Дисертації з теми "Skeletal muscle satellite cells"
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Blackwell, Danielle. "The role of Talpid3 in skeletal muscle satellite cells and skeletal muscle regeneration." Thesis, University of East Anglia, 2017. https://ueaeprints.uea.ac.uk/66948/.
Повний текст джерелаThompson, Steven Howard 1958. "The effect of trenbolone on skeletal muscle satellite cells." Thesis, The University of Arizona, 1987. http://hdl.handle.net/10150/276633.
Повний текст джерелаRathbone, Christopher R. "Mechanisms regulating skeletal muscle satellite cell cycle progression." Diss., Columbia, Mo. : University of Missouri-Columbia, 2006. http://hdl.handle.net/10355/5866.
Повний текст джерелаThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. "December 2006" Includes bibliographical references.
Collins, Charlotte Anne. "An investigation of the stem cell potential of skeletal muscle satellite cells." Thesis, University College London (University of London), 2004. http://discovery.ucl.ac.uk/1446604/.
Повний текст джерелаMorisi, F. "AUTOPHAGY AND SKELETAL MUSCLE WASTING: EFFECTS ON SATELLITE CELLS POPULATION." Doctoral thesis, Università degli Studi di Milano, 2016. http://hdl.handle.net/2434/347854.
Повний текст джерелаJudson, Robert Neil. "The role of Yes-associated protein (YAP) in skeletal muscle satellite cells and myofibres." Thesis, University of Aberdeen, 2012. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=189444.
Повний текст джерелаLindström, Mona. "Satellite cells in human skeletal muscle : molecular identification quantification and function." Doctoral thesis, Umeå universitet, Anatomi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-29817.
Повний текст джерелаBrandt, Amanda Maverick. "Regulation of satellite cells by extrinsic factors during recovery from exercise in horses." Diss., Virginia Tech, 2019. http://hdl.handle.net/10919/89089.
Повний текст джерелаDoctor of Philosophy
The horse is well-known as an athletic creature and is often used in amateur and professional athletic events. Despite its popularity as a pastime in low and high-stakes competition, certain facets directly related to performance during exercise remain relatively unstudied. One crucial component of recovery from exercise is the intrinsic ability of skeletal muscle to repair exercise-induced muscle damage. This is accomplished largely through the incorporation of new nuclei, which originate from a position orbiting the muscle, hence the name satellite cells. This cell is essential to muscle regeneration from injury as often demonstrated in rodent models, but the role of satellite cells in recovery from exercise remains elusive in all species, but particularly so in horses. For instance, whether satellite cells only contribute nuclei after exercise to stimulate gains in muscle mass or whether they may also play a role in the process of adaptation to exercise is not clearly understood. The purpose of my work was to define the response of satellite cells to hepatocyte growth factor, a factor present in skeletal muscle during exercise that is already well-studied in rodent models. Additionally, to determine whether the addition of the non-essential amino acid, citrulline, would influence satellite cells and nutrient reserves after a session of submaximal exercise. I found that hepatocyte growth factor does not influence satellite cells isolated from horses in the same way it influences those from rodents, nor through the same mechanisms. Additionally, I found that satellite cells were not stimulated after a session of submaximal exercise, but a factor involved in regulation of genetic expression that is associated with satellite cells and skeletal muscle was downregulated with the addition of citrulline. Together, these results suggest that satellite cells may behave like other species in some ways, such as some responses to hepatocyte growth factor and the lack of response to a submaximal bout of exercise, but that there is still much to be learned in order to begin to influence management and training decisions as regards skeletal muscle recovery.
Mofarrahi, Mahroo. "Regulation of skeletal muscle satellite cell proliferation by NADPH oxidase." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111521.
Повний текст джерелаCorrera, Rosa Maria. "Pw1/Peg3 regulates skeletal muscle growth and satellite cell self-renewal." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066339.
Повний текст джерелаPw1/Peg3 is a parentally imprinted gene expressed from the paternal allele. It is expressed in all adult progenitor/stem cell populations examined to date including muscle satellite cells. We examined the impact of loss-of-function of Pw1/Peg3 in skeletal muscle, a tissue that greatly contributes to body mass. We found that constitutive loss of Pw1/Peg3 results in reduced muscle mass resulting from a decrease in muscle fiber number. The reduced fiber number is present at birth. Mice lacking both the paternal and maternal alleles display a lower fiber number as compared to mice carrying the paternal deletion, suggesting that the maternal allele is functional during prenatal development. Hybrid analyses (C57BL6J and Cast/Ei) of muscle tissue reveal a bi-allelic expression of Pw1/Peg3 around 10%. Pw1/Peg3 is strongly up-regulated in response to muscle injury. Using the constitutive Pw1/Peg3 knock out mouse, we observed that satellite cells display a reduced self-renewal capacity following muscle injury. Pw1/Peg3 is expressed in satellite cells as well as a subset of muscle interstitial cells (PICs). To determine the specific role of Pw1/Peg3 in satellite cells, we crossed our conditional Pw1/Peg3 allele with the Pax7-CreER line. Interestingly, these mice displayed a more pronounced phenotype of impaired regeneration revealing a clear and direct role for Pw1/Peg3 in satellite cells. Taken together, our data show that Pw1/Peg3 plays a role during fetal development in the determination of muscle fiber number that is gene-dosage dependent and plays a specific role in muscle satellite cell self-renewal
Mohd, Imran Kamalliawati. "Up-regulation of Hedgehog signalling in satellite cells and skeletal muscle regeneration." Thesis, University of Sheffield, 2019. http://etheses.whiterose.ac.uk/22909/.
Повний текст джерелаScaramozza, Annarita <1982>. "The regulation of Satellite Cells during skeletal muscle regeneration and neuromuscular disease." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2012. http://amsdottorato.unibo.it/4258/1/Scaramozza_Annarita_tesi.pdf.
Повний текст джерелаScaramozza, Annarita <1982>. "The regulation of Satellite Cells during skeletal muscle regeneration and neuromuscular disease." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2012. http://amsdottorato.unibo.it/4258/.
Повний текст джерелаLi, Grace T. Y. "C/EBPbeta is a Negative Regulator of Skeletal Muscle Differentiation." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/20110.
Повний текст джерелаFlann, Kyle. "The Role of Satellite Cells in Skeletal Muscle Revascularization: A Potential Factor in Muscular Dystrophy." Diss., The University of Arizona, 2010. http://hdl.handle.net/10150/195799.
Повний текст джерелаPunch, Vincent. "Genome-Wide Studies on the Molecular Functions of Pax7 in Adult Muscle Satellite Cells." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/20050.
Повний текст джерелаLibergoli, Michela. "CD90 marks satellite cells into two subpopulations with distinct dynamics of activation and proliferation." Doctoral thesis, Università degli studi di Trento, 2021. http://hdl.handle.net/11572/323156.
Повний текст джерелаKosek, David J. "Aging differences in mechanisms of human skeletal muscle hypertrophy." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2009r/kosek.pdf.
Повний текст джерелаTan, Kah Yong. "Stem Cell-Based Strategies to Enhance Muscle Regeneration through Extrinsic and Intrinsic Regulators." Thesis, Harvard University, 2011. http://dissertations.umi.com/gsas.harvard:10009.
Повний текст джерелаSchirwis, Elija. "Skeletal muscle growth and maintenance depend on BMP signaling." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066057.
Повний текст джерелаGrowth factors of the TGF-β superfamily play a role in all stages of prenatal myogenesis and govern adult muscle maintenance. Bone morphogenetic proteins (BMPs) are members of the TGF-β subfamily and are key signals that regulate embryonic and fetal muscle development. This work investigates the role of BMP signaling in muscle stem cells of the postnatal muscle, the satellite cells. I showed that BMPs regulate satellite cell-dependent growth of postnatal fibers and the generation of the satellite cell pool. After inhibition of BMP signaling, I observed that myogenic precursor cells become quiescent and fail to progress towards differentiation, whereas treatment with BMP4 on its own is sufficient to reactivate the myogenic program. BMP signaling also affects the size of the muscle in a satellite cell-independent manner. I found that BMPs provide a hypertrophic signal and protect from denervation-induced muscle atrophy. Under such condition, BMP signaling inhibits the expression of the E3 ubiquitin ligase Fbxo30. I further analyzed the interaction between myostatin and BMP signaling. Myostatin is another member of TGF-β superfamily, but myostatin and BMPs bind to different receptors for signaling. Large muscles in absence of myostatin entirely depend on the presence of BMP signaling. Denervation of muscle in myostatin mutant mice causes a strong muscle atrophy, which is aggravated by the inhibition of BMP signaling. Therefore, the BMP pathway is a fundamental hypertrophic signal in adult muscle and is dominant over myostatin signaling
Sorensen, Jacob R. "Repair and Adaptation of Aged Skeletal Muscle to Nonpathological Muscle Damage: The Influence of Macrophage Polarization." BYU ScholarsArchive, 2018. https://scholarsarchive.byu.edu/etd/7691.
