Dissertations / Theses on the topic 'Myoblasts'
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Elia, Ines. "SNAI1 target genes in myoblasts." Doctoral thesis, Università di Siena, 2021. http://hdl.handle.net/11365/1142998.
Full textMahabir, Mark Ashford. "Senescence in normal and DMD myoblasts." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ58835.pdf.
Full textZhao, Shuai. "Effects of Hypoxic Conditions on Skeletal Myoblasts." Cleveland State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=csu1482831468411105.
Full textBabić, Nikolina. "Regulation of energy metabolism of heart myoblasts /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/11563.
Full textYazid, Muhammad Da'In Bin. "Analysis of cell signalling in dystrophin-deficient myoblasts." Thesis, University of Birmingham, 2017. http://etheses.bham.ac.uk//id/eprint/7342/.
Full textAkohene-Mensah, Paul. "Examining the Role of L-Type Amino Acid Transporter 1 (SLC7A5) in Myoblasts." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/41036.
Full textGersbach, Charles Alan. "Runx2-Genetically Engineered Skeletal Myoblasts for Bone Tissue Engineering." Diss., Georgia Institute of Technology, 2006. http://hdl.handle.net/1853/11600.
Full textMazzuca, Delfina Maria. "Regulation and function of glucose transporters in rat myoblasts." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ30668.pdf.
Full textRen, Huiping. "MBD2bdemethylase is involved in the myogenesis of C2C12 myoblasts." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=80861.
Full textPromoter methylation is one of the normal mechanisms inactivating gene expression. A single CpG site in the 5' flanking region of myogenin is reported to undergo demethylation during C2C12 differentiation. Considering the demethylase feature of MBD2b and its expression profile during C2C12 differentiation, I propose the hypothesis that MBD2b/demethylase is involved in C2C12 differentiation by demethylating the promoter of the myogenin gene as well as other genes involved in myogenic differentiation.
To test this hypothesis, I determined the consequences of up-regulation and down-regulation of MBD2b/demethylase in C2C12 cells.
The state of the myogenin promoter was also altered as determined using a probe recognizing a single HpaII site, which was previously reported to become demethylated during C2C12 differentiation. (Abstract shortened by UMI.)
Lund, Dane. "It's a Jungle Out There| Myoblasts, Matrix, and MMPs." Thesis, University of Missouri - Columbia, 2016. http://pqdtopen.proquest.com/#viewpdf?dispub=10182609.
Full textRazvadauskaite, Giedre. "Survival and differentiation of implanted skeletal myoblasts in the native and in the cryoinjured myocardium." Link to electronic thesis, 2003. http://www.wpi.edu/Pubs/ETD/Available/etd-0106103-155714.
Full textKeywords: myoblasts; dexamethasone; infarction; cryoinjury; desmin; myosin heavy chain; differentiation. Includes bibliographical references (p. 54-59).
Cowan, Joanne L. "Translational control during cellular stress and differentiation of C2C12 myoblasts." Thesis, University of Sussex, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.436824.
Full textSwailes, Nathan. "Actin and non-muscle myosin II in pre-fusion myoblasts." Thesis, University of Leeds, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.416842.
Full textBriggs, D. "An investigation into sub-populations of satellite cells and myoblasts." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1386193/.
Full textPouliot, Yannick 1963. "Study of L6 myoblast cell-cell adhesion." Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=61797.
Full textButler, David Christopher. "The role of Id2 phosphorylation at serine 5 in C2C12 myoblasts." Morgantown, W. Va. : [West Virginia University Libraries], 2008. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=5669.
Full textTitle from document title page. Document formatted into pages; contains v, 42 p. : ill. (some col.). Includes abstract. Includes bibliographical references.
Bray, Jonathan Alexander. "Comparing insulin and insulin-like growth factor-1 signalling in myoblasts." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596876.
Full textHou, Yuguo. "Roles of cholesterol in the proliferation and differentiation of bovine myoblasts." Thesis, Virginia Tech, 2017. http://hdl.handle.net/10919/87466.
