation of WT and delete mtDNA after cell division. Daughter cells that inherit large amounts of delete mtDNA will be unable to continue to proliferate. If efforts to “gene shift” in these patients will involve the activation of satellite cells to repair damaged muscle, it is paramount that this process does not exhaust the muscle stem cell pool. Satellite cell numbers have been determined in patients harbouring sporadically occurring mtDNA deletions, who will be considered potential beneficiaries of exercise based interventions. No significant difference was observed in satellite cell numbers when patients were compared to controls. In addition, a single patient was examined for satellite cell numbers over eleven years and no reduction in numbers was found. Given that the large majority of single deletion patients will lose their mtDNA mutation during the process of muscle regeneration and that they will not suffer from an exhaustion of the satellite cell pool, “gene shifting” remains a viable therapy in these patients. However, the mechanisms behind the process are somewhat different to what was originally hypothesised.

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Iyer, Dharini. "Generation of epicardium and epicardium-derived coronary-like smooth muscle cells from human pluripotent stem cells." Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708997.

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Izzard, Tanya. "Extracellular matrix and the cell cycle in vascular smooth muscle cells." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322616.

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Holder, Emma L. (Emma Lesley). "Gene expression in muscle tissue and cells." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=69755.

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Cellular differentiation is accompanied by the modulation of gene expression. I have compared the expression of various genes, using the slot-blot technique, in two different systems. First, the level of expression of a wide variety of genes was analyzed in the hypertrophied heart of transgenic mice expressing the polyomavirus large T-antigen gene, and compared to normal control heart. I have shown that most changes in gene expression occurred mainly during early stages of heart hypertrophy. These genes code for proteins known to play a role in signal transduction, and transcriptional and growth control. The latter stages of cardiac hypertrophy are accompanied by changes in the expression of genes that are mostly involved in stress responses. Second, we analyzed the expression of various genes in three mouse myogenic cell lines undergoing differentiation in several culture conditions. The adult (C2C12) and fetal-derived (G7 and G8) myoblast cell lines were exposed to either retinoic acid, dimethyl sulfoxide, or transforming growth factor $ beta$. These three molecules are known to have profound effects on cellular growth and differentiation. I have shown that these treatments result in significant changes in expression of a wide variety of genes. Interestingly, all three cell lines differed considerably in their pattern of gene expression. Results from the analysis of these two systems demonstrate that differentially induced morphological changes of muscle cells, result in cell type specific changes in expression of a variety of genes.

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Haddad, Mansour Emil Goerge. "GPCRs in rat primary skeletal muscle cells." Thesis, University of Nottingham, 2012. http://eprints.nottingham.ac.uk/14176/.