Повний текст джерелаHelsel, Patricia J. "The effects of furosemide on equine skeletal muscle satellite cell myogenesis and metabolism in vitro." Thesis, Virginia Tech, 2020. http://hdl.handle.net/10919/96608.
Повний текст джерелаMaster of Science
Thoroughbred racehorses often bleed from the lungs as a result of high-intensity exercise. This condition can oftentimes be fatal depending on severity. Furosemide, is used in the industry to reduce blood pressure within the lungs during racing to prevent bleeding. Furosemide, a diuretic given four hours prior to a race, causes a horse to excrete up to 4% of its body weight. This effect of furosemide decreases the weight a horse must carry during a race, thus allowing the horse to run faster. Therefore, deemed as a performance enhancing drug due to its effects on the kidney, to our knowledge, no research has been conducted on what effects furosemide might have on muscle generation. High-intensity exercise causes massive muscle damage and therefore must be repaired to prepare for the next bout of exercise. Muscle generation is called myogenesis. Stem cells, or satellite cells, that lie within the muscle become activated, recognizing the need for muscle repair. Satellite cells divide, increasing in cell number and then fuse together, forming new muscle fibers. Satellite cells undergo different types of metabolism depending on their state of development. For example, proliferating cells require glucose for energy, while cells fusing together forming myotubes, require oxidative metabolism for long-lasting energy. Therefore, the objective of this study was to determine the effects furosemide might have on muscle formation and metabolism. The excess furosemide dose (100 µg/mL) decreased cell proliferation. The expression of regulatory factors responsible for forming myotubes at different stages of muscle development are decreased when cells were treated with the defined excess furosemide dose. Furosemide decreased the ability of satellite cells to generate myotubes. Glycogen concentration was also decreased as a result of excess furosemide treatment. Gene expression of enzymes involved in glycogen synthesis were increased from treatment with our excess furosemide dose. No effect of furosemide was seen on glycolysis, whereas oxidative metabolism suffered as a result of treatment with excess furosemide. In conclusion, furosemide does indeed affect muscle generation and oxidative metabolism.
Matsumura, Marc Shigeru. "The Role of Growth Arrest Specific 6 and Axl Signaling in Skeletal Muscle Regeneration." BYU ScholarsArchive, 2019. https://scholarsarchive.byu.edu/etd/9112.
Повний текст джерелаCalderbank, Emma Ruth. "Identification of genes involved in the quiescence and early activation of skeletal muscle satellite cells." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.502606.
Повний текст джерелаRossi, CA. "Skeletal muscle reconstruction through in vivo tissue engineering and characterization of satellite cell heterogeneity." Doctoral thesis, Università degli studi di Padova, 2010. http://hdl.handle.net/11577/3426563.
Повний текст джерелаUna delle sfide più intriganti nell’ambito dell’ingegneria tissutale è la ricostruzione completa di un organo. Questa dipende dal trovare la combinazione più efficace tra cellule staminali e uno scaffold biocompatibile, in grado di fornire supporto per la proliferazione e la migrazione cellulare, oltre ad una struttura fisica. Durante i miei studi per il dottorato di ricerca mi sono concentrato specificamente nella ricostruzione del muscolo in seguito ad una consistente rimozione di tessuto, e ho disegnato e sviluppato un protocollo sperimentale sia per l’impianto di cellule precursori muscolari (MPCs) che di cellule satelliti (SCs) attraverso un idrogel a base di acido ialuronico iniettabile e fotopolimerizzabile in situ. Impiantando muscoli tibialis anterioris (TA), parzialmente ablati, di topi C57BL/6J con SCs isolate a fresco e GFP-positive, inserite in idrogel, ho potuto documentare un consistente recupero di massa muscolare, se paragonato a TAs che avevano ricevuto idrogel+MPCs o il solo idrogel. Inoltre le SCs isolate a fresco e inserite in idrogel hanno portato ad un recupero funzionale, monitorato attraverso misurazione della forza contrattile. Questo recupero è stato associato alla generazione sia di un network neurale che vascolare e alla ricostituzione di una nicchia di SCs funzionale. Questo lavoro costituisce la prima realizzazione di un approccio di ingegneria tissutale in vivo, con le potenzialità per superare le limitazioni incontrate in precedenza nell’ingegnerizzazione del tessuto muscolare. In seguito a questi risultati mi sono focalizzato nella caratterizzazione di una sottopopolazione di SCs, con elevata capacità proliferativa e di migrazione nel muscolo ricevente, nonché in grado di promuovere una efficace rigenerazione in seguito a danno. Le SCs sono state inizialmente considerate cellule staminali unipotenti, in grado cioé di dare origine ad un unico fenotipo specializzato. In seguito è stato dimostrato in topo come anche il differenziamento in senso alternativo verso le pathways osteogenica e adipogenica fosse possibile. Anche se si conviene che la popolazione delle SCs sia la maggiore, e probabilmente l’unica fonte di mionuclei per il muscolo, è verosimile che le cellule satelliti non siano tutte cellule staminali multipotenti, in quanto evidenze di diversità all’interno del compartimento miogenico sono state descritte sia in vitro che in vivo. Nel mio studio, attraverso l’isolamento di singole fibre da muscolo flexor digitorum brevis (FDB) di ratto, ho potuto identificare e caratterizzare clonalmente due principali sottopopolazioni di SCs: i cloni a bassa proliferazione (LPC), presenti in proporzione maggiore (~75%), e i cloni ad alta proliferazione (HPC), presenti invece in minor quantità (~25%). I LPC generano spontaneamente miotubi mentre i HPC differenziano in adipociti, con la proprietà di skippare il programma adipogenico se messi in co-coltura con LPC. LPC e HPC differiscono anche per il potenziale di membrana (ΔΨm), il bilancio dell’ATP e la generazione di specie reattive dell’ossigeno (ROS), mettendo in evidenza diversità nel metabolismo che precedono il differenziamento. Inoltre l’eterogeneità delle SCs è mantenuta anche in vivo. Posso così concludere che il pool delle SCs sembra comprendere due popolazioni cellulari distinte, anche se non irreversibilmente determinate, distinguibili in base a notevoli differenze riguardo a parametri biologici basali, come proliferazione, metabolismo e differenziamento.
Sidique, Idris L. "Evaluation of skeletal muscle satellite cell activity in rodent models depicting muscle hypertrophy and atrophy." Thesis, University of Nottingham, 2013. http://eprints.nottingham.ac.uk/13899/.
Повний текст джерелаLuk, Hui Ying. "Effect of the Resistance Exercise-Induced Hormonal Changes on Satellite Cell Myogenic State." Thesis, University of North Texas, 2018. https://digital.library.unt.edu/ark:/67531/metadc1157528/.
Повний текст джерелаFan, Huitao [Verfasser]. "Epigenetic and molecular mechanisms underlying gene expression in porcine skeletal muscle and satellite cells / Huitao Fan." Bonn : Universitäts- und Landesbibliothek Bonn, 2012. http://d-nb.info/1043055800/34.
Повний текст джерелаRepele, Andrea. "Differentiation potential and metabolic analysis of satellite cells and amniotic fluid stem cells." Doctoral thesis, Università degli studi di Padova, 2012. http://hdl.handle.net/11577/3422458.