Full textMaster of Science
Evans, Darrell John Rhys. "The behaviour and commitment of myoblasts during mammalian skeletal muscle formation." Thesis, University of Aberdeen, 1994. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU603173.
Full textPeduto, Giovanni. "Long-term accommodation to encapsulated xenogeneic myoblasts engineered to secrete erythropoietin /." [S.l.] : [s.n.], 1999. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.
Full textEl, Haddad Marina. "Approche pharmacologique dans la thérapie cellulaire : rôle de l'acide rétinoïque dans la survie et la différenciation des myoblastes humains." Thesis, Montpellier, 2015. http://www.theses.fr/2015MONTT003.
Full textMouse and human satellite cells have been shown to be functional muscle stem cells. Since myoblasts, the progeny of satellite cells can be transplanted and fuse with endogenous muscle fibers to form hybrid cells, myoblast transplantation represents a potential approach for the treatment of muscle diseases. Although other limitations, such as immune rejection or limited spread into the host tissue are also important, failure of myoblast transfer in the initial clinical trials was at least partly related to poor survival rate of transplanted myoblasts. Several approaches have been developed to reduce early loss of injected myoblasts. The approach in the laboratory was to select and purify a pool of myoblasts characterized by an improved survival response. Aldehyde dehydrogenases (ALDH) are a family of enzymes that efficiently detoxify aldehydic products generated by reactive oxygen species and might therefore participate in cell survival. Their findings indicate that high ALDH activity is present in a majority of human myoblasts. This activity is correlated ex vivo to resistance to hydrogen peroxide (H2O2)-induced cytotoxic effect and in vivo to improved cell viability when ALDHhigh myoblasts were transplanted into host muscle of immune deficient scid mice. They demonstrated that Aldh1a1 protein contributes to most if not all ALDH activity in human myoblasts. Aldh1a1 catalyzes the irreversible oxidation of vitamin A (retinol) to retinoic acid (RA) which binds and activates nuclear retinoic acid receptor (RAR)/Retinoic X receptor (RXR) heterodimers. Since high ALDH activity is correlated to improved cell viability, we will ask whether part of this biological activity is mediated by retinoic acid synthesis. In this project, we propose to determine whether retinoids (vitamin A and retinoic acid) protect human muscle precursor cells from cytotoxic damages and improved cell survival in transplantation assays. During my M2R training, I showed that human myoblasts exposed to an oxidative stress lost their integrity. Treatment with retinoic acid impaired these cytotoxic damages ex vivo. Microarray analysis of retinoic acid treated myoblasts revealed glutathione peroxidase 3 and superoxide dismutase 2, genes encoding antioxidant enzymes, as a potential RA target genes. In this project, aim 1, I propose to extend these results to myoblasts derived from patients with Facioscapulohumeral dystrophy (FSHD), a muscle degenerative disease. Since the team of Winokur and our team found that FSHD myoblasts were highly susceptible to an induced oxidative stress, we postulate that retinoid signalling pathway may stabilise this oxidative stress and protect FSHD myoblasts during the process of transplantation. In aim2, I will inactivate Gpx-3 and SOD2 using shRNA to determine whether SOD-2 and GPx3 mediate the anti-apoptotic effects of retinoic acid. In the aim 3, I will determine whether retinoic acid improves myoblast survival in transplantation assays in animals. Finally, in a more long-term project, aim 4, I will test the hypothesis that vitamin A status (the precursor of retinoic acid) is important for satellite cell survival and expansion in the offspring. Therefore, manipulating cell survival in order to increase the mass of muscle produced from a pool of muscle precursor cells could be an important therapeutic strategy to counteract the course of muscular dystrophy
Sudarsan, Vikram. "Coordinating cell fate signalling during Drosophila development." Thesis, University of Sheffield, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247190.