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GPCRs are the largest family of proteins in the human genome and a target for huge numbers of therapeutic drugs. However, the role of skeletal muscle in the action of these drugs is unclear. Given the unique importance of GPCR signalling in terms of glucose and fatty acid turnover in other tissues, it would be anticipated that GPCR identified to influence metabolism in these tissues might well be expressed in skeletal muscle. This study investigated the expression of genes encoding GPCRs in skeletal muscle and in cultured preparations thereof. In particular, this study focussed on the expression and signalling of adenosine receptors, a2-adrenoceptor, P2Y receptors and CBI cannabinoid receptors and the impact of CBI receptor modulation upon insulin signalling in rat primary skeletal muscle cells. All experiments in this work looked at GPCR expression and their signalling; with either tissues or cultured cells from rats. These experiments included: 1. Transcriptional profiling of skeletal muscle tissue in Wistar rats for GPCRs and proteins in associated signalling pathways. 2. Signalling of GPCRs (adenosine, a2A-adrenoceptor, P2y) in rat primary skeletal muscle cells. 3. Cannabinoid signalling pathways and cross-talk with insulin signalling. 4. CBI cannabinoid receptor antagonist/inverse agonist/agonist treatment of rat primary skeletal muscle cells. Expression of example members of the three major G protein coupling GPCR families was observed in rat skeletal muscle tissue. mRNA encoding Gs- (A2Aadenosine receptor, P2-adrenoceptor), Gi- (AI adenosine receptor, (l2A-adrenoceptor), and Gq-coupled (P2Y 1. P2Y2 and P2Y6 receptors) receptors were detected using gene microarray (Agilent, all ranked <10220 out of 41090). QRT-PCR (Taqman) identified (l2A-adrenoceptor and CBI cannabinoid receptor mRNA expression at low level similar across myoblasts, myotubes and skeletal muscle tissue. Functional responses to example members of the three major G protein coupling families of GPCR were also observed in rat primary skeletal muscle preparations. First, treatment of myotubes with the non-selective adenosine receptor agonist NECA elicited increases in cAMP, which were inhibited in the presence of the A2Badenosine receptorselective antagonist, PSB603. In contrast, the A2A-selective agonist, CGS21680 failed to evoke a significant cAMP elevation in myotubes. Second, neither basal nor forskolinevoked elevation of cAMP was altered in the presence of the Ar-selective agonist, SENBA. Third, the (l2-adrenoceptor agonist UK14304 inhibited forskolin-evoked cAMP levels, however, rauwolscine did not prevent this effect. Treatment with UK14304 also increased phosphorylation of ERK1/2; these responses, however, were inhibited by rauwolscine. In addition, rauwolscine in the absence of other ligands also inhibited ERK phosphorylation. Fourth, ATP and UTP, P2Y receptor agonists, elevated intracellular calcium ion levels in myoblasts. Although expression of mRNA for CBI cannabinoid receptors was detected in myoblasts, myotubes and skeletal muscle tissue, forskolin-evoked elevation of cAMP was unaltered in the presence of the CBI receptor-selective agonist ACEA or the antagonist/inverse agonist rimonabant in cultured myotubes. AICAR-stimulated AMPactivated protein kinase activity was also unaltered by ACEA. However, treatment with ACEA increased activation ofERK1I2 and p38 mitogen-activated protein kinases; these responses were significantly inhibited by rimonabant. Insulin treatment of myotubes increased the activation (phosphorylation) of AKT/protein kinase B, glycogen synthase kinase 3(1 and ~, ERK1I2 and p38 MAP kinases; however, pre-treatment with ACEA for 24 hours failed to alter these responses. In conclusion, these studies indicate expression and functional responses to select members of the three major G protein coupling families of GPCR in rat skeletal muscle preparations. These findings also provided evidence for expression of functionally active CB) cannabinoid receptors in skeletal muscle. However, they fail to support previous reports suggesting an interaction between insulin and CB) receptor signalling in these cells. The impact of CB) receptor function in skeletal muscle should be the subject of further investigation.

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Books on the topic "Muscle cells"

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Perdiguero, Eusebio, and DDW Cornelison, eds. Muscle Stem Cells. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6771-1.

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Rassier, Dilson E. Muscle biophysics: From molecules to cells. New York: Springer, 2010.

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Asakura, Atsushi, ed. Skeletal Muscle Stem Cells. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3036-5.

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A, Sassoon D., ed. Stem cells and cell signalling in skeletel myogenesis. Amsterdam: Elsevier, 2002.

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1933-, Sugi Haruo, and Gordon A. M. 1934-, eds. Muscle contraction and cell motility: Molecular and cellular aspects. Berlin: Springer-Verlag, 1992.

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Wang, Yong-Xiao, ed. Calcium Signaling In Airway Smooth Muscle Cells. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-01312-1.

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Dhoot, Gurtej Kaur. Development and differentiation of striated muscle cells. Birmingham: University of Birmingham, 1992.

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M, Carlson Bruce, ed. Growth and hyperplasia of cardiac muscle cells. London, U.K: Harwood Academic Publishers, 1991.

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D, Huizinga Jan, ed. Pacemaker activity and intercellular communication. Boca Raton: CRC Press, 1995.

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Kaba, Nubia Kristen. Effect of urea on cell volume regulation in smooth muscle cells. [s.l.]: [s.n.], 1998.

