Relevant bibliographies by topics / Human skeletal muscle myoblast

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Academic literature on the topic 'Human skeletal muscle myoblast'

Author: Grafiati
Published: 14 March 2023

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Journal articles on the topic "Human skeletal muscle myoblast"

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Jurdana, Mihaela, Maja Cemazar, Katarina Pegan, and Tomaz Mars. "Effect of ionizing radiation on human skeletal muscle precursor cells." Radiology and Oncology 47, no. 4 (December 1, 2013): 376–81. http://dx.doi.org/10.2478/raon-2013-0058.

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Abstract Background. Long term effects of different doses of ionizing radiation on human skeletal muscle myoblast proliferation, cytokine signalling and stress response capacity were studied in primary cell cultures. Materials and methods. Human skeletal muscle myoblasts obtained from muscle biopsies were cultured and irradiated with a Darpac 2000 X-ray unit at doses of 4, 6 and 8 Gy. Acute effects of radiation were studied by interleukin - 6 (IL-6) release and stress response detected by the heat shock protein (HSP) level, while long term effects were followed by proliferation capacity and cell death. Results. Compared with non-irradiated control and cells treated with inhibitor of cell proliferation Ara C, myoblast proliferation decreased 72 h post-irradiation, this effect was more pronounced with increasing doses. Post-irradiation myoblast survival determined by measurement of released LDH enzyme activity revealed increased activity after exposure to irradiation. The acute response of myoblasts to lower doses of irradiation (4 and 6 Gy) was decreased secretion of constitutive IL-6. Higher doses of irradiation triggered a stress response in myoblasts, determined by increased levels of stress markers (HSPs 27 and 70). Conclusions. Our results show that myoblasts are sensitive to irradiation in terms of their proliferation capacity and capacity to secret IL-6. Since myoblast proliferation and differentiation are a key stage in muscle regeneration, this effect of irradiation needs to be taken in account, particularly in certain clinical conditions.
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Quinn, LeBris S., Barbara G. Anderson, and Stephen R. Plymate. "Muscle-specific overexpression of the type 1 IGF receptor results in myoblast-independent muscle hypertrophy via PI3K, and not calcineurin, signaling." American Journal of Physiology-Endocrinology and Metabolism 293, no. 6 (December 2007): E1538—E1551. http://dx.doi.org/10.1152/ajpendo.00160.2007.

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The insulin-like growth factors (IGF-I and IGF-II), working through the type 1 IGF receptor (IGF-1R), are key mediators of skeletal muscle fiber growth and hypertrophy. These processes are largely dependent on stimulation of proliferation and differentiation of muscle precursor cells, termed myoblasts. It has not been rigorously determined whether the IGFs can also mediate skeletal muscle hypertrophy in a myoblast-independent fashion. Similarly, although the phosphatidylinositol 3-kinase (PI3K) and calcineurin signaling pathways have been implicated in skeletal muscle hypertrophy, these pathways are also involved in skeletal myoblast differentiation. To determine whether the IGFs can stimulate skeletal muscle hypertrophy in a myoblast-independent fashion, we developed and validated a retroviral expression vector that mediated overexpression of the human IGF-1R in rat L6 skeletal myotubes (immature muscle fibers), but not in myoblasts. L6 myotubes transduced with this vector accumulated significantly higher amounts of myofibrillar proteins, in a ligand- and receptor-dependent manner, than controls and demonstrated significantly increased rates of protein synthesis. Stimulation of myotube hypertrophy was independent of myoblast contributions, inasmuch as these cultures did not exhibit increased levels of myoblast proliferation or differentiation. Experiments with PI3K and calcineurin inhibitors indicated that myoblast-independent myotube hypertrophy was mediated by PI3K, but not calcineurin, signaling. This study demonstrates that IGF can mediate skeletal muscle hypertrophy in a myoblast-independent fashion and suggests that muscle-specific overexpression of the IGF-1R or stimulation of its signaling pathways could be used to develop strategies to ameliorate muscle wasting without stimulating proliferative pathways leading to carcinogenesis or other pathological sequelae.
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Hicks, Michael R., Thanh V. Cao, David H. Campbell, and Paul R. Standley. "Mechanical strain applied to human fibroblasts differentially regulates skeletal myoblast differentiation." Journal of Applied Physiology 113, no. 3 (August 1, 2012): 465–72. http://dx.doi.org/10.1152/japplphysiol.01545.2011.