Full textLim, Sean. "The Relationship Between Metabolic Circumstance and Epigenetic Acetylation in Myoblast Fate and Function." Thesis, Université d'Ottawa / University of Ottawa, 2021. http://hdl.handle.net/10393/42659.
Full textJoshi, Shilpy. "Specific and redundant roles of the Tead family of transcription factors in myogenic differentiation of C2C12 cells and primary myoblasts in vitro." Thesis, Strasbourg, 2015. http://www.theses.fr/2015STRAJ093/document.
Full textThe Tead family of transcription factors recognise the MCAT element found in thepromoters of muscle-specific genes. Genetic analysis of their function in muscledifferentiation has proved elusive likely due to redundancy amongst the family members.We previously used shRNA-mediated silencing to show that loss of Tead4 function resultedin abnormal differentiation characterised by the formation of shortened myotubes. ChIP-chipcoupled to RNA-seq data identified a set of potential target genes that are either activatedor repressed by Tead4 during differentiation. In this study, we have used siRNA-mediatedsilencing to address the role of the Tead factors in primary myoblast differentiation. Incontrast to C2C12 cells where Tead4 plays a critical role, its silencing in primary myoblastshad little effect on their differentiation. Silencing of individual Tead factors had no significanteffect on primary myoblast differentiation, whereas combinatorial silencing led to inhibitionof their differentiation indicating redundancy amongst these factors. In C2C12 cells also,combinatorial Tead silencing had much more potent effects than silencing of Tead4 aloneindicating a contribution of other Teads in this process. By integrating Tead1 and Tead4ChIP-seq data with RNA-seq data following combinatorial Tead1/4 silencing, we identifydistinct but overlapping sets of Tead regulated genes in both C2C12 cells and primarymyoblasts. We also integrated the Tead1/4 ChIP-seq data with public data sets on Myogand Myod1 ChIP-seq and chromatin modifications to identify a series of active regulatoryelements bound by Tead factors alone or together with Myog and Myod1. These datadissect the specific and combinatorial functions of these transcription factors in muscledifferentiation regulatory networks
Beauchamp, Pascal. "The functional role of the RNA-binding protein HuR in the regulation of muscle cell differentiation /." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111586.
Full textLi, Hongmei. "An Investigarion of PAX3 Isoforms (PAX3c, e AND g) in C2c12 Myoblasts." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492771.
Full textRapa, Elizabeth. "Characterisation of the differences in gene expression between rhabdomyosarcoma cells and myoblasts." Thesis, University of Oxford, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.510209.
Full textAlsharidah, Mansour. "Behaviour of human myoblasts in vitro : role of ageing and inflammatory cytokines." Thesis, King's College London (University of London), 2012. https://kclpure.kcl.ac.uk/portal/en/theses/behaviour-of-human-myoblasts-in-vitro-role-of-ageing-and-inflammatory-cytokines(f544ecce-946d-40f1-91a4-fd750aacee11).html.
Full textParolini, D. "CALCIUM HANDLING IN MYOGENIC PROGENITORS AND SKELETAL MYOBLASTS: THE ROLE OF CD20." Doctoral thesis, Università degli Studi di Milano, 2013. http://hdl.handle.net/2434/217445.
Full textBensimon, Maharaj Victoria. "Novel Cell Cycle Regulation of the Transcription Factor p53 and the Kinase c-Abl in Skeletal Myoblast Cultured in Differentiation Media and the Fusion of Myoblasts." Cleveland State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=csu1600275796611256.
Full textLee, Antonio Seung Jin, and n/a. "Myogenic mononucleated cell populations in the developing vertebrate limb in vivo." University of Otago. Department of Anatomy & Structural Biology, 2007. http://adt.otago.ac.nz./public/adt-NZDU20070321.143922.
Full textLu, Lin, and 鹿琳. "Mechanisms involved in the release of ATP from skeletal myoblasts at low pH." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B47323772.