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Book chapters on the topic "Muscle cells"

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Bagshaw, Clive R. "Muscle cells." In Muscle Contraction, 21–32. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-015-6839-5_3.

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Gooch, Keith J., and Christopher J. Tennant. "Muscle Cells." In Mechanical Forces: Their Effects on Cells and Tissues, 101–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-662-03420-0_5.

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Gayford, Chris. "Muscle Contraction." In Energy and Cells, 154–65. London: Macmillan Education UK, 1986. http://dx.doi.org/10.1007/978-1-349-08159-2_10.

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Saucedo, Leslie. "Muscle." In Getting to Know Your Cells, 43–47. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-30146-9_8.

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Canale, Enrico D., Gordon R. Campbell, Joseph J. Smolich, and Julie H. Campbell. "Cardiac Muscle Cells in Culture." In Cardiac Muscle, 195–221. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-50115-9_10.

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Kuang, Shihuan, and Michael A. Rudnicki. "Muscle Stem Cells." In Cell Cycle Regulation and Differentiation in Cardiovascular and Neural Systems, 105–20. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-60327-153-0_6.

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Lynch, Gordon S., David G. Harrison, Hanjoong Jo, Charles Searles, Philippe Connes, Christopher E. Kline, C. Castagna, et al. "Stem Cells, Muscle." In Encyclopedia of Exercise Medicine in Health and Disease, 814–16. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_257.

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Stewart, Alastair G., Darren J. Fernandes, Valentina Koutsoubos, Aurora Messina, Claire E. Ravenhall, Ross Vlahos, and Kai-Feng Xu. "Airway smooth muscle cells." In Cellular Mechanisms in Airways Inflammation, 263–302. Basel: Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8476-1_10.

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Riascos-Bernal, Dario F., and Nicholas E. S. Sibinga. "Vascular Smooth Muscle Cells." In Atherosclerosis, 117–28. Hoboken, NJ: John Wiley & Sons, Inc, 2015. http://dx.doi.org/10.1002/9781118828533.ch10.

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Halayko, Andrew J., and Pawan Sharma. "Airway Smooth Muscle Cells." In Inflammation and Allergy Drug Design, 163–71. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444346688.ch12.

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Conference papers on the topic "Muscle cells"

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Sorrentino, Carmela, Giulia Gentile, Rosa D’Angiolo, Carmela Barra, Ferdinando De Stefano, Fabrizio Licitra, Emilia Sabbatino, et al. "The Role of the Androgen Receptor in Skeletal Muscle and Its Utility as a Target for Restoring Muscle Functions." In Cells 2023. Basel Switzerland: MDPI, 2023. http://dx.doi.org/10.3390/blsf2023021005.

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BLAES, N., and C. COVACHO. "PLATELET AGGREGATION INDUCED BY TUMORIGENIC ARTERIAL SMOOTH MUSCLE CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643413.

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A focal proliferation of intimal smooth muscle cells is assumed to be an early event in atherogenesis. In addition, platelets have been suggested to play a role at different steps of the disease process. Blood platelets can be aggregated by a number of tumor cells of various tissue origin. Rat arterial smooth muscle cells presenting a tumorigenic and metastatic phenotype (NBC1 and NBC2 cell lines) have been obtained in the laboratory (BLAES N. et al, Arch. Mai. Coeur Vais., 1986, 79, 55a). The aim of the present work was to assay the proaggregant abilities of these tumor cells of vascular origin. Smooth muscle cells derived from normal rat aortic media. NBC1 and NBC2 cells were spontaneously transformed in cell culture. Interactions between cells and platelets were studied in an homologous in vitro system containing 0.5 ml of PRP (300 000 platelets per ul) from heparinized rat blood and 50 ul of rat smooth muscle cells suspension. Proaggregant activity was tested for control non tumorigenic smooth muscle cells and tumorigenic cells (after 10 or 240 passages). Experiments showed that NBC2 cells elicited a proaggregant ability, weak after 10 passages but very significant after 240 passages. This effect depended on the number of cells added to the platelet suspension (it increased from 105 to 2.106 cells per 0.5 ml suspension). Aggregation profiles appeared biphasic and could be abolished by aspirin. The first reversible phase occured immediately and was reduced dose-dependently by apyrase. Hirudin was shown to affect the aggregation profile suggesting an activation of the clotting system in the NBC2-induced platelet activation. By comparison, non tumorigenic arterial smooth muscle cells showed no effect at comparable cell numbers and NBC1 cells (less metastatic than NBC2 cells) exhibited only a monophasic profile. These results suggest that NBC2 cells are able to induce platelet aggregation by mechanisms involving ADP and thrombin generation. This ability could be related to their tumorigenic and metastatic phenotype.