Повний текст джерелаIl nostro gruppo ha recentemente caratterizzato due distinte popolazioni di cellule satelliti, classificate come cloni a bassa proliferazione (LPC) e ad alta proliferazione (HPC), che si differenziano in termini di proliferazione, potenziale rigenerativo e metabolismo mitocondriale. Nel mio lavoro di dottorato, abbiamo valutato e caratterizzato la loro biologia cellulare con particolare attenzione a quelle differenze intrinseche presenti anche prima della loro clonazione. Infatti, ambo le tipologie clonali possono essere distinte mediante il potenziale di membrana mitocondriale (ΔΨm) subito dopo l’isolamento dalla fibra. Questo dato è in accordo con lo stato ossido riduttivo mitocondriale misurato tramite NAD+/NADH e la quantificazione della produzione di CO2. Questi risultati sono responsabili delle differenze metaboliche e possono essere spiegati dalla diversa espressione dell’enzima glicolitico Pfkfb3. Inoltre la concentrazione mitocondriale del Ca2+ e la sensibilità all’apoptosi sono modificate così come la dimensione della rete mitocondriale. In conclusione, siamo stati in grado di determinare quale clone rappresenta la cellula staminale all’interno della popolazione di cellule satelliti. Queste nuove osservazioni sperimentali rivelano caratteristiche fisiologiche della biologia delle popolazioni delle cellule satelliti prima e dopo la clonazione, mettendo in luce un’eterogeneità intrinseca della cellula satellite. Nella seconda parte della mia tesi abbiamo esplorato la possibilità che le cellule satelliti possano, se opportunamente stimolate, trans-differenziarsi in cellule muscolari lisce. Il sistema nervoso enterico normalmente interagisce con le cellule muscolari per controllare l’attività peristaltica e secretoria della parete intestinale. L’incompleta colonizzazione dell’intestino da parte delle cellule della cresta neurale provoca la malattia di Hirschsprung, caratterizzata da aganglionosi del colon distale. Le neurosfere (NLBs), precursori enterici in grado di auto-rinnovarsi, possono generare neuroni e glia; essere isolate dall’intestino di topi, ratti e umani e sono in grado di colonizzare l'intestino dopo il trapianto. Il nostro obiettivo è di capire la relazione tra i precursori di cellule satelliti (MPCs) e NLBs utilizzando un modello in vitro di co-coltura: questo sarà utile in prospettiva di un approccio di ingegneria tissutale per la rigenerazione intestinale e muscolo scheletrico. I nostri dati hanno evidenziato che NLBs, in presenza di MPCs, sono in grado di formare nuovi miotubi. L’uso di terreni di coltura miogenici ha evidenziato un notevole aumento della differenziazione in senso muscolare, promuovendo la formazione di striature ed aumentando l’espressione di desmina. Dall’altra parte, l’utilizzo di terreni di coltura neurogenici ha mostrato un fenotipo simil neurale. Come prospettive future, dobbiamo comprendere ulteriormente la relazione tra MPCs e NLBs e se le sinapsi sono coinvolte in questo processo; si deve verificare se un loro utilizzo su polimeri biocompatibili ne possa influenzare il comportamento, ed infine è necessaria una conferma dei suddetti dati tramite un’analisi di differenziazione in vivo in muscolo scheletrico e liscio. Nella terza ed ultima fase del mio lavoro, ci siamo focalizzati ad esplorare la possibilità che cellule non-muscolari possano, se opportunamente stimolate, differenziare in senso muscolare liscio. Il nostro obiettivo è stato quello di ottenere cellule muscolari lisce (SMCs) partendo da cellule staminali del fluido amniotico umano (hAFSC). hAFSC sono state trasdotte utilizzando un virus codificante per ZsGreen sotto il promotore αSMA. SMhAFSC così ottenute hanno evidenziate un alto livello d’espressione dei geni del muscolo liscio (come αSMA, desmina, calponina e smoothelin). Queste caratteristiche sono state confermate da molteplici analisi: di immunofluorescenza, dimostrando la positività a marcatori specifici per il muscolo liscio; microscopia a trasmissione elettronica (TEM), dove si verificava l’aumento della presenza di filamenti intermedi, di corpi densi e depositi di glicogeno, modello simile rispetto alle SMCs. Analisi in timelapse di SMhAFSC hanno dimostrato che queste possiedono un potenziale contrattile superiore rispetto hAFSC e studi su singola cellula hanno evidenziato la presenza di canali calcio voltaggio-dipendenti attivati da potassio solamente su SMhAFSC. In conclusione, siamo stati in grado di generare di cellule muscolari lisce funzionali da un precursore nonmuscolare ed in secondo luogo il processo di trasduzione può rappresentare un valido strumento per distinguere e selezionare differenti popolazioni. Questa fase può eventualmente superare il ben noto problema dell’espansione di progenitori di cellule muscolari lisce, rendendo queste cellule suscettibili per approcci d’ingegneria tessutale.
Chen, Ying. "Regulation of protein metabolism in skeletal muscle of low-birth-weight neonatal pigs." Diss., Virginia Tech, 2017. http://hdl.handle.net/10919/88511.
Повний текст джерелаPHD
Latil, Mathilde. "Conditions de survie des cellules souches du muscle squelettique à des conditions extrêmes d'hypoxie : caractérisation phénotypique et fonctionnelle des sous populations de cellules pour optimiser la régénération tissulaire et les thérapies cellulaires." Thesis, Paris Est, 2013. http://www.theses.fr/2013PEST0065.
Повний текст джерелаA major issue in stem cell biology for basic and clinical research is the accessibility to stem cells from healthy or diseased individuals, and the maintenance of their potency for experimentation, therapeutic drug screens, or transplantations. Here we report conditions for the isolation of viable and functional skeletal myogenic cells from human up to 17 days, and mouse up to 14 days post mortem, significantly beyond previous reports. Muscle stem cells were enriched in post mortem tissue suggesting a selective survival advantage compared to other cell types. Transplantations of 4 day post mortem mouse muscle and haematopoietic stem cells regenerated tissues robustly. Cellular quiescence contributes to this muscle stem cell viability where cells adopt a reversible dormant state characterised by reduced metabolic activity, a prolonged lag phase before the first cell division, and a transcriptional status less primed for commitment. Further, we show that the stress response of stem cells to the post mortem environment is NF-κB-independent, and that post mortem muscle stem cells are characterised by elevated levels of ROS, higher mitochondrial DNA content, and lower activity of super oxide dismutases, yet they do not display changes in redox levels. Finally, severe hypoxia, or anoxia is critical for maintaining stem cell viability and robust regenerative capacity. Ces découvertes ont des implications majeures pour des études fondamentales et cliniques sur des cellules souches et ils peuvent aussi être prolongés(étendus) à d'autres systèmes de cellule souche de normal et des patients de malade (comme un exemple que nous avons aussi montré que des cellules souches hematopoietic survivent pendant une période prolongée(étendue) après la mort dans des mouchoirs en papier(des tissus) et restent fonctionnelles in vivo)
Kocamis, Hakan. "Functional profiles of growth related genes during embryogenesis and postnatal development of chicken and mouse skeletal muscle." Morgantown, W. Va. : [West Virginia University Libraries], 2001. http://etd.wvu.edu/templates/showETD.cfm?recnum=2026.
Повний текст джерелаTitle from document title page. Document formatted into pages; contains ix, 109 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 88-104).
Papaefthymiou, Aikaterini. "Role of the Srf transcription factor in adult muscle stem cells." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB120/document.
Повний текст джерелаThe adult skeletal muscle is a high plastic tissue as it adapts its size upon overload and it is capable of regeneration upon muscle lesion. The skeletal muscle is composed of a specialized syncytium, the myofiber, which is the functional unit of the muscle and a small population of myogenic progenitors, residing adjacent to the myofibers, termed as satellite cells (SCs). SCs are the muscle-specific stem cells which endow the skeletal muscle with its remarkable capacity to repair and to maintain homeostasis during muscle turnover. In resting adult muscles, SCs are quiescent but they activate upon exposure to stimuli. The activated SCs (myoblasts) proliferate extensively and subsequently differentiate and fuse between them or pre-existing myofibers, a series of cellular events called myogenesis. In parallel to the myogenesis, a reserve population of SCs escapes the myogenic program and self-renews to replenish the SC pool. The current project aims to further characterize the signalling pathways involved in SC functions during muscle regeneration and compensatory hypertrophy (CH). Srf is a muscle-enriched transcription factor with Srf-target genes implicated in cell proliferation, differentiation (sarcomeric proteins), adhesion, migration and cellular cytoskeleton. Studies in C2C12 mouse myogenic cell line showed that Srf loss prevent the myoblast proliferation and differentiation by down-regulating the expression of the myogenic determinant MyoD gene. We used a genetic murine model for adult SC-specific Srf-loss in order to conduct in vivo and ex vivo studies for the Srf role in SCs. Compensatory hypertrophy and regeneration are the two means by which SCs were recruited. We show that loss of Srf in SCs affects the regeneration process and the CH suggesting the Srf role in the SC fate. Srf-depleted SCs display probably no defect in their proliferation and differentiation but reduced capacity in motility and fusion. Transcriptomic analysis revealed altered actin cytoskeleton and signalling. Srf-depleted SCs show reduced actin expression and altered actin cytoskeleton. Rescue of actin expression in Srf-depleted SCs partially restored the cytoskeleton organization and the fusion process. Interestingly by actin overexpression only the heterotypic/asymmetric fusion was established but not the homotypic/symmetric fusion. Therefore actin overexpression restored the hypertrophic growth in the CH (in vivo model of heterotypic fusion) but failed to do so in the regeneration (in vivo model of homotypic fusion). This study contributed to the in vivo investigation of the Srf mechanistic role in adult SCs and underlined the importance of actin cytoskeleton maintenance in the fusion of myogenic cells
Van, Niekerk Gustavus. "The effects of low level laser therapy on satellite cells." Thesis, Stellenbosch : University of Stellenbosch, 2009. http://hdl.handle.net/10019.1/4074.