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Physiology
Master
Master of Philosophy
Abbas, Hesham Magdi. "Estrogenic Compounds Protect Rat Cardiac Myoblasts (H9c2 Cells) Against Doxorubicin-Induced Cell Death." VCU Scholars Compass, 2006. http://scholarscompass.vcu.edu/etd_retro/131.
Full textLIBETTI, DEBORA. "ROLE OF NF-YA ISOFORMS IN MOUSE EMBRYONIC STEM CELLS AND MYOBLASTS DIFFERENTIATION." Doctoral thesis, Università degli Studi di Milano, 2020. http://hdl.handle.net/2434/732914.
Full textWang, Kun. "Development of new fibrin-based biomaterials." Electronic Thesis or Diss., Sorbonne université, 2021. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2021SORUS430.pdf.
Full textFibrin is widely used in clinic, but hydrogels formed by this protein generally suffer from poor mechanical property and very rapid biodegradation. To overcome these limitations, we have developed three strategies. The first was to form hybrid materials by adding different sources of silanes. The certain silanes at low concentration could promote fibrillogenesis and lead to stabilization of the gels. At a higher concentration of silane or in the presence of condensed silica, the self-assembly of fibrin is disturbed. The second approach involved the addition of cellulose nanocrystals. Studies under dilute condition shown the adsorption of fibrinogen to the nanocrystals, which facilitates their alignment. Composite hydrogels from high concentrated fibrinogen and nanocrystals showed a notable mechanical reinforcement. In addition, a slowing down of the gelation kinetics have led to new injectable formulations. The third approach was to form the interpenetrate network with type I collagen. Through the process of gelation of fibrinogen under acidic conditions, it was possible to obtain mixed gels but the rheological properties of which were little modified. For the three strategies adopted, the materials have been shown to have the ability to promote proliferation and differentiation of myoblast cells. Interesting results have been obtained in the presence of cellulose nanocrystals. This work has therefore made it possible to elucidate the interactions of fibrin with various inorganic or bio-organic fillers and opens up new perspectives for its application in the biomedical field
Harrison, Adrian Paul. "Regulation of porcine skeletal muscle growth and differentiation." Thesis, University of Cambridge, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360936.
Full textGe, Xiaomei. "Roles of Growth Hormone, Insulin-Like Growth Factor I, and Sh3 and Cysteine Rich Domain 3 in Skeletal Muscle Growth." Diss., Virginia Tech, 2012. http://hdl.handle.net/10919/77332.
Full textPh. D.
Miller, Mathew Gordon. "Integrin-linked kinase 1 (ILK1) is necessary for myogenic differentiation in rat L6 myoblasts." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0018/MQ54079.pdf.
Full textWhitney, Marsha L. "Molecular control of skeletal myoblast proliferation for cardiac repair /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/8008.
Full textTalarico, Alexander Phillip. "Myf5 Does Not Induce Apoptosis In Skeletal Myoblasts But Is Regulated By Oncogenic Ras Expression." Cleveland State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=csu1234402667.
Full textCogan, John G. "DNA-binding proteins regulating vascular smooth muscle alpha-actin gene expression in myoblasts and fibroblasts /." The Ohio State University, 1995. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487863429091115.
Full textEngelbrecht, Lize. "Grape seed extract affects adhesion competence and maturation of primary isolated rat myoblasts after contusion injury." Stellenbosch : Stellenbosch University, 2013. http://hdl.handle.net/10019.1/80380.