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Soker, Shay, Dawn Delo, Samira Neshat, and Anthony Atala. "Amniotic Fluid Derived Stem Cells for Cardiac Muscle Therapies." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192492.

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Many forms of pediatric and adult heart disease are accompanied by high morbidity and mortality, as the heart muscle has limited regenerative potential. Cell therapy has been proposed as a means to promote the regeneration of injured heart muscle. We have established lines of broad spectrum multipotent stem cells derived from primitive fetal cells present in human amniotic fluid (hAFS) cells (1). AFS cells offer several advantages: They are easy to isolate and grow (no feeder layers needed), are highly expansive including clonal growth and they can differentiate into all germ layers. In the current study, we demonstrate that AFS cells can differentiate into cardiac muscle cells and be used for cardiac tissue regeneration.

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Suzuki, YJ, L. Liu, and A. Park. "Differential Mechanisms of Apoptosis in Pulmonary Artery Smooth Muscle Cells and in Cardiac Muscle Cells." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5359.

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Ahsan, Taby, Adele M. Doyle, Garry P. Duffy, Frank Barry, and Robert M. Nerem. "Stem Cells and Vascular Regenerative Medicine." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193591.

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Vascular applications in regenerative medicine include blood vessel substitutes and vasculogenesis in ischemic or engineered tissues. For these repair processes to be successful, there is a need for a stable supply of endothelial and smooth muscle cells. For blood vessel substitutes, the immediate goal is to enable blood flow, but vasoactivity is necessary for long term success. In engineered vessels, it is thought that endothelial cells will serve as an anti-thrombogenic lumenal layer, while smooth muscle cells contribute to vessel contractility. In other clinical applications, what is needed is not a vessel substitute but the promotion of new vessel formation (vasculogenesis). A simplified account of vasculogenesis is that endothelial cells assemble to form vessel-like structures that can then be stabilized by smooth muscle cells. Overall, the need for new vasculature to transfer oxygen and nutrients is important to reperfuse not only ischemic tissue in vivo, but also dense, structurally complex engineered tissue. The impact of these vascular therapies, however, is limited in part by the low yield and inadequate in vitro proliferation potential of primary endothelial and smooth muscle cells. Thus, there is a need to address the cell sourcing issue for vascular cell-based therapies, potentially using stem cells.

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DeClerck, Y. A., R. Bock, and W. E. Laug. "PRODUCTION OF A TISSUE INHIBITOR OF METALLOPROTEINASES BY BOVINE VASCULAR CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644603.