Повний текст джерелаENGLISH ABSTRACT: Although muscle tissue demonstrates a remarkable capacity for regeneration following injury, this process is slow and often accompanied by the formation of scar tissue and a subsequent decrease in contractile capacity following regeneration. Treatment options are few and mostly supportive in nature. This regeneration process involves muscle stem cells (satellite cells) which ultimately give rise to the regenerated muscle. The contentious field of low level laser therapy (LLLT) has made remarkable claims in facilitating wound healing in soft tissue injuries of various types. Yet, the mechanism(s) invoked in these beneficial effects are poorly understood. We have investigated the effects of LLLT using a 638 nm laser on satellite cells in culture and in-vivo. Using an array of techniques we have measured, amongst other things, metabolic responses to laser irradiation, signaling pathways activated/altered and antioxidant status. In response to laser irradiation satellite cells in culture showed an increase in MTT values (a measure of metabolic activity) and a decrease in antioxidant status (measured using the ORAC assay). In addition laser irradiation also altered the expression and phosphorylation state of several signaling pathways, including Akt and STAT-3. Following on from this the effects of laser irradiation on satellite cells in-vivo was assessed in a rat model of contusion injury. No significant differences in satellite cell number was found following laser irradiation, changes were seen in tissue antioxidant status and blood antioxidant status (measured using the ORAC assay). In the course of this study several standard techniques were used to investigate the effects of laser irradiation on satellite cells both in-vitro and invivo. It has become apparent that several of these techniques have problems associated with them that possibly make them inappropriate for vi further use in studies involving laser irradiation. However the results indicate that laser therapy is induces satellite cell behavior and further study is warranted in this field.
AFRIKAANSE OPSOMMING: Alhoewel spierweefsel merkwaardige regenerasie kapasiteit vertoon ten opsigte van besering, is hierdie proses stadig en word soms vergesel met die vorming van letselweefsel asook ‘n gevolglike afname in kontaktiele kapasiteit na afloop van regenerasie. Behandelingsmoontlikhede is skaars en meesal ondersteunend van aard. Hierdie proses sluit spierstamselle (satelietselle), wat uiteindelik die ontstaan van die regenerasie van spier tot gevolg het, in. Die kontroversiële veld van lae vlak laserterapie (Engels: Low level laser therapy (LLLT)) het merkwaardige aansprake in die fasilitering met verskeie sagteweefsel wondgenesing. Nietemin, die meganisme(s) wat voordelige effekte induseer, word nog nie goed begryp nie. Ons het die effek van LLLT, deur gebruik te maak van ‘n 638 nm laser op kultuur in vitro satelietselle sowel in-vivo, ondersoek. Deur gebruik te maak van verskeie tegnieke is onder meer die metaboliese, sowel die seinstransduksie weë en antioksidantstatus na laserbestraling, gemeet. In reaksie op die laserbestraling het satelietselle (in kultuur) ‘n toename in MTT waardes getoon (‘n maatstaf van die metaboliese aktiwiteit) en ‘n afname in die antioksidantstatus (gemeet deur van die ORAC toets). Addisioneel het laserbestraling ook uitdrukking en fosforilering van verskeie proteïene betrokke in seintransduksieweë beïnvloed, insluitend Akt, STAT-3). Na afloop van hierdie effekte op satelietselle na laserbestraling, is daar gebruik gemaak van ‘n kneusbeseringsrotmodel om hierdie effekte in vivo te ondersoek. Geen betekenisvolle verskille in die aantal satelietselle na laserbestraling is opgemerk nie, maar veranderings is wel opgemerk in weefsel- en bloed-antioksidantstatus (gemeet deur van die ORAC toets gebruik te maak). Gedurende die verloop van die studie is van verskeie standaardtegnieke gebruik gemaak om die effekte van laserbestraling op beide satelietselle in vitro en in vivo te ondersoek. iv Dit het duidelik na vore gekom dat daar wel gepaardgaande probleme met van hierdie tegnieke voorgekom het, en dat van hierdie tegnieke nie gepas is vir ondersoek in laserbestralingsstudies nie. Nietemin, die resultate toon wel dat laserbehandeling. satelietselgedrag induseer wat verdere studie in hierdie veld noodsaak
Nearing, Marie. "The Role of the Regenerating Protein Family on Skeletal Muscle Regeneration." Diss., The University of Arizona, 2013. http://hdl.handle.net/10150/268516.
Повний текст джерелаZhang, Yafei. "Role of the Sh3 and Cysteine-Rich Domain 3 (STAC3) Gene in Proliferation and Differentiation of Bovine Satellite Cells." Thesis, Virginia Tech, 2013. http://hdl.handle.net/10919/76864.
Повний текст джерелаMaster of Science
Victor, Pedro Sousa. "Skeletal muscle aging: stem cell function and tissue homeostasis." Doctoral thesis, Universitat Pompeu Fabra, 2012. http://hdl.handle.net/10803/81933.
Повний текст джерелаEl envejecimiento del tejido muscular está caracterizado concretamente por una reducción global de la masa muscular y un empeoramiento de la función de tejido, particularmente prominentes en individuos muy viejos (geriátricos) que padecen sarcopenia. La pérdida muscular asociado a la edad, se acompaña de una reducción en la capacidad de regeneración del músculo y en una reducción del número y la función de las células madre residentes en el músculo (células satélite). Aunque la sarcopenia sea una de las causas principales de la pérdida general de función fisiológica del músculo, los mecanismos implicados en la reducción de la homeostasis muscular y de actividad de las células satélite no han sido completamente caracterizados. Mediante el análisis comparativo del transcriptoma de células madre musculares aisladas de ratones jóvenes y de ratones viejos (geriátricos), hemos encontrado cambios específicos en su perfil de expresión génica que apuntan a los procesos biológicos dominantes y a los marcadores moleculares potencialmente asociados con el envejecimiento de las células satélite, entre los que destaca p16INK4a. Por ello, hemos utilizado ratones deficientes en Bmi1 para explorar más profundamente las implicaciones de la sobreexpresión de p16INK4a en la función de las células satélite. Hemos encontrado que células satélite jóvenes del ratón Bmi1-/- presentan sobrexpresión de p16INK4a, que correlacionan con una reducción en el número de la células, y en su capacidad de proliferación y autorenovación. Además hemos identificado un grupo de procesos biológicos comunes entre las células satélite viejas y las deficientes en Bmi1, sugiriendo que la regulación epigenética mediada por Bmi1 puede ser la base de muchos de los cambios intrínsecos que ocurren en células envejecidas fisiológicamente. Además, demostramos que la pérdida Bmi1 causa defectos en el crecimiento postnatal/adulto del músculo, caracterizado por pérdida de masa muscular con fibras más pequeñas, típico del músculo atrofiado senescente o sarcopénico. Puesto que la expresión de p16 está aumentada específicamente en el músculo de ratones viejos, sarcopénicos y en un modelo del ratón con envejecimiento (senescencia) acelerado (SAMP8), proponemos que el eje Bmi1/p16 puede actuar particularmente en las células madre musculares de los ancianos. La pérdida de masa muscular es una de las consecuencias fisiológicas de la sarcopenia y la identificación de nuevos factores que regulen el crecimiento y atrofia del músculo es de gran importancia para aplicaciones terapéuticas. Hemos descubierto un nuevo papel de las Sestrinas como factores promotores del crecimiento del músculo esquelético en el adulto. Hemos encontrado que la expresión de las Sestrinas se regula en modelos del ratón de atrofia y de hipertrofia muscular y en miopatías humanas. Mediante experimentos de ganacia de función hemos demostrado que las Sestrinas inducen el crecimiento del músculo esquelético, activando el ruta de señalización de IGF1/PI3K/AKT
Tardif, Derek. "Implication du facteur de transcription GATA-6 dans la régénération musculaire." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112311.
Повний текст джерелаKeywords. GATA-6, muscle regeneration, mdx, satellite cells
Molon, Sibilla. "Role of collagen VI in skeletal muscle regeneration and intestinal homeostasis." Doctoral thesis, Università degli studi di Padova, 2016. http://hdl.handle.net/11577/3424420.