Full textENGLISH ABSTRACT: Contusion injuries cause significant muscle damage, activating a series of cellular events. Satellite cells (SC), the key role players in muscle regeneration, are activated to proliferate and develop into mature myoblasts, which could fuse to form new myotubes or to repair damaged fibres. Evidence suggests that anti-oxidants, such as those found in grape seed extract (GSE), enhance repair, but their effect on SCs is still unclear. This study aimed to harvest and culture primary rat myoblasts to investigate the effect of chronic in vivo GSE supplementation on SCs following a standardised crush injury. Using a modified pre-plate technique, myoblasts were harvested from rat muscle and then compared with the immortal C2C12 cell line for proliferation and differentiation competence. Several media options were compared: i) DMEM with or without L-glutamine, ii) Ham‘s F10 or iii) DMEM with L-glutamine and Ham‘s F10 combined. Primary myoblasts proliferated and differentiated at a much slower rate than C2C12 cells. The combined media was selected for further use. To investigate the effects of GSE on the recovery, rats were supplemented daily with GSE or placebo 14 days prior to a standardised mass-drop crush injury to the gastrocnemius. SCs were isolated and cultured from uninjured (NI, baseline) and from injured rats 4 hours (4h), 3 days (3d) or 14 days (14d) post-injury. Expression of myogenic proteins Pax7, M-cadherin, MyoD, CD56, desmin and CD34 was determined by flow cytometry. Myoblasts were sorted according to their CD56 and CD34 expression and three sub-sets were collected and re-cultured, namely CD56+/CD34-, CD56-/CD34+ and CD56+/CD34+. After 24 hours, sorted cells were stained for desmin expression. Pax7, M-cadherin and MyoD were present in 100% of isolated cells from all groups confirming their myogenic SC identity. For all groups, desmin was expressed only in ~80% of SCs. Lower adhesion competency in GSE supplemented groups resulted in lower yield obtained for culturing. Expression of CD56 increased significantly 3d post-injury in the placebo group. In contrast, with GSE, CD56 already increased 4h post-injury and decreased again 3d post-injury. Although CD34 expression did not differ dramatically, expression pattern resembled that of CD56. Immunocytochemistry revealed a range in morphology and desmin expression of sorted myoblasts. More myoblasts with high desmin expression were observed in the two CD56+ sub-sets (irrespective of CD34 expression), indicating that CD56 is still expressed in more mature myoblasts. Flow cytometry revealed a population of myoblasts expressing particularly high levels of desmin, primarily in the non-injured baseline GSE group. We hypothesise that this result is an indication of preparedness of myoblasts to respond earlier to injury, enabling quicker repair. This cell population with high desmin content is restored in skeletal muscle after repair (14d), only when supplemented with GSE. In conclusion, GSE attenuated adhesion competence of primary myoblasts in culture, but resulted in earlier maturation of SCs, possibly due to baseline preparedness of myoblasts in uninjured muscle for a quick response. Both reduced adhesion competence and early progression of myoblasts could enhance wound healing in skeletal muscle.