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Tissue Inhibitor of Metalloproteinases (TIMP) plays an important role in collagen turnover in tissue due to its ability to irreversibly inhibit mammalian collagenases. We have investigated the production of such an inhibitor by various cells of bovine vessels including endothelial cells of arterial, venous and capillary origin and arterial smooth muscle cells. While large amounts of collagenase inhibitor (800 mU/106 cells/24 hr) were produced by vascular smooth muscle cells, smaller amounts were detected in* the medium conditioned by either arterial, capillary or venous endothelial cells (90, 1.7 and 1.1 mU/106 cells/24 hr respectively). An inhibitor with a Mr of 28,500 was purified from serum free medium conditioned by bovine smooth muscle cells using molecular sieve followed by heparin sepharose and carboxy-methylcellulose chromatography. It inhibited several vertebrate collagenases but was inactive against bacterial collagenase. This inhibitor was resistant to treatment with acid and heat but sensitive to trypsin and reduction alkylation. It formed with vertebrate collagenase an enzyme-inhibitor complex resistant to organomercurials or trypsin. This inhibitor, therefore, is similar to a collagenase inhibitor produced by human fibroblasts and a tissue inhibitor of metalloproteinases extracted from human amniotic fluid and rabbit bone.The production of TIMP by bovine vascular smooth muscle cells markedly increased during cell proliferation. In addition, when endothelial cells were grown on a preformed layer of smooth muscle cells, the production of TIMP was more than additive suggesting an enhancing effect of endothelial cells on vascular smooth muscle cells.These data suggest that the large amount of TIMP produced by vascular muscle cells may be responsible for the accumulation of collagen characteristically observed in conjunction with smooth muscle cells hyperplasia in atherosclerotic plaques.

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Cassino, Theresa R., Masaho Okada, Lauren Drowley, Johnny Huard, and Philip R. LeDuc. "Mechanical Stimulation Improves Muscle-Derived Stem Cell Transplantation for Cardiac Repair." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192941.

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Muscle-derived stem cells (MDSCs) have been successfully transplanted into both skeletal (1) and cardiac muscle (2) of dystrophin-deficient (mdx) mice, and show potential for improving cardiac and skeletal dysfunction in diseases like Duchenne muscular dystrophy (DMD). Our previous study explored the regeneration of dystrophin-expressing myocytes following MDSC transplantation into environments with distinct blood flow and chemical/mechanical stimulation attributes. After MDSC transplantation within left ventricular myocardium and gastrocnemius (GN) muscles of the same mdx mice, significantly more dystrophin-positive fibers were found within the myocardium than in the GN. We hypothesized that the differences in mechanical loading of the two environments influenced the transplantation and explored whether using MDSCs exposed to mechanical stimulation prior to transplantation could improve transplantation. Our study shows increased engraftment into the heart and GN muscle for cells pretreated with mechanical stretch for 24 hours. This increase was significant for transplantation into the heart. These studies have implications in a variety of applications including mechanotransduction, stem cell biology, and Duchenne muscular dystrophy.

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Hsiao, Amy Y., Teru Okitsu, Hiroaki Onoe, Mahiro Kiyosawa, Hiroki Teramae, Shintaroh Iwanaga, Shigenori Miura, Tomohiko Kazama, Taro Matsumoto, and Shoji Takeuchi. "Self-assembly of cell springs using smooth muscle-like cells differentiated from multipotent cells." In 2013 IEEE 26th International Conference on Micro Electro Mechanical Systems (MEMS). IEEE, 2013. http://dx.doi.org/10.1109/memsys.2013.6474179.

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Tsvankin, Vadim, Dmitry Belchenko, Devon Scott, and Wei Tan. "Anisotropic Strain Effects on Vascular Smooth Muscle Cell Physiology." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176284.

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Biological development is a complex and highly-regulated process, a significant part of which is controlled by mechanostimulus, or the strain imparted on a cell by its environment. Mechanostimulus is important for stem cell differentiation, from cytoskeletal assembly to cell-cell and cell-matrix adhesion [1]. The mechanics of cells and tissues play a critical role in organisms, under both physiological and pathological conditions; abnormal mechanotransduction — the mechanism by which cells sense and respond to strain — has been implicated in a wide range of clinical pathologies [2,3].

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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.

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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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Reports on the topic "Muscle 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.

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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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C. Uy, Genevieve, Raymond L. Rosales, and Satish Khadilkar. Myopathies in Clinical Care: A Focus on Treatable Causes. Progress in Neurobiology, February 2024. http://dx.doi.org/10.60124/j.pneuro.2024.10.01.