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Cyclic short-duration stretches (CSDS) such as those resulting from repetitive motion strain increase the risk of musculoskeletal injury. Myofascial release is a common technique used by clinicians that applies an acyclic long-duration stretch (ALDS) to muscle fascia to repair injury. When subjected to mechanical strain, fibroblasts within muscle fascia secrete IL-6, which has been shown to induce myoblast differentiation, essential for muscle repair. We hypothesize that fibroblasts subjected to ALDS following CSDS induce myoblast differentiation through IL-6. Fibroblast conditioned media and fibroblast-myoblast cocultures were used to test fibroblasts' ability to induce myoblast differentiation. The coculture system applies strain to fibroblasts only but still allows for diffusion of potential differentiation mediators to unstrained myoblasts on coverslips. To determine the role of IL-6, we utilized myoblast unicultures ± IL-6 (0–100 ng/ml) and cocultures ± α-IL-6 (0–200 μg/ml). Untreated uniculture myoblasts served as a negative control. After 96 h, coverslips ( n = 6–21) were microscopically analyzed and quantified by blinded observer for differentiation endpoints: myotubes per square millimeter (>3 nuclei/cell), nuclei/myotube, and fusion efficiency (%nuclei within myotubes). The presence of fibroblasts and fibroblast conditioned media significantly enhanced myotube number ( P < 0.05). However, in coculture, CSDS applied to fibroblasts did not reproduce this effect. ALDS following CSDS increased myotube number by 78% and fusion efficiency by 96% vs. CSDS alone ( P < 0.05). Fibroblasts in coculture increase IL-6 secretion; however, IL-6 secretion did not correlate with enhanced differentiation among strain groups. Exogenous IL-6 in myoblast uniculture failed to induce differentiation. However, α-IL-6 attenuated differentiation in all coculture groups ( P < 0.05). Fibroblasts secrete soluble mediators that have profound effects on several measures of myoblast differentiation. Specific biophysical strain patterns modify these outcomes, and suggest that myofascial release after repetitive strain increases myoblast differentiation and thus may improve muscle repair in vivo. Neutralization of IL-6 in coculture significantly reduced differentiation, suggesting fibroblast-IL-6 is necessary but not sufficient in this process.
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Lee, Nicole K. L., Jarrod P. J. Skinner, Jeffrey D. Zajac, and Helen E. MacLean. "Ornithine decarboxylase is upregulated by the androgen receptor in skeletal muscle and regulates myoblast proliferation." American Journal of Physiology-Endocrinology and Metabolism 301, no. 1 (July 2011): E172—E179. http://dx.doi.org/10.1152/ajpendo.00094.2011.

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The aim of this study is to determine if the Odc1 gene, which encodes ornithine decarboxylase (ODC), the rate-limiting enzyme in polyamine biosynthesis, is directly regulated by the androgen receptor (AR) in skeletal muscle myoblasts and if Odc1 regulates myoblast proliferation and differentiation. We previously showed that expression of Odc1 is decreased in muscle from AR knockout male mice. In this study, we show in vivo that Odc1 expression is also decreased >60% in muscle from male muscle-specific AR knockout mice. In normal muscle homeostasis, Odc1 expression is regulated by age and sex, reflecting testosterone levels, as muscle of adult male mice expresses high levels of Odc1 compared with age-matched females and younger males. In vitro, expression of Odc1 is 10- and 1.5-fold higher in proliferating mouse C2C12 and human skeletal muscle myoblasts, respectively, than in differentiated myotubes. Dihydrotestosterone increases Odc1 levels 2.7- and 1.6-fold in skeletal muscle cell myoblasts after 12 and 24 h of treatment, respectively. Inhibition of ODC activity in C2C12 myoblasts by α-difluoromethylornithine decreases myoblast number by 40% and 66% following 48 and 72 h of treatment, respectively. In contrast, overexpression of Odc1 in C2C12 myoblasts results in a 27% increase in cell number vs. control when cells are grown under differentiation conditions for 96 h. This prolonged proliferation is associated with delayed differentiation, with reduced expression of the differentiation markers myogenin and Myf6 in Odc1-overexpressing cells. In conclusion, androgens act via the AR to upregulate Odc1 in skeletal muscle myoblasts, and Odc1 promotes myoblast proliferation and delays differentiation.
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Rauen, Melanie, Dandan Hao, Aline Müller, Eva Mückter, Leo Cornelius Bollheimer, and Mahtab Nourbakhsh. "Free Fatty Acid Species Differentially Modulate the Inflammatory Gene Response in Primary Human Skeletal Myoblasts." Biology 10, no. 12 (December 12, 2021): 1318. http://dx.doi.org/10.3390/biology10121318.

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Age-related loss of skeletal muscle is associated with obesity and inflammation. In animal models, intramuscular fat deposits compromise muscle integrity; however, the relevant fat components that mediate muscular inflammation are not known. Previously, we hypothesized that free fatty acids (FFAs) may directly induce inflammatory gene expression in skeletal muscle cells of obese rats. Here, we examined this hypothesis in primary human skeletal myoblasts (SkMs) using multiplex expression analysis of 39 inflammatory proteins in response to different FFA species. Multiplex mRNA quantification confirmed that the IL6, IL1RA, IL4, LIF, CXCL8, CXCL1, CXCL12 and CCL2 genes were differentially regulated by saturated and unsaturated C16 or C18 FFAs. Fluorescence staining revealed that only saturated C16 and C18 strongly interfere with myoblast replication independent of desmin expression, mitochondrial abundance and oxidative activity. Furthermore, we addressed the possible implications of 71 human receptor tyrosine kinases (RTKs) in FFA-mediated effects. Phosphorylated EphB6 and TNK2 were associated with impaired myoblast replication by saturated C16 and C18 FFAs. Our data suggest that abundant FFA species in human skeletal muscle tissue may play a decisive role in the progression of sarcopenic obesity by affecting inflammatory signals or myoblast replication.
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Chen, Xiaoping, Zebin Mao, Shuhong Liu, Hong Liu, Xuan Wang, Haitao Wu, Yan Wu, et al. "Dedifferentiation of Adult Human Myoblasts Induced by Ciliary Neurotrophic Factor In Vitro." Molecular Biology of the Cell 16, no. 7 (July 2005): 3140–51. http://dx.doi.org/10.1091/mbc.e05-03-0218.