Повний текст джерелаDurante il mio percorso di dottorato mi sono occupata di studiare il ruolo del collagene VI nella rigenerazione del muscolo scheletrico e nell’omeostasi dell’intestino. Il collagene VI è una glicoproteina della matrice extracellulare (MEC) costituita da tre catene geneticamente distinte, le quali si organizzano in modo da formare un’estesa rete di microfilamenti in grado di connettere cellule e altri componenti della MEC. Mutazioni a carico dei geni codificanti le catene del collagene VI causano diverse patologie muscolari, principalmente la miopatia di Bethlem e la distrofia muscolare congenita di Ullrich. Gli studi condotti sul modello knockout murino privo di collagene VI hanno permesso di chiarire i difetti patomolecolari causati dall’assenza di questa proteina, dimostrandosi utile anche per l’identificazione di nuovi trattamenti farmacologici per le malattie umane. Nel coso degli anni, molteplici studi hanno messo in luce le diverse funzioni esercitate dal collagene VI nel regolare diversi eventi cellulari e tissutali, tra cui l’apoptosi e il danno ossidativo, l’autofagia, il differenziamento cellulare, il mantenimento della staminalità ai fini rigenerativi e le proprietà biomeccaniche. Nel corso del mio dottorato ho partecipato inizialmente alla caratterizzazione del ruolo del collagene VI durante la rigenerazione del muscolo scheletrico e la sua influenza sull’attività delle cellule satelliti, la popolazione principale di cellule staminali adulte nei muscoli scheletrici. Da tali studi è emerso che il collagene VI è un componente essenziale della nicchia delle cellule satelliti. La mancanza di tale proteina determina una ridotta rigenerazione tissutale e una diminuita capacità delle cellule satelliti di compiere self-renewal in seguito a danni muscolari multipli. I muscoli dei topi privi di collagene VI sono caratterizzati da una minore stiffness e approfondite analisi condotte in vitro hanno rivelato che le proprietà staminali e rigenerative delle cellule satelliti sono fortemente compromesse quando coltivate su biomateriali con un modulo elastico che mima la condizione patologica. Le capacità rigenerative e le proprietà meccaniche dei muscoli di topi privi di collagen VI vengono ripristinate in seguito alla deposizione di collagene VI, ristabilita tramite grafting di fibroblasti muscolari isolati da topi wild-type. Complessivamente, questi studi hanno dimostrato che modulando le proprietà meccaniche del muscolo, il collagene VI è in grado di regolare l’attività delle cellule satelliti. Abbiamo inoltre dimostrato che la somministrazione di ciclosporina A è in grado di stimolare la miogenesi in condizioni fisiologiche, inducendo la formazione di nuove fibre muscolari, e di migliorare la rigenerazione muscolare e l’omeostasi delle cellule satelliti in seguito a danni muscolari nei topi privi di collagene VI. Successivamente mi sono dedicata ad indagare il ruolo del collagene VI nell’omeostasi dell’intestino. Sebbene questa proteina sia ampiamente distribuita nella mucosa e nello strato muscolare, la sua assenza sembra non comportare alterazioni macroscopiche sull’architettura intestinale. L’analisi della funzionalità del sistema gastrointestinale ha evidenziato un’aumentata motilità e una ridotta permeabilità paracellulare in assenza di collagene VI. Esperimenti di induzione di colite acuta mediante sodio solfato destano hanno rivelato che i topi privi di collagene VI presentano una ridotta risposta e severità, associate ad una minore perdita di peso corporeo e minore infiammazione della mucosa del colon rispetto ai topi wild-type. Inoltre, durante la fase di colite acuta il reclutamento di cellule infiammatorie è risultato essere aumentato nei topi wild-type, comportando un aumento del numero di macrofagi e di attività dei neutrofili, mentre si riduce durante la fase di recupero seguente la colite acuta, favorendo la rigenerazione tissutale. Di contro, nei topi privi di collagene VI l’infiammazione è risultata essere ancora attiva durante la fase di recupero, con un elevato numero di macrofagi pro-infiammatori M1, un’alta attività dei neutrofili e un peggioramento della perdita di peso. Inoltre l’assenza di collagene VI ha dimostrato influenzare il comportamento dei macrofagi della mucosa del colon, sia in condizioni fisiologiche sia durante i primi giorni di infiammazione acuta, la cui attività è essenziale per assicurare l’omeostasi della mucosa intestinale. Nel complesso, da questi studi è emerso che il collagene VI esercita un ruolo da chemoattrattore per le cellule infiammatorie durante la fase di colite acuta, mentre nella successiva fase di risoluzione la sua presenza è necessaria nell’indurre una corretta rigenerazione tissutale. Studi di immunofluorescenza hanno inoltre rivelato nei topi wild-type un’elevata espressione di collagene VI in stretto contatto con i macrofagi della mucosa del colon durante la fase di colite acuta. L’evidenza di un’aumentata espressione di collagene VI su biopsia di ileo di paziente affetto da morbo di Crohn, associata ad un elevato numero di macrofagi rispetto al controllo sano, suggerisce un coinvolgimento di questo componente della MEC nel decorso delle malattie infiammatorie intestinali. In conclusione, le evidenze emerse in questo mio lavoro di tesi avvalorano l’importanza del ruolo della matrice extracellulare nell’omeostasi tissutale.
Doreste, Gonzalez Bruno. "The effect of modulating the dystrophic skeletal muscle environment on satellite cell engraftment." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10051216/.
Повний текст джерелаHardy, David. "Le rôle clef de la chimiokine CXCL12/SDF1 au sein du couplage angiogenèse/myogenèse au cours de la régénérescence du muscle strié squelettique." Thesis, Paris Est, 2015. http://www.theses.fr/2015PESC0035.
Повний текст джерелаMuscle regeneration needs specialized stem cells but it also requires coordinated action of stromal cells and supporting tissue. The study of muscle regeneration can not be only limited to the study of the activation, proliferation and differentiation of muscle stem cells. The aim of this thesis was to approach the mechanisms involved in the harmonious regeneration of the muscle beside satellite cells to know the different cellular elements of the supporting tissues and also the stroma through the study of CXCL12 chemokine and its anchorage to the GAG of the muscle extracellular matrix.First, we made the observation that muscle damage models were numerous and were used indistinctly with ignorance of their own specificities. Thus, the first part of this thesis consisted of comparing different injury models commonly used in the literature to determine their potential targets and choose the most adapted to scientific questions asked. secondarily, we used an animal model genetically invalidated for anchoring of CXCL12 gamma isoform to the matrix to study the skeletal muscle development, stem cells and the organization of their niche and finally, the repair.We showed initially that the initial choice of the injury model is important during pathophysiological studies. Although all muscle injury models lead to an ad integrum restitution, regeneration processes vary considerably and the impact on different cell types also varies widely. In addition, we have shown that the only histological parameters, are not entirely sufficient to say that muscle regeneration is complete and each cell type should be considering in detail as well as functional parameters that should be measured in perspectives of this work.We used as a study model, mice knock in CXCL12Gagtm/Gagtm recently developed in the laboratory and in which CXCL12 gene has been mutated for the region coding the controlling anchoring of CXCL12 to HS. In this mouse, CXCL12 is present but unable to bind to the extracellular matrix HS while keeping its activity via CXCR4. In this case CXCL12 is unable to generate a gradient responsible for the attraction, retention and migration of target cells.Although this change does not affect the development of the mouse and the muscle at basal state is normal, we have shown a lack of muscle regeneration in these mice with fibrosis and fat infiltartion.The muscle stem cell compartment seems not to be altered in the mutant mice in the basal state and during the regeneration of the muscle. We have shown that the absence of CXCL12 gradient leads to deregulated angiogenesis through vascular hyperproliferation at the basal state. This deregulation seems to be responsible of an altered vascular regeneration after injury with the presence of non-stabilized mural cells (smooth muscle cells and pericytes). This lack of vascular regeneration appears to be responsible for a muscle regeneration failure
Mougeolle, Alexis. "Effet du stress oxydant sur les cavéoles dans les cellules musculaires squelettiques." Thesis, Bordeaux, 2014. http://www.theses.fr/2014BORD0298/document.
Повний текст джерелаSarcopenia is an age-related degenerative disease which is characterized by a progressive and involuntary loss of muscle mass and strength. It is accompanied by an impairment of muscle regeneration and accumulation of reactive oxygen species. Caveolae are invaginations of the plasma membrane. In muscle, they play a role in the differentiation of satellite cells and in maintaining the contractile unit of the differentiated skeletal muscle. Some myopathies are resulting from the absence of caveolae in muscle. Caveolae are also involved in mediating signals related to the regulation of oxidative stress. To better understand the mechanisms involved in the development of sarcopenia, we investigated here the relationship between oxidative stress and caveolae. Mouse muscle cells were treated with H2O2 and decreased levels of caveolin-1 and -3 were demonstrated in myoblasts and myotubes, respectively. It therefore appears that caveolae constituent proteins are actually sensitive to oxidative stress in muscle cells. In the presence of H2O2, caveolae functions (endocytosis and resistance to mechanical stress) were also significantly degraded in myoblasts. Altogether, these data suggest that oxidative stress would affect caveolae, which could have consequences on regeneration and maintenance of muscle integrity during aging
Parato, Giulia. "Regulation of muscle satellite cell proliferation and differentiation by local trophic factors." Doctoral thesis, Università degli studi di Trieste, 2014. http://hdl.handle.net/10077/10153.