AFRIKAANSE OPSOMMING: Kneuswonde veroorsaak aansienlike skade aan skeletspier, wat ‘n reeks sellulêre prosesse in werking stel. Satellietselle, die hoofrolspelers tydens spierregenerasie, vermenigvuldig en ontwikkel tot volwasse mioblaste, wat saamsmelt om nuwe spiervesels te vorm. Antioksidante, soos die wat in druiwepit-ekstrak voorkom, bespoedig herstel, maar hul uitwerking op satellietselle is steeds onduidelik. Die doel van hierdie studie was om mioblaste uit rotspiere te isoleer en te kweek om die effek van langdurige in vivo aanvulling van druiwepit-ekstrak op satellietselle na ‘n kneusbesering te bepaal. 'n Aangepaste protokol is gebruik om primêre mioblaste te isoleer, wat daarna met C2C12 selle, ten opsigte van hul vermenigvuldigings- en differensiasievermoë vergelyk is. Verskeie groeimedia is gebruik: i) DMEM met of sonder L-glutamien, ii) Ham F10 en iii) ‘n kombinasie van DMEM, L-glutamien en Ham F10. Primêre mioblaste het stadiger vermenigvuldig en gedifferensieer as C2C12 selle. Die gekombineerde medium is vir verdere gebruik gekies. Om die uitwerking van druiwepit-ekstrak op spierherstel te ondersoek, is rotte vir 14 dae onderwerp aan daaglikse aanvullings van druiwepit-ekstrak of placebo voor ‘n gestandardiseerde kneusbesering aan die gastrocnemius. Satellietselle is geïsoleer vanuit onbeseerde spier (basiskontrole) en vanuit beseerde spier 4 ure (4h), 3 dae (3d) en 14 dae (14d) na die besering. Die uitdrukking van spierverwante proteïene Pax7, M-cadherin, MyoD, CD56, desmin en CD34 is vasgestel met 'n vloeisitometer. Mioblaste is daarna gesorteer op grond van hul CD56- en CD34-uitdrukking. Drie sub-groepe is versamel en verder gekweek, nl. CD56+/CD34-, CD56-/CD34+ en CD56+/CD34+. Na 24 uur is gesorteerde selle gekleur om desmin-uitdrukking te bepaal. Pax7, M-cadherin en MyoD is deur 100% satellietselle in alle groepe uitgedruk, wat hul spierverwante identiteit bevestig, alhoewel slegs 80% selle in alle groepe desmin uitgedruk. Druiwepit-ekstrak het die vermoë van selle om aan plate te heg onderdruk, wat gelei het tot ‘n laer opbrengs van mioblaste. Drie dae na die besering in die placebo groep het die CD56-uitdrukking beduidend toegeneem. In teenstelling hiermee het CD56-uitdrukking in die druiwepit-ekstrak groep 4 ure na die besering beduidend toegeneem en weer afgeneem na 3 dae. Hoewel daar nie sulke dramatiese verskille was tussen groepe ten opsigte van CD34-uitdrukking nie, was daar ‘n soortgelyke tendens as vir CD56-uitdrukking. Immunositochemie het ‘n verskeidenheid van morfologieë en variërende desminvlakke in gesorteerde mioblaste blootgestel. In die twee CD56+ groepe is meer mioblaste wat hoë desmin vlakke uitdruk gevind, wat aandui dat CD56 uitgedruk word deur meer volwasse mioblaste, ongeag van CD34-uitdrukking. Tydens vloeisitometrie is ‘n populasie selle wat hoë desminvlakke uitdruk, hoofsaaklik in die onbeseerde en 14d druiwepit-ekstrak groepe gevind. Dit is ‘n aanduiding dat sommige mioblaste voorbereid is om na 'n besering vinniger te reageer. Na die herstelproses word hierdie groep selle hernu in die teenwoordigheid van druiwepit-ekstrak-aanvulling. Die resultate het gevolglik daartoe gelei dat druiwepit-ekstrak die hegtingsvemoë van mioblaste verlaag, maar dat die aanvulling in vivo tot vroeër ontwikkeling van mioblaste lei, waarskynlik deur satellietselle voor te berei vir 'n vinnige respons na ‘n besering. Beide die onderdrukking van aanhegting aan kultuurplate en die vroeë ontwikkeling van mioblaste, kan die herstel van die skeletspier verbeter.
NRF and the Harry Crossley bursary for funding
Horner, Ellias. "Six1 Is Important for Myoblast Proliferation Through Direct Regulation of Ccnd1." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/34186.
Full textEl, Khatib Nour. "Identification des mécanismes moléculaires et physiopathologiques impliqués dans la dystrophie facioscapulohumérale." Thesis, Montpellier, 2016. http://www.theses.fr/2016MONTT039.