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Ciliary neurotrophic factor (CNTF) is primarily known for its important cellular effects within the nervous system. However, recent studies indicate that its receptor can be highly expressed in denervated skeletal muscle. Here, we investigated the direct effect of CNTF on skeletal myoblasts of adult human. Surprisingly, we found that CNTF induced the myogenic lineage-committed myoblasts at a clonal level to dedifferentiate into multipotent progenitor cells—they not only could proliferate for over 20 passages with the expression absence of myogenic specific factors Myf5 and MyoD, but they were also capable of differentiating into new phenotypes, mainly neurons, glial cells, smooth muscle cells, and adipocytes. These “progenitor cells” retained their myogenic memory and were capable of redifferentiating into myotubes. Furthermore, CNTF could activate the p44/p42 MAPK and down-regulate the expression of myogenic regulatory factors (MRFs). Finally, PD98059, a specific inhibitor of p44/p42 MAPK pathway, was able to abolish the effects of CNTF on both myoblast fate and MRF expression. Our results demonstrate the myogenic lineage-committed human myoblasts can dedifferentiate at a clonal level and CNTF is a novel regulator of skeletal myoblast dedifferentiation via p44/p42 MAPK pathway.
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Kagawa, Yuki, and Masahiro Kino-oka. "An in silico prediction tool for the expansion culture of human skeletal muscle myoblasts." Royal Society Open Science 3, no. 10 (October 2016): 160500. http://dx.doi.org/10.1098/rsos.160500.

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Regenerative therapy using autologous skeletal myoblasts requires a large number of cells to be prepared for high-level secretion of cytokines and chemokines to induce good regeneration of damaged regions. However, myoblast expansion culture is hindered by a reduction in growth rate owing to cellular quiescence and differentiation, therefore optimization is required. We have developed a kinetic computational model describing skeletal myoblast proliferation and differentiation, which can be used as a prediction tool for the expansion process. In the model, myoblasts migrate, divide, quiesce and differentiate as observed during in vitro culture. We assumed cell differentiation initiates following cell–cell attachment for a defined time period. The model parameter values were estimated by fitting to several predetermined experimental datasets. Using an additional experimental dataset, we confirmed validity of the developed model. We then executed simulations using the developed model under several culture conditions and quantitatively predicted that non-uniform cell seeding had adverse effects on the expansion culture, mainly by reducing the existing ratio of proliferative cells. The proposed model is expected to be useful for predicting myoblast behaviours and in designing efficient expansion culture conditions for these cells.
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Broholm, Christa, Matthew J. Laye, Claus Brandt, Radhika Vadalasetty, Henriette Pilegaard, Bente Klarlund Pedersen, and Camilla Scheele. "LIF is a contraction-induced myokine stimulating human myocyte proliferation." Journal of Applied Physiology 111, no. 1 (July 2011): 251–59. http://dx.doi.org/10.1152/japplphysiol.01399.2010.

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The cytokine leukemia inhibitory factor (LIF) is expressed by skeletal muscle and induces proliferation of myoblasts. We hypothesized that LIF is a contraction-induced myokine functioning in an autocrine fashion to activate gene regulation of human muscle satellite cell proliferation. Skeletal muscle LIF expression, regulation, and action were examined in two models: 1) young men performing a bout of heavy resistance exercise of the quadriceps muscle and 2) cultured primary human satellite cells. Resistance exercise induced a ninefold increase in LIF mRNA content in skeletal muscle, but LIF was not detectable in plasma of the subjects. However, electrically stimulated cultured human myotubes produced and secreted LIF, suggesting that LIF is a myokine with local effects. The well established exercise-induced signaling molecules PI3K, Akt, and mTor contributed to the regulation of LIF in cultured human myotubes as chemical inhibition of PI3K and mTor and siRNA knockdown of Akt1 were independently sufficient to downregulate LIF. Human myoblast proliferation was increased by recombinant exogenous LIF and decreased by siRNA knockdown of the endogenous LIF receptor. Finally, the transcription factors JunB and c-Myc, which promote myoblast proliferation, were induced by LIF in cultured human myotubes. Indeed, both JunB and c-Myc were also increased in skeletal muscle following resistance exercise. Our data suggest that LIF is a contraction-induced myokine, potentially acting in an autocrine or paracrine fashion to promote satellite cell proliferation.
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Zhang, Haifeng, Junfei Wen, Anne Bigot, Jiacheng Chen, Renjie Shang, Vincent Mouly, and Pengpeng Bi. "Human myotube formation is determined by MyoD–Myomixer/Myomaker axis." Science Advances 6, no. 51 (December 2020): eabc4062. http://dx.doi.org/10.1126/sciadv.abc4062.