Повний текст джерелаThe skeletal muscle is a terminally differentiated tissue. Its capacity to repair following injury or disease depends on a population of myogenic precursors, named satellite cells. These cells are localized beneath the skeletal muscle fiber, in a specialized microenvironment, the niche. The niche preserves the homeostatic conditions of satellite cell quiescence, but at the same time, it ensures their responsiveness to mechanical, physical and chemical triggers from the surrounding environment. Therefore, the composition of the external milieu is critical in determining satellite cell behavior. As a matter of fact, during aging or under pathological conditions, alterations of the extracellular environment entail a severe impairment of satellite cell ability to sustain regeneration and repair of the skeletal muscle tissue. The general goal of this thesis was to focus on some of the trophic factors potentially present in the satellite cell niche in vivo and to characterize their role on the modulation of satellite cell functions in vitro. The first part of the research activity dealt with the study of the trophic effect of ATP on mouse myoblast proliferation. From literature, it emerged that ATP is a potential regulator of the skeletal muscle regenerative program, however the signalling mechanism remained partially unknown. We observed that ATP increased myoblast growth rate, effect that was mimicked by low concentrations of H2O2. Reactive oxygen species (ROS) imaging revealed that ATP induced H2O2 production, at concentrations comparable to those effective in triggering myoblast proliferation. Interestingly, the exposure to equimolar concentrations of adenosine did not mimic the effect of ATP, excluding any role for the main hydrolysis product of ATP in the control of cell cycling. This result was in agreement with data reporting that the specific enzymes responsible for ATP degradation are poorly expressed in myoblasts and become upregulated after cell differentiation. In line with the latter observation, it appeared reasonable that the differentiating skeletal muscle cells were more exposed to ATP-derived adenosine than proliferating myoblasts, and this suggested a potential physiological role for the nucleoside adenosine in the later phases of myogenesis. Taking into account that adenosine receptors (ARs) are present in mouse myotubes, in a second study we hypothesized a crosstalk between nAChRs and ARs. Using the Ca2+-imaging technique, we observed that the pharmacological modulation of ARs triggered variations in the nAChR-driven ([Ca2+]i) spikes. Moreover, our preliminary results suggest not only an interplay between the two receptors but also that endogenous adenosine is tonically released by twitching myotubes and activates its receptors. The third research project was aimed at exploring the role of neural agrin, a heparan sulphate proteoglycan, so far known as the key organizer of post-synaptic elements during skeletal muscle differentiation/regeneration. Besides agrin’s canonical effect on the maturation of the NMJ, novel roles have been discovered in the recent years, suggesting that the neurotrophic factor has pleiotropic effects. In this new context, we pursued the identification of potential new roles for neural agrin in the determination of satellite cell behaviour. Firstly, the analysis of different cell models, including C2C12 cell line and primary mouse and human cells, and revealed an increase in IL-6 secretion following exposure to agrin. Secondly, we addressed the hypothesis of agrin as a potential modulator of human myoblasts proliferation. Our preliminary results demonstrate that agrin enhances the proliferative capacity of human satellite cells and suggest the potential mechanism involved in the signaling cascade.
Il muscolo scheletrico è un tessuto terminalmente differenziato. La sua capacità rigenerativa in seguito a danno o patologia dipende da una popolazione di precursori miogenici, le cellule satelliti. Esse sono localizzate sulla superficie della fibra muscolare, racchiuse in un ambiente altamente specializzato, la nicchia. La nicchia assicura il mantenimento della quiescenza cellulare, ma allo stesso tempo fa sì che la cellula satellite risponda a stimoli meccanici, fisici o chimici, provenienti dall’ambiente esterno. Per questo motivo, la composizione dell’ambiente circostante condiziona altamente il comportamento della cellula satellite. Infatti, le alterazioni che si verificano con l’invecchiamento o in seguito a patologia compromettono la capacità dei precursori miogenici di sostenere la rigenerazione del tessuto. Lo scopo di questo lavoro di tesi è stato quello di individuare e caratterizzare alcuni dei fattori trofici che compongono il microambiente della cellula satellite in vivo, per cercare di capire come essi modulino le funzioni dei precursori miogenici durante la rigenerazione in vitro. La prima parte dell’attività di ricerca ha riguardato lo studio dell’effetto trofico dell’ATP sulla proliferazione mioblastica. Studi in letteratura hanno fatto emergere il potenziale ruolo regolatore dell’ATP nella rigenerazione muscolare, anche se i meccanismi attraverso cui opera non sono ancora chiari. I risultati da noi ottenuti hanno dimostrato che l’ATP aumenta la proliferazione mioblastica e che un effetto simile si osserva in presenza di H2O2. L’imaging per le specie reattive dell’ossigeno (ROS) ha inoltre dimostrato che l’ATP induce la produzione di H2O2, a concentrazioni paragonabili a quelle capaci di aumentare la proliferazione. In presenza di concentrazioni equimolari di adenosina non è stato osservato alcun effetto sulla proliferazione cellulare, fatto che suggerisce che il ruolo dell’ATP non sia attribuibile all’adenosina, il suo principale prodotto di degradazione. Questo risultato è in accordo con quanto già riportato da altri Autori a proposito degli enzimi responsabili dell’idrolisi dell’ATP: essi sono poco espressi nei mioblasti in proliferazione, mentre la loro espressione aumenta notevolmente con il differenziamento cellulare. Alla luce di queste osservazioni, risultava verosimile che i miotubi fossero più esposti rispetto ai mioblasti all’adenosina derivante dall’ATP e che pertanto l’adenosina avesse un ruolo fisiologico preponderante nelle fasi avanzate della miogenesi. Dal momento che i recettori per l’adenosina (ARs) sono espressi nei miotubi murini, un secondo lavoro ha avuto come obiettivo quello di investigare un possibile “crosstalk” tra i ARs e i nAChRs. Esperimenti di Ca2+- imaging hanno dimostrato come la modulazione farmacologica dei ARs si traduca in una variazione nelle oscillazioni di [Ca2+]i indotte dall’attività del nAChR. Questi risultati, sebbene preliminari, suggeriscono non solo che i due recettori interagiscono tra loro, ma anche che l’adenosina è tonicamente secreta dai miotubi in contrazione e agisca attivando i suoi recettori. Il terzo progetto di ricerca è stato finalizzato allo studio del ruolo dell’agrina neuronale, un proteoglicano eparan solfato, già noto per la sua capacità di aggregare elementi sinaptici durante la fase di differenziamento e di rigenerazione del muscolo scheletrico. Accanto al ruolo canonico che la vede coinvolta nella maturazione della giunzione neuromuscolare, negli ultimi anni sono state descritte nuove funzioni per l’agrina neuronale, che la indicano come un fattore pleiotropico. In questo contesto, abbiamo esplorato nuove proprietà dell’agrina. In primo luogo, l’analisi di diversi modelli cellulari, incluse la linea cellulare C2C12 e cellule primarie murine e umane, ha dimostrato che il fattore neurotrofico potenzia il rilascio di IL-6. In un secondo studio, è stato ipotizzato un potenziale effetto di modulazione della proliferazione di mioblasti umani da parte dell’agrina neuronale. Risultati preliminari hanno dimostrato che l’agrina aumenta la capacità proliferativa delle cellule satelliti umane. Inoltre, sono stati individuati alcuni dei fattori molecolari che partecipano alla cascata di segnalazione.
XXVI Ciclo
1986
Awaya, Tomonari. "Selective Development of Myogenic Mesenchymal Cells from Human Embryonic and Induced Pluripotent Stem Cells." Kyoto University, 2013. http://hdl.handle.net/2433/180602.
Повний текст джерелаSteyn, Paul. "Cytokine super-families affect adult stem cells : IL-6 and the skeletal muscle niche." Thesis, Stellenbosch : University of Stellenbosch, 2011. http://hdl.handle.net/10019.1/6550.
Повний текст джерелаIncludes bibliography.
ENGLISH ABSTRACT: Background: IL-6 belongs to a cytokine super-family known to affect cell proliferation, although other family members are better characterized. Proliferation promoting factors (IL-6) compete with differentiation promoting factors (myogenic regulatory factors: MyoD and myogenin) to affect cell cycle. Cell cycle progression is assessed by determining the proportion of cells shifting from arrest to chromatin synthesis and mitosis phases (G0/G1 and S and G2/M respectively). Methods: This study assessed the effects of IL-6 on cell cycle progression and proliferation vs. differentiation of C2C12 skeletal myoblasts. Physiological doses (10 or 100 pg/ml) were compared to a high dose (10 ng/ml), with exposure lasting 48 hours (addition of IL-6 dose to proliferation medium at 0 and 24 hours). Acute signaling downstream of the IL-6 gp130 receptor was assessed after the first exposure. Results: Propidium iodide analysis of nuclear material using flow cytometry indicated shifts in forward scatter. Both Low and Medium doses shifted a greater proportion (p<0.05) of cells from G0/G1 to S and G2M phases at 24 hours and all doses resulted in the same shift (p<0.05) at the 48 hour time point. However, the High dose significantly (p<0.05) increased myogenin expression at the 48 hour time point. Microscopy indicated that confluence was prevented by low seeding density and did not influence the result. Cells harvested at 5 minutes post stimulation indicated that all doses significantly increased STAT3 phosphorylation. 10 minutes post stimulation the High dose group sustained elevated levels of STAT3 phosphorylation. Conclusions: Low and medium doses of IL-6 increase proliferation in a muscle satellite cell line by activating cell division and allowing myoblasts to remain in the active cell cycle. High doses of IL-6 increase differentiation by mediating upregulation of myogenic regulatory factors and this is thought to be due to prolonged STAT3 activation. Physiological control of myoblast behaviour by cytokines is evident and such control would be influenced by the severity of the endogenous cytokine response to various stimuli.