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Myopathies present a wide range of clinical symptoms that affect the skeletal muscles, including weakness, fatigue, and pain. While acquired myopathies receive significant attention due to the availability of treatment options, it is important to note that some inherited myopathies can also be effectively managed. These myopathies can be classified based on their underlying causes, such as infectious agents, autoimmune disorders leading to muscle inflammation, granulomatous inflammation, metabolic abnormalities within the muscle cells, skeletal muscle channel dysfunctions, prolonged ICU stay, and inherited conditions such as Duchenne muscular dystrophy. In this review, we initially present a clinical approach to neuromuscular diseases and subsequently place specific emphasis on myopathies, particularly to those that have treatment options available.

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Robson, Richard M., and Ted W. Huiatt. Properties of Synemin, a Protein Important in Maintaining the Structural Integrity of Muscle Cells. Ames (Iowa): Iowa State University, January 2004. http://dx.doi.org/10.31274/ans_air-180814-956.

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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.

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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.

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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.

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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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Zhang, Zhibing, Qian Huang, Yonghong Man, Wei Li, Qi Zhou, Shuo Yuan, Yi Tian Yap, et al. Inactivation of Cops5 in smooth muscle cells causes abnormal reproductive hormone homeostasis and development in mice. Peeref, June 2023. http://dx.doi.org/10.54985/peeref.2306p3662949.

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Tran, Emily, Jasmine J. Park, Nandini N. Kulkarni, and Vinay S. Gundlapalli. Left Facial Primary Leiomyosarcoma Misdiagnosed as Atypical Fibroxanthoma and Immunochemical Markers Relevant to Diagnosis: A Case Report. Science Repository, February 2024. http://dx.doi.org/10.31487/j.ajscr.2023.04.03.

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Abstract:

Soft tissue sarcomas are relatively rare neoplasms of mesenchymal origin that generally make up less than 2% of all adult malignant neoplasms. Atypical fibroxanthoma is a benign soft tissue tumor often confused with malignant variants of similar tumors such as leiomyosarcoma due to similar staining markers and cell morphology. We report a case of a 70-year-old caucasian male who initially presented with a 2 cm exophytic left facial lesion that was misdiagnosed as atypical fibroxanthoma upon biopsy. The patient underwent a wide local excision of the growing 11 cm mass and immediate reconstruction with a cervicofacial flap and full thickness skin graft. Pathological analysis of the specimen revealed the final diagnosis as confirmed primary leiomyosarcoma. Both the patient’s biopsy report and the surgical pathology report revealed similar negative findings (desmin, cytokeratin AE1/AE3, p63, SOX10) as well as similar positive findings (smooth muscle actin and CD68). Critical distinctions that led to a change in diagnosis from atypical fibroxanthoma to leiomyosarcoma emerged during the final pathological analysis, which revealed more widespread positive staining for smooth muscle actin and muscle-specific actin throughout the surgical specimen along with detailed cell and nucleus morphology of atypical spindle cells in the dermis and subcutis. This valuable information was not available during the initial biopsy when the lesion was smaller. It is possible that earlier diagnosis of primary leiomyosarcoma could have resulted in advanced pre-operative treatment and excision of the facial lesion, preventing involvement of surrounding areas such as the patient’s left eye, ear, and facial nerve.

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Kanatous, Shane B. Proof of Concept to Isolate and Culture Primary Muscle Cells from Northern Elephant Seals to Study the Mechanisms that Maintain Aerobic Metabolism Under the Hypoxic Conditions of Breath-hold Diving. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada573541.

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Kanatous, Shane B. Proof of Concept to Isolate and Culture Primary Muscle Cells from Northern Elephant Seals to Study the Mechanisms that Maintain Aerobic Metabolism Under the Hypoxic Conditions of Breath-hold Diving. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada597966.

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Kanatous, Shane B. Proof of Concept to Isolate and Culture Primary Muscle Cells from Northern Elephant Seals to Study the Mechanisms that Maintain Aerobic Metabolism Under the Hypoxic Conditions of Breath-Hold Diving. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada617630.

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