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Myoblast fusion is essential for formations of myofibers, the basic cellular and functional units of skeletal muscles. Recent genetic studies in mice identified two long-sought membrane proteins, Myomaker and Myomixer, which cooperatively drive myoblast fusion. It is unknown whether and how human muscles, with myofibers of tremendously larger size, use this mechanism to achieve multinucleations. Here, we report an interesting fusion model of human myoblasts where Myomaker is sufficient to induce low-grade fusion, while Myomixer boosts its efficiency to generate giant myotubes. By CRISPR mutagenesis and biochemical assays, we identified MyoD as the key molecular switch of fusion that is required and sufficient to initiate Myomixer and Myomaker expression. Mechanistically, we defined the E-box motifs on promoters of Myomixer and Myomaker by which MyoD induces their expression for multinucleations of human muscle cells. Together, our study uncovered the key molecular apparatus and the transcriptional control mechanism underlying human myoblast fusion.
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Badu-Mensah, Agnes, Paola Valinski, Hemant Parsaud, James J. Hickman, and Xiufang Guo. "Hyperglycemia Negatively Affects IPSC-Derived Myoblast Proliferation and Skeletal Muscle Regeneration and Function." Cells 11, no. 22 (November 18, 2022): 3674. http://dx.doi.org/10.3390/cells11223674.

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Diabetic myopathy is a co-morbidity diagnosed in most diabetes mellitus patients, yet its pathogenesis is still understudied, which hinders the development of effective therapies. This project aimed to investigate the effect of hyperglycemia on human myoblast physiology, devoid of other complicating factors, by utilizing human myoblasts derived from induced pluripotent stem cells (iPSCs), in a defined in vitro system. IPSC-derived myoblasts were expanded under three glucose conditions: low (5 mM), medium (17.5 mM) or high (25 mM). While hyperglycemic myoblasts demonstrated upregulation of Glut4 relative to the euglycemic control, myoblast proliferation demonstrated a glucose dose-dependent impedance. Further cellular analysis revealed a retarded cell cycle progression trapped at the S phase and G2/M phase and an impaired mitochondrial function in hyperglycemic myoblasts. Terminal differentiation of these hyperglycemic myoblasts resulted in significantly hypertrophic and highly branched myotubes with disturbed myosin heavy chain arrangement. Lastly, functional assessment of these myofibers derived from hyperglycemic myoblasts demonstrated comparatively increased fatigability. Collectively, the hyperglycemic myoblasts demonstrated deficient muscle regeneration capability and functionality, which falls in line with the sarcopenia symptoms observed in diabetic myopathy patients. This human-based iPSC-derived skeletal muscle hyperglycemic model provides a valuable platform for mechanistic investigation of diabetic myopathy and therapeutic development.
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Dissertations / Theses on the topic "Human skeletal muscle myoblast"

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Cesare, Maria Michela. "ANTIOXIDANT PROTECTION OF TUSCAN TOMATO PEEL POLYPHENOLS IN A CELLULAR MODEL OF SARCOPENIA." Doctoral thesis, Università di Siena, 2022. http://hdl.handle.net/11365/1186467.

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Background: Tomato by-products contain a great variety of biologically active substances and might represent a significant source of natural antioxidant supplements of the human diet. The preliminary studies were carried out on two ancient Tuscan tomato peel varieties, Rosso di Pitigliano (RED) and Perina a Punta della Valtiberina (PER), obtained by growing plants in normal (-Ctr) or in drought stress conditions (-Ds) present in the Regional Bank of the Germplasm of Tuscany. The variety chosen was Rosso di Pitigliano for the best beneficial effects on vascular related dysfunction. The preliminary aim of the thesis was to create an in vitro model of sarcopenia, induced by dexamethasone using human skeletal muscle myoblasts (HSMM). Sarcopenia is a disease that affects athletes who practice endurance physical activity. In these, an excessive exercise increased reactive oxygen species (ROS) levels, that, if not properly balanced by the endogenous antioxidant system, can compromise the performance of the athletes. Furthermore, in controlling muscle mass an important role is played by serine/threonine kinase and a decreased activation of the Akt-mTOR pathway by sarcopenia contributes to protein synthesis reduction. The main aim of study was to evaluate the cytoprotective properties of tomato peel polyphenols from Rosso di Pitigliano, cultivated in normal or in drought stress conditions, on an in vitro model of sarcopenia. Methods: The antioxidant activity and total polyphenol content (TPC) were measured. The identification of bioactive compounds of several tomato peel was performed by HPLC. HUVEC were pre-treated with different TPC of RED-Ctr or RED-Ds, then stressed with H2O2. Cell viability, ROS production and CAT, SOD and GPx activities were evaluated. Permeation of antioxidant molecules contained in RED across excised rat intestine was also studied. The phenol content of both peel extracts was investigated by Ultra High-Performance Liquid Chromatography (UHPLC) analyses coupled to electrospray ionization high-resolution mass spectrometry (ESI-HR-MS). Morphological sarcopenia induction and treatment with tomato peels extracts were performed. The effector’s expression was evaluated by Real-Time PCR reactions after setting the optimal reaction conditions. Myotubes-differentiated were examined for the expression of Myosin heavy chain-2 (MYH2), Troponin T type 1 (TNNT) and Myogenin (MYOG). Furthermore, Protein kinase B (AKT1) and Forkhead Box O1 (FOXO1) mRNA expression was evaluated. Superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities were performed. Results: RED-Ds tomato peel extract possessed higher TPC than compared to RED-Ctr (361.32 ± 7.204 mg vs. 152.46 ± 1.568 mg GAE/100 g fresh weight). All extracts were non-cytotoxic. Two hours pre-treatment with 5 μg GAE/mL from RED-Ctr or RED-Ds showed protection from H2O2-induced oxidative stress and significantly reduced ROS production raising SOD and CAT activity (* p < 0.05 and ** p < 0.005 vs. H2O2, respectively). The permeation of antioxidant molecules contained in RED-Ctr or RED-Ds across excised rat intestine was high with non-significant difference between the two RED types (41.9 ± 9.6% vs. 26.6 ± 7.8%). Phenolic acids increase in the stressed tomato peel extract, while flavonoids decrease. Data shows a protective effect of 5μg GAE/ml TPC of Red DS extract on the sarcopenia. FOXO1 mRNA expression was significantly increased when cells treated with Dexa, but this expression was significantly decreased in Red Ds+Dexa (p <0.0001 vs control). AKT1 mRNA expression was increased in myotubes pre-treated with Red Ds and Dexa (p <0.0001 vs control). Myosin heavy chain 2 (MYH2), troponin T (TNNT1), miogenin (MYOG), were express in myotubes differentiated (p<0.001 vs Control). DEXA significantly reduces the antioxidant enzyme activity of SOD compared with untreated cells (p < 0.0001), but RED-Ds increased SOD activity. Conclusions: The final results show that the tomato peel extract of Rosso di Pitigliano, grown in conditions of drought stress, represents a good source of bioactive molecules, which protects the endothelium from oxidative stress even at low concentrations. Furthermore, the polyphenols from tomato peel show a cytoprotective effect in the in vitro model of sarcopenia without the use of vehicles for absorption.
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Wilson, Alyssa A. "Exploring the Role of Myoblast Fusion in Skeletal Muscle Development and Homeostasis." University of Cincinnati / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1504781294099666.