AFRIKAANSE OPSOMMING: Agtergrond: IL-6 behoort aan n sitokien super-familie bekend vir die affektering van sel verspreiding, alhoewel ander familie lede beter gekenmerk is. Bevordering van verspreiding faktore (IL-6) kompeteer met bevordering van differensiasie fatore (myogenic regulatory factors: MyoD en myogenin) om die sel siklus te affekteer. Sel siklus progressie word geassesseer deur die bepaling van die proporsie selle wat verskuif van arrestasie na chromatien sintese en mitose fases (G0/G1 en S en G2/M onderskeidelik). Metodes: Hierdie studie het die effekte van IL-6 op die progressie van die sel siklus geassesseer asook die proliferasie vs. differensiasie van C2C12 skelet spier satelliet selle. Fisiologiese dosisse (10 en 100 pg/ml) was vergelyk tot n hoog dose (10 ng/ml), met blywende blootstelling van 48 uur (byvoeging van IL-6 dose tot verspreidings medium op 0 and 24 uur). Akute sein stroomaf van die IL-6 gp130 reseptor was ook geassesseer na die eerste blootstelling. Resultate: Propidium iodide analise van kern materiaal deur vloei sitometrie het voorwaarts verskuiwing aangedui. Beide Laag and Medium doses het n groter proporsie (p<0.05) selle verskuif van die G0/G1 tot die S en G2M fases na 24 uur en alle dosisse het gelei in die selfde verskuiwing (p<0.05) by die 48 huur tyd punt. Alhoewel die Hoog dose myogenin uitdrukking aansienlik (p<0.05) verhoog het na 48 uur. Mikroskopie het aangedui dat samevloeiing voorkom was deur n lae loting digtheid en dit het nie resultate geaffekteer nie. Selle wat geoes was 5 minute na stimulasie het aangedui dat alle dosisse STAT3 fosforilasie laat toeneem het. 10 minute na stimulasie het die Hoog dose groep volgehoue vlakke van STAT3 fosforilasie besit. Gevolgtrekkings: Laag en Medium dosisse van IL-6 verhoog verspreiding in n spier satelliet sel lyn deur die aktivering van sel deling en deur selle toe te laat om in die aktiewe sel siklus te bly. Hoog dosisse van IL-6 verhoog differensiase deur bemiddelende opstoot van myogenic regulatory factors en die gedagte is dat dit bewerkstellig word deur aanhoudende aktivering van STAT3. Fisiologies beheer van satelliet selle deur sitokiene is duidelik en die beheer sal beinvloed word deur die erns van die endogene sitokien reaksie op verskillende stimuli.
Van, Tubbergh Karen. "Skeletal muscle repair after micro-damage : effect of ice therapy on satellite cell activation." Thesis, Stellenbosch : University of Stellenbosch, 2005. http://hdl.handle.net/10019.1/16623.
Повний текст джерелаENGLISH ABSTRACT: Cryotherapy is one of the popular treatments used to alleviate muscle soreness, especially in the competitive sports arena. However, the therapeutic use of cryotherapy is unsubstantiated because of a lack of proper investigations in the literature, especially a hypothesised effect on muscle recovery. Thus, our aims were to characterise satellite cell (SC) activity in human subjects with delayed onset muscle soreness (DOMS) and to shed light on the effect of cryotherapy on SC activity. DOMS was induced in six male subjects (24 ± 3 years) by completion of a downhill-run (DHR) protocol (5 x 8 min bouts, 2 min rest between bouts) at 70 or 80% of their individual peak treadmill speed. Ice application was applied to only one leg per subject for 3 days: 30 min every 2 hours, 5 times per day. In total 5 muscle biopsies were obtained from each subject: 1 baseline and 4 post-DHR. Post-DHR biopsies: 1 from each leg on day 1 and 7 (1st group, n=3) and 1 from each leg on day 2 and 9 (2nd group, n=3). DOMS was successfully induced as indicated by significant increases in muscle soreness at days 1 and 2 post-DHR (P < 0.01), and creatine kinase activity at day 1 post-DHR (P < 0.01). No difference in muscle soreness was found between treated and untreated legs. SC quiescence and activation were characterised by their expression of the cell surface markers CD34 and CD56 respectively. No significant change in quiescent SC was observed in the untreated or treated legs over time. However, at day 1 post-DHR the number of quiescent SC was significantly lower in the untreated compared with the treated leg (P < 0.05). There was a significant increase in activated SC numbers at day 2 post-DHR in the untreated leg, which was sustained up to day 9 post-DHR (P < 0.01). However, no such increase was found in biopsies taken on days 1 and 7. Also, no change was found in the treated leg, however a significant difference between the number of activated SC in untreated and treated legs on days 2 and 9 post-DHR (P < 0.01) was seen. No significant effect of DOMS or ice treatment was observed for the expression of the myogenic regulatory factors, MyoD and myogenin. C2C12 cell cultures induced to differentiate, however, did stain using these antibodies. This is the first study to report an effect of cryotherapy at the tissue level. In conclusion, this study highlights many unanswered questions on the SC response to DOMS at tissue level, and lays a good foundation for future studies.
AFRIKAANSE OPSOMMING: Kreoterapie is een van die gewilde behandelings wat gebruik word om spierseerheid te verlig, veral in die kompeterende sport arena, maar die gebruik van kreoterapie is onbevestig as gevolg van ‘n gebrek aan voldoende ondersoeke in die literatuur, veral ‘n hipotese oor die effek op spier-herstel. Ons doelstellings was dus om satellietsel (SC) aktiwiteit te ondersoek in mens proefpersone met vertraagde aanvang spierseerheid (DOMS) en ook om lig te werp op die effek van kreoterapie op SC aktiwiteit. DOMS was in ses mans proefpersone (24 ± 3 jare) geїnduseer deur voltooїng van ‘n afdraend-hardloop (DHR) protokol (5 x 8 min rondtes, 2 min rus tussen rondtes) teen 70 of 80% van elkeen se individuele maksimum trapmeul-spoed. Ys was vir 3 dae op net een been per proefpersoon aangewend: 30 min elke 2 ure, 5 keer per dag. 5 spierbiopsies in totaal was van elke proefpersoon verkry: 1 basislyn en 4 post-DHR. Post-DHR biopsies: 1 van elke been op dae 1 en 7 (1ste groep, n=3) en 1 van elke been op dae 2 en 9 (2de groep, n=3). DOMS was suksesvol geїnduseer soos aangedui deur die betekenisvolle verhogings in spierseerheid op dae 1 en 2 post-HR (P < 0.01) en kreatien kinase aktiwiteit op dag 1 post-DHR (P < 0.01). Geen verskil in spierseerheid is gevind tussen die onbehandelde en behandelde bene nie. SC dormansie en aktivering was gekarakteriseer deur die onderskeidelike uitdrukking van die sel oppervlak merkers CD34 en CD56. Geen betekenisvolle verandering is in SC dormansie in die onbehandelde en behandelde bene waargeneem nie, maar op dag 1 post-DHR was die getal dormante SC betekenisvol laer in die onbehandelde been as in die behandelde been (P < 0.05). Daar was ‘n betekenisvolle verhoging in die getalle geaktiveerde SC op dag 2 post-DHR in die onbehandelde been wat volgehou was tot op dag 9 post-DHR (P < 0.01), maar so ‘n verhoging was nie in biopsies wat op dae 1 en 7 geneem is gevind nie. Daar is ook geen verandering in die behandelde been gevind nie, maar ‘n betekenisvolle verskil in die getal geaktiveerde SC is tussen die onbehandelde en behandelde bene op dae 2 en 9 post-DHR gevind(P < 0.01). Geen betekenisvolle effek van DOMS en ys-aanwending vir die uitdrukking van die miogeniese (myogenic) regulatoriese faktore, MyoD en myogenin, is waargeneem nie. C2C12 sel kulture wat geїnduseer is om te differensieer het wel gekleur vir hierdie antiliggame. Dit is die eerste studie wat ‘n effek van kreoterapie op weefselvlak rapporteer. Ten slotte, hierdie studie beklemtoon baie onbeantwoorde vrae oor die SC respons op DOMS op weefselvlak en dit lê ‘n goeie grondslag neer vir toekomstige studies.