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Tallon, Mark J. "Carnosine metabolism in human skeletal muscle." Thesis, University of Chichester, 2005. http://eprints.chi.ac.uk/843/.

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Aviss, Kathryn Jane. "A synthetic biodegradable oriented scaffold for skeletal muscle tissue engineering." Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/a-synthetic-biodegradable-oriented-scaffold-for-skeletal-muscle-tissue-engineering(baed422d-940f-4489-b180-0bed3f4fc6ee).html.

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The aim of this project was to create a novel biodegradable, synthetic scaffold that will provide the correct topographical cues for myoblast alignment and efficient differentiation into myotubes. Skeletal muscle repair after major surgery or serious burns is often overlooked leading to poor healing and consequent loss of power in movements of affected limbs. In order to overcome this problem a tissue engineered construct could be utilised as a grafting patch to encourage further regeneration and enhance possible power to the limb. Using a biodegradable polymer can provide structural support until the tissue is established, and will be excreted by the body's natural processes as it degrades. A synthetic polymer is desirable as it can reduce the risk of immunogenic responses thus reduce risk of graft rejection. For successful in vitro growth of skeletal muscle, the cells must be encouraged to arrange themselves into parallel arrays in order for efficient fusion and consequent contraction. By incorporating the correct topographical cues into the scaffold to promote contact guidance for cellular alignment this can be achieved. Electrospinning is a reliable technique which yields highly reproducible aligned fibres from the micro- to the nanoscale. This project focuses upon creating and characterising the electrospun scaffold, checking biocompatibility with myoblasts by monitoring the topography, residual solvent within the scaffold, the mechanical properties of the scaffold, and a brief investigation into the degradation profile of the electrospun fibres. The immunogenicity of the scaffold was investigated by monitoring cytokine release from macrophages. Myoblast morphology was monitored, as was the efficiency of the cells to differentiate and their potential to become contractile myofibres. Cellular adhesion to the scaffold was also looked into by measuring the expression of integrins during early and late adhesion and on substrates with different topographies. It was found that the electrospun scaffold did not contain a significant amount of residual solvent, and macrophages were not activated any more than on tissue culture plastic. Myoblasts responded to the topography of the aligned fibres by aligning along the length of the fibres, showing elongation and bi-axial cytoskeletal arrangement after just 30 minutes culture on the aligned fibres. This elongation prompted fusion and differentiation of the myoblasts to occur faster than cells which were not exposed to the aligned topography, and this global alignment was maintained in long term culture.
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Leng, Xinyan. "Roles of proteasome, arachidonic acid, and oxytocin in bovine myoblast proliferation and differentiation." Diss., Virginia Tech, 2018. http://hdl.handle.net/10919/82707.

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The overall objective of this dissertation project was to identify factors and mechanisms that control bovine myoblast proliferation, differentiation, and fusion. Three studies were conducted during this project. The objective of the first study was to determine the effect of oxytocin (OXT) on myoblast proliferation, differentiation and fusion. Treating primary bovine myoblasts in culture with 10 nM and 100 nM OXT for 24 h increased their proliferation rate by 7% (P < 0.05) and 10% (P < 0.05), respectively. Treating bovine myoblasts with either concentration of OXT for 48 h had no effect on their differentiation and fusion, as indicated by no changes in mRNA expression of selected myoblast differentiation markers and fusion index. The objective of the second study was to determine the effects of arachidonic acid (AA) and its major metabolites prostaglandin E2 (PGE2), PGF2a, and PGI2 on myoblast proliferation, differentiation and fusion. Treating myoblasts with 10 μM AA, 1 μM PGE2, 1 μM PGF2α, and 1 μM PGI2 for 24 h each increased the number of proliferating cells by 13%, 24%, 16%, and 16%, respectively, compared to the control (P < 0.05). At the same concentrations, AA, PGE2, and PGF2a stimulated myoblast differentiation and PGE2 improved myoblast fusion (P < 0.05). Treating myoblasts with AA and the cyclooxygenase (COX)-1 and COX-2 inhibitor indomethacin or the COX-2-specific inhibitor NS-398 reversed the stimulatory effect of AA on myoblast proliferation (P < 0.05). The objective of the third study was to determine the role of the proteasome in bovine myoblast differentiation and fusion. It was found that the proteasome activity increased (P < 0.05) during myoblast differentiation and fusion. Adding 5 μM lactacystin, a specific inhibitor of the proteasome, to the differentiation medium nearly completely blocked myoblast differentiation and fusion. Inhibitor of DNA-binding 1 (ID1) is known to inhibit myoblast differentiation and to be degraded by the proteasome in some cells. Both ID1 protein and mRNA expression were found to decrease during myoblast differentiation and fusion, and the decrease in ID1 protein but not ID1 mRNA was reversed (P < 0.05) by treating the cells with lactacystin. In summary, this project reveals that OXT and AA are stimulators of bovine myoblast proliferation and that AA is a stimulator of bovine myoblast differentiation. This project also indicates that the proteasome plays a positive role in bovine myoblast differentiation and fusion, and that it does so perhaps by reducing the accumulation of the ID1 protein.
Ph. D.
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Renna, L. V. "MOLECULAR BASIS OF SKELETAL MUSCLE ATROPHY IN MYOTONIC DYSTROPHY." Doctoral thesis, Università degli Studi di Milano, 2015. http://hdl.handle.net/2434/333083.

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Myotonic dystrophy (DM) is an autosomal dominant multisystemic disorder characterized by a variety of multisystemic features including myotonia, muscular dystrophy, cardiac dysfunctions, cataracts and insulin-resistance. DM1 is caused by an expanded (CTG)n in the 3’ UTR of the DMPK gene, while DM2 is caused by the expansion of a (CCTG)n repeat in the intron 1 of the CNBP gene. In both forms, the mutant transcripts accumulate in nuclear foci altering the function of some alternative splicing regulators which are necessary for the physiological processing of mRNAs. However, the downstream pathways by which these RNA binding proteins cause skeletal muscle alteration are not well understood. For these reasons the aim of my PhD project was to analyze the molecular mechanisms behind DM skeletal muscle atrophy. In the first part of my PhD we have performed different studies to better define the molecular pathogenesis of DM. In particular, we have analysed the histopathological and biomolecular features of skeletal muscle biopsies from a cohort of DM1 and DM2 patients presenting different phenotypes. The results indicated that the splicing and muscle pathological alterations observed are related to the clinical DM1 and DM2 phenotype and that CUGBP1 seems to play a role only in DM1, confirming that the molecular pathomechanism of DM is more complex than the one actually suggested. These data were confirmed by the analysis of two different biopsies obtained from 5 DM2 patients that showed that morphological alterations evolve more rapidly over time than the molecular changes suggesting that the molecular mechanisms that drive to skeletal muscle atrophy are still unclear and that these features cannot be explained only by spliceopathy. For all these reasons we decided to analyse DM satellite cells activity in vitro. Satellite cells are the muscle fibre precursor cells and our data indicated that both DM1 and DM2 skeletal muscle cells have lower proliferative capability than control myoblasts. Moreover, the premature proliferative growth arrest observed in DM cells appears to be caused by an overexpression of p16 in DM1 muscle cells, while DM2 muscle cells stop dividing with telomeres shorter than controls, suggesting that in these cells the signaling involved in premature senescence depend on a telomere-driven pathway. Finally, we decided to analyze the insulin pathway which is involved in the regulation of skeletal muscle atrophy. Our data have shown that DM1 and DM2 cells exhibit a lower glucose uptake and a lower proteins activation after 10 nM insulin stimulation when compared to controls suggesting that also this pathway could play a role in the molecular mechanisms that drive skeletal muscle atrophy in DM patients. In conclusion, we have shown that the molecular mechanisms behind skeletal muscle atrophy in DM1 and DM2 patients are more complicated than that previously suggested and further analysis are necessary to understand why skeletal muscle atrophy affect mainly type 1 fibres in DM1 patients, while on the contrary it affects selectively type 2 fibres in DM2 patients.
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Adamo, Kristi Bree. "Proglycogen and macroglycogen in human skeletal muscle." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ31807.pdf.

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Saxton, John Michael. "Exercise-induced damage to human skeletal muscle." Thesis, University of Wolverhampton, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385185.

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Hurel, Steven J. "Insulin action in cultured human skeletal muscle." Thesis, University of Newcastle Upon Tyne, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363891.