Rayagiri, Shanti sree Sandeepani. "Analysis of the remodelling of the satellite cell basal lamina during skeletal muscle regeneration." Thesis, University of Sheffield, 2014. http://etheses.whiterose.ac.uk/6713/.
Повний текст джерелаLupi, Ryan Alexander. "Regulation of human satellite cells in vitro via inflammatory cytokines and myogenic transcription factors across proliferation and differentiation." Thesis, Virginia Tech, 2019. http://hdl.handle.net/10919/90390.
Повний текст джерелаMaster of Science
Skeletal muscle is responsible for conscious, voluntary movement. In addition, the tissue is responsible for the majority of energy expenditure in the human body. Skeletal muscle is able to adapt to exercise programs through the fusion of undifferentiated stem cells – called satellite cells – in the skeletal muscle fiber. In long-term diseased conditions, the immune response involves chronic rises in inflammation and results in the loss of skeletal muscle and corresponding loss of ability to move. A shorter rise in inflammation is also linked with the positive exercise response. Our study features satellite cells harvested from muscle samples of 12 male human research participants. We were interested in evaluating the relationships between the expression and secretion of two proteins associated with inflammation and regulation of the satellite cell cycle. The two proteins of interest in our study are tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6). We also measure the gene expression of another inflammatory protein, transforming growth factor beta (TGF-β). In order to know where the cells were in their life cycle, we measured expression of genes associated with the division (Pax7), early fusion (MyoD), and late fusion of satellite cells (myogenin). Our study found a decrease in IL-6 secretion and expression as the process of satellite cells turning into muscle fibers was initiated. Additionally, a 50-fold increase in IL-6 expression was found at day 7 compared to day 0 of the satellite cell cycle. Additionally, we found a positive correlation between TGF-β and myogenin and a negative correlation between IL-6 and MyoD. Although we found correlations between satellite cell cycle genes and inflammation genes, more research is necessary to see if there is a pathway causing this relationship.
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.
Повний текст джерелаLuin, Elisa. "The Ca 2+ currents and homeostasis during the aging process of skeletal muscle." Doctoral thesis, Università degli studi di Trieste, 2008. http://hdl.handle.net/10077/2574.
Повний текст джерелаAims: The mechanisms involved in sarcopenia, the decline in muscle mass with aging coupled with loss of force and function, has been actively investigated in animal and human models over the last years [reviewed in Di Iorio et al., Sarcopenia: age-related skeletal muscle changes from determinants to physical disability, Int. J. Immunopathol. Pharmacol. 19 (2006) 703-719]. An important age-associated deficit may be the alteration of the mechanisms controlling Ca2+ handling. Moreover, it has already been proposed that defective fibres in old humans could result from a reduced efficiency of aged satellite cells (a distinct muscle cell subtype, responsible for post-natal growth and repair of damaged fibres) in properly differentiating into myotubes with a mature E-C coupling mechanism [see: Lorenzon et al., Aging affects the differentiation potential of human myoblasts, Exp. Gerontol. 39 (2004) 1545-1554]. Proceeding from these results, the main goal of the present Ph.D. thesis was to investigate whether the inefficiency of aged satellite cells to generate functional skeletal muscle fibres could be partly due to defective voltage-dependent Ca2+ currents. Methods: The whole-cell patch clamp and the videoimaging techniques were employed to measure respectively T- and L-type Ca2+ currents and [Ca2+]i transients in myoblasts and/or myotubes derived from murine and human satellite cells, obtained respectively from young murine skeletal muscle and then aged in vitro under culture conditions, and from human skeletal muscle tissue of healthy donors aged 2, 12, 76 and 86 years. Results: First of all, I confirmed that both murine and human senescent satellite cells fuse more slowly and less efficiently, leading to smaller and thinner myotubes, as known from previous work. Moreover, I showed for the first time that both in myotubes derived from in vitro aged murine satellite cells and in human myotubes derived from satellite cells of old donors the functional expression and the biophysical properties of T- and L-type voltage-dependent Ca2+ channels are impaired. In fact, extensively, less Ca2+ can be available via T-type and L-type channels in old myotubes than in the young ones, and this can be put in relation to the age-related decrease in the quality of myoblast fusion. I also confirmed a specific responsibility of the decrease of the L-type channel number and/or activity for the age-related lowering of intracellular Ca2+ release (the so-called E-C uncoupling; see: Delbono et al., Excitation-calcium release uncoupling in aged single human skeletal muscle fibers, J. Membr. Biol. 148 (1995) 211-222]. Conclusions: From these results one can infer a clear parallelism between the results obtained with the in vitro aging of murine satellite cells model and that concerning the physiological process of human skeletal muscle aging in vivo. In the final analysis, aging effects on voltage-dependent L- and T-type currents could be one of the causes of the inability of old satellite cells to efficiently counteract age-related impairment in muscle force. So, a further strong evidence has been given that in humans, as in other mammals, the satellite cells and the regulation of Ca2+ homeostasis have a decisive role in the physiological process of skeletal muscle aging.
**************************************************************************************** Scopo della ricerca: Nel corso dell’invecchiamento il muscolo scheletrico subisce cambiamenti significativi, quali la perdita di forza e di massa muscolare (sarcopenia; per una rassegna recente vedere: Di Iorio et al., Sarcopenia: age-related skeletal muscle changes from determinants to physical disability, Int. J. Immunopathol. Pharmacol. 19 (2006) 703-719). Era già noto che le disfunzioni correlate all’età potrebbero essere almeno in parte dovute all’inabilità delle cellule satelliti, le cellule staminali per eccellenza del muscolo scheletrico, di rigenerare fibre muscolari funzionali nell’individuo anziano (vedere: Lorenzon et al., Aging affects the differentiation potential of human myoblasts, Exp. Gerontol. 39 (2004) 1545-1554). Il principale scopo di questa Tesi di Dottorato è stato quello di studiare le possibili modificazioni dei meccanismi che regolano l’omeostasi calcica in cellule satelliti murine ed umane, rispettivamente nel corso dell’invecchiamento in vitro (senescenza replicativa in coltura) ed in vivo. In particolare l’attenzione è stata focalizzata sull’effetto delle alterazioni, collegate all’età, delle correnti al Ca2+ voltaggio-dipendenti di tipo L e di tipo T in miotubi provenienti dalla proliferazione e dal differenziamento di cellule satelliti a vari stadi di invecchiamento. Metodologia: Le cellule satelliti murine utilizzate derivavano da una linea primaria espansa denominata i28; le cellule satelliti umane sono state ottenute da biopsie di individui di diversa età (2, 12, 76 e 86 anni). Esperimenti di elettrofisiologia e di videomicroscopia hanno permesso lo studio rispettivamente delle correnti al Ca2+ e dei transienti di Ca2+ intracellulare, nonché delle loro modifiche collegate all’invecchiamento in vitro e in vivo nei modelli murino ed umano. Risultati: Vengono confermati, sia nel modello murino di invecchiamento in vitro che nel modello umano di invecchiamento in vivo, i dati sulla relazione tra sarcopenia e difficoltà di cellule satelliti invecchiate nel formare un numero sufficiente di nuovi miotubi, che anche morfologicamente risultano diversi da quelli derivanti dalla fusione di cellule satelliti giovani. Inoltre, si dimostra per la prima volta che le correnti al Ca2+ in esame sono espresse in minor percentuale e densità, e più tardivamente nel corso del differenziamento, in miotubi derivati da cellule satelliti murine a stadi avanzati di senescenza replicativa, e in cellule umane da donatore anziano. Anche le proprietà biofisiche dei canali di tipo L e T, presenti in miotubi derivati da cellule satelliti invecchiate in vitro e in vivo, appaiono compromesse; complessivamente, meno Ca2+ può entrare attraverso i due tipi di canale e ciò può essere messo in relazione alla riduzione, correlata all’età, della capacità differenziativa e di fusione in miotubi. Viene ulteriormente messo in rilievo il ruolo determinante, nel corso dell’invecchiamento, del calo in numero e in attività dei canali di tipo L, come meccanismo alla base del minor rilascio di calcio intracellulare (fenomeno del disaccoppiamento eccitazione-contrazione; vedere: Delbono et al., Excitation-calcium release uncoupling in aged single human skeletal muscle fibers, J. Membr. Biol. 148 (1995) 211-222). Conclusioni: Dai risultati ottenuti si evince un netto parallelismo tra il modello dell’invecchiamento in vitro di cellule satelliti murine e l’invecchiamento in vivo di cellule satelliti umane. In ultima analisi, si avvalora l’ipotesi che alterazioni età-dipendenti delle correnti al Ca2+ voltaggio-attivate possano essere alla base dell’impossibilità di cellule satelliti invecchiate di contrastare efficacemente la riduzione di forza muscolare caratteristica dell’anziano.
XX Ciclo
1980