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Ruiz, Carlos Ariel. "Transcriptional and Post-Transcriptional Regulation of Synaptic Acetylcholinesterase in Skeletal Muscle." Scholarly Repository, 2009. http://scholarlyrepository.miami.edu/oa_dissertations/370.

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myotubesProper muscle function depends upon the fine tuning of the different molecular components of the neuromuscular junction (NMJ). Synaptic acetylcholinesterase (AChE) is responsible for rapidly terminating neurotransmission. Neuroscientists in the field have elucidated many aspects of synaptic AChE structure, function, and localization during the last 75 years. Nevertheless, how the enzyme is regulated and targeted to the NMJ is not completely understood. In skeletal muscle the synaptic AChE form derives from two separate genes encoding the catalytic and the collagenic tail (ColQ) subunits respectively. ColQ-AChE expression is regulated by muscle activity; however, how this regulation takes place remains poorly understood. We found that over or down-regulation of ColQ is sufficient to change the levels of AChE activity by promoting assembly of higher order oligomeric forms including the collagen-tailed forms. Furthermore, when peptides containing the Proline Rich Attachment Domain (PRAD), the region of ColQ that interacts with the AChE, are fed to muscle cells or cell lines expressing AChE, they are taken up by the cells and retrogradely transported to the endoplasmic reticulum (ER)/Golgi network where they induce assembly of newly synthesize AChE into tetramers. This results in an increase, as a consequence, in total cell associated AChE activity and active tetramer secretion, making synthetic PRAD peptides potential candidates for the treatment of organophosphate pesticides and nerve gas poisoning. To study the developmental regulation of ColQ-AChE we determined the levels of ColQ and ColQ mRNA in primary quail muscle cells in culture and as a function of muscle activity. Surprisingly, we found dissociation between transcription and translation of ColQ from its assembly into ColQ-AChE indicating the importance of posttranslational controls in the regulation of AChE folding and assembly. Furthermore, we found that the vast majority of the ColQ molecules in QMCs are not assembled into ColQ-AChE, suggesting that they can have alternative function(s). Finally, we found that the levels of ER molecular chaperones calnexin, calreticulin, and particularly protein disulfide isomerase are regulated by muscle activity and they correlate with the levels of ColQ-AChE. More importantly, our results suggest that newly synthesized proteins compete for chaperone assistance during the folding process.
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Books on the topic "Human skeletal muscle myoblast"

1

Kinesiology: The skeletal system and muscle function. 2nd ed. St. Louis, Mo: Mosby/Elsevier, 2011.

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A, Stone Judith, ed. Atlas of the skeletal muscles. Dubuque, Iowa: Wm. C. Brown, 1989.

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Child, R. B. Exercise and free radical induced damage to human skeletal muscle. Wolverhampton: University of Wolverhampton, 1997.

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A, Stone Judith, ed. Atlas of skeletal muscles. 3rd ed. Boston: McGraw-Hill, 2000.

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Stone, Robert J. Atlas of skeletal muscles. 6th ed. Boston: McGraw-Hill Higher Education, 2009.

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A, Stone Judith, ed. Atlas of skeletal muscles. 6th ed. Boston: McGraw-Hill Higher Education, 2009.

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Stone, Robert J. Atlas of skeletal muscles. 2nd ed. Dubuque, IA: Wm. C. Brown Publishers, 1997.

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Stone, Robert J. Atlas of skeletal muscles. 6th ed. Boston: McGraw-Hill Higher Education, 2009.

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Kadyan, Mamta. The capillary supply of human skeletal muscle in health and disease. St. Catharines, Ont: Brock University, Faculty of Applied Health Sciences, 2006.

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Kadyan, Mamta. The capillary supply of human skeletal muscle in health and disease. St. Catharines, Ont: Brock University, Faculty of Applied Health Sciences, 2006.

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Book chapters on the topic "Human skeletal muscle myoblast"

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Ham, Richard G., Judy A. St. Clair, and Sarah D. Meyer. "Improved Media for Rapid Clonal Growth of Normal Human Skeletal Muscle Satellite Cells." In Myoblast Transfer Therapy, 193–99. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5865-7_21.

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Carpenter, Stirling. "Regeneration of Skeletal Muscle Fibers after Necrosis." In Myoblast Transfer Therapy, 13–15. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5865-7_3.

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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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van der Ven, Peter F. M. "Skeletal Muscle." In Human Cell Culture, 65–101. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/0-306-46870-0_5.

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Malatesta, Manuela, Marzia Giagnacovo, Rosanna Cardani, Giovanni Meola, and Carlo Pellicciari. "Human Myoblasts from Skeletal Muscle Biopsies: In Vitro Culture Preparations for Morphological and Cytochemical Analyses at Light and Electron Microscopy." In Stem Cells and Aging, 67–79. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-317-6_6.

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Ernst, Linda M., and Patrick Shannon. "Skeletal Muscle." In Color Atlas of Human Fetal and Neonatal Histology, 367–74. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-11425-1_33.

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Windhorst, U., and W. F. H. M. Mommaerts. "Physiology of Skeletal Muscle." In Comprehensive Human Physiology, 911–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-60946-6_46.

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Miranda, A. F., T. Mongini, E. Bonilla, A. D. Miller, and W. E. Wright. "Myogenic Conversion of Human Non-Muscle Cells for the Diagnosis and Therapy of Neuromuscular Diseases." In Myoblast Transfer Therapy, 205–10. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5865-7_23.

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Langlois, Stéphanie, and Kyle N. Cowan. "Regulation of Skeletal Muscle Myoblast Differentiation and Proliferation by Pannexins." In Advances in Experimental Medicine and Biology, 57–73. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/5584_2016_53.

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Yamada, Hiroshi, and Eiichi Tanaka. "Active Stress Models of Cardiac Muscle, Smooth Muscle and Skeletal Muscle." In Human Biomechanics and Injury Prevention, 161–66. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-66967-8_21.

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Conference papers on the topic "Human skeletal muscle myoblast"

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Mason, Andrew K., Ryan A. Koppes, Douglas M. Swank, and David T. Corr. "Mechanical and Electrical Stimulation Induces Calcium-Sensitive Mechanical Properties of Myoblast Derived Engineered Fibers." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14646.

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Skeletal muscle loss, through injuries, myopathies, and interventional medicine, presents major challenges in physiological function and clinical interventions [1]. Autologous tissue transplantation necessitates tissue loss from the donor site, and autologous grafts do not attain the strength of the original tissue. Exogenous tissue grafting faces similar strength issues, as well as the added challenge of immunorejection [2,3]. In vitro skeletal muscle tissue engineering holds promise for addressing these issues. However, these tissues have not yet shown proper dynamic response when compared to physiological muscle [2]. Mechanical and electrical stimulation have shown promise in improving construct properties [4], but mainly limited to 2D and scaffold-based constructs.
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Burmeister and Lehman. "Force Relaxation In Human Skeletal Muscle." 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.1992.589829.

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Burmeister, E. E., and S. L. Lehman. "Force relaxation in human skeletal muscle." In 1992 14th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.5761946.

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"A NEW METABOLISM MODEL FOR HUMAN SKELETAL MUSCLE." In International Conference on Biomedical Electronics and Devices. SciTePress - Science and and Technology Publications, 2008. http://dx.doi.org/10.5220/0001051202380243.

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Williams, K., M. Mullen, T. LaRocca, K. Hamilton, C. Bahney, and N. Ehrhart. "Myoblast Exosome Production, Function, and MiRNA Cargo Is Altered by Mechanical Stimulation: Therapeutic Implications for Skeletal Muscle Regeneration." In Abstracts of the 6th World Veterinary Orthopedic Congress. Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1758266.

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Pagliara, Valentina, Rosarita Nasso, Antonio Ascione, Mariorosario Masullo, and Rosaria Arcone. "Myostatin and plasticity of skeletal muscle tissue." In Journal of Human Sport and Exercise - 2019 - Summer Conferences of Sports Science. Universidad de Alicante, 2019. http://dx.doi.org/10.14198/jhse.2019.14.proc5.12.

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Ito, Akira, Hirokazu Akiyama, Yasunori Yamamoto, Yoshinori Kawabe, and Masamichi Kamihira. "Skeletal muscle tissue engineering using functional magnetite nanoparticles." In 2009 International Symposium on Micro-NanoMechatronics and Human Science (MHS). IEEE, 2009. http://dx.doi.org/10.1109/mhs.2009.5351986.

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Nagamine, Kuniaki, Shingo otani, Mai Takeda, Makoto Kanzaki, and Matsuhiko Nishizawa. "Hydrogel-supported skeletal muscle cell-based bioassay system." In 2011 International Symposium on Micro-NanoMechatronics and Human Science (MHS). IEEE, 2011. http://dx.doi.org/10.1109/mhs.2011.6102223.

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Calve, Sarah, and Hans-Georg Simon. "The Mechanical and Biochemical Environment Controls Cellular Differentiation During Muscle Regeneration." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53767.

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Urodele amphibians like the newt, are able to completely regenerate lost organs and appendages without scarring. Differentiated tissues are considered a reservoir for uncommitted blastema cells that participate in the regeneration of the lost structure. To determine the influence of the extracellular matrix (ECM) on the recruitment of progenitor cells from the skeletal muscle, we immunohistochemically mapped the limb in 3D and found that a transitional ECM rich in hyaluronic acid (HA), tenascin-C (TN) and fibronectin (FN) is dynamically expressed during the early stages of regeneration [1]. Functional in vitro testing of different ECM components on primary muscle cells revealed that HA and TN support myoblast migration, inhibit differentiation and enhance the fragmentation of multinucleate myotubes and production of viable mononucleate myoblasts, cellular behaviors necessary for blastema formation [1]. In contrast, myoblasts plated on matrices that mimic ECM around differentiated muscle (FN, Matrigel and laminin) induced both proliferation and fusion.
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GOLLNICK, PHILIP, V. EDGERTON, and BENGT SALTIN. "Human skeletal muscle responses to spaceflight and possible countermeasures." In Space Programs and Technologies Conference. Reston, Virigina: American Institute of Aeronautics and Astronautics, 1990. http://dx.doi.org/10.2514/6.1990-3809.

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Reports on the topic "Human skeletal muscle myoblast"

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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.

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: 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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