Full textFacioscapulohumeral muscular dystrophy (FSHD) is an autosomal dominant disease, characterized by progressive weakness and atrophy of specific skeletal muscles. FSHD is linked to an inefficient repeat-mediated epigenetic repression of the D4Z4 macrosatellite repeat array on chromosome 4, resulting in the unappropriated expression in skeletal muscle of the double homeobox 4 (DUX4) retrogene. DUX4 overexpression leads to atrophic myotubes phenotype and dysregulation of antioxidant genes. Despite major progress in the understanding of the genetic locus, exact mechanisms that lead to FSHD defects are not completely understood and no curative treatment is available. However, several lines of evidence have proposed oxidative stress and myogenesis defect as the major biological processes affected in FSHD. Recently, we characterized oxidative stress in skeletal muscle biopsies and blood samples from patients with FSHD. We demonstrated that oxidative stress is associated with reduced physical performance in patients with FSHD and that antioxidants adapted strategy was effective to reduce oxidative stress and maintain muscle functions. Furthermore, satellite cell-derived myoblasts from these patients were more susceptible to pro-oxidant agents than control myoblasts and showed a defect in differentiation. The originality of this project relies on creating a synergy between basic and clinical research. The major goal of this work is to identify molecular mechanisms involved in FSHD oxidative stress in order to identify therapeutic approaches.Using in vitro cell model of FSHD, recently developed and optimized in our team, we demonstrate the presence of oxidative stress in FSHD primary myoblast cultures that corroborates previous observations at systemic and muscular levels. Furthermore, treatments with different pro-oxidant agents (paraquat and hydrogen peroxide) have a differential effect on the expression of antioxidant enzymes compared to controls, suggesting a defect in the oxidative stress adaptive response in FSHD myoblasts.Furthermore, in order to improve rehabilitation procedures for patients affected with FSHD, we proposed to investigate the feasibility, safety, and effectiveness of neuromuscular electrostimulation (NMES) strength training to counteract quadriceps muscle weakness in these patients. This ongoing study appears to be a promising rehabilitation strategy and shows no adverse effect for patients with FSHD
Streppa, Laura. "Characterizing mechanical properties of living C2C12 myoblasts with single cell indentation experiments : application to Duchenne muscular dystrophy." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSEN008/document.
Full textThis interdisciplinary thesis was dedicated to the atomic force microscopy (AFM) characterization of the mechanical properties of myoblasts (murine and human) and myotubes (murine). We reported that the mechanical properties of these cells were modified when their actin cytoskeleton (CSK) dynamics was inhibited or altered. Recording single AFM force indentation curves, we showed that adherent layers of myoblasts and myotubes introduced on the AFM cantilever an extra hydrodynamic drag as compared to a solid wall. This phenomenon was dependent on the cantilever scan speed and not negligible even at low scan velocities (1μm/s). We observed that the mechanical properties of the muscle precursor cells became non-linear (plastic behaviour) for large local deformations (>1μm) and that they varied depending on the state, type and environment of the cells. Combining AFM experiments, viscoelastic modeling and multi-scale analyzing methods based on the wavelet transform, we illustrated the variability of the mechanical responses of these cells (from viscoelastic to viscoplastic). Through AFM force indentation curves analysis, morpho-structural imaging (DIC, fluorescence microscopy) and pharmacological treatments, we enlightened the important role of active (ATP-dependent) processes in myoblast mechanics, focusing especially on those related to the molecular motors (myosin II) coupled to the actin filaments. In particular, we showed that the perinuclear actin stress fibers could exhibit some abrupt remodelling events (ruptures), which are characteristic of the ability of these cells to tense their CSK. Finally, we showed that this approach can be generalized to some human clinical cases, namely primary human myoblasts from healthy donors and patients affected by Duchenne muscular dystrophy, paving the way for broader studies on different cell types and diseases
Gu, Jinmo. "An NF-kappaB - EphrinA5 - Dependent Communication between NG2+ Interstitial Cells and Myoblasts Promotes Muscle Growth in Neonates." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1458152802.
Full textChung, Kevin. "Augmentation of alignment and differentiation in C2C12 skeletal myoblasts through use of nano-to-microscale biochemical patterns." Diss., [La Jolla] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p1467778.
Full textTitle from first page of PDF file (viewed September 15, 2009). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 71-76).
Powell, Gareth Thomas. "The zebrafish homologues of JAM-B and JAM-C are essential for myoblast fusion." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609399.
Full textWilliams, Drew. "Identification of a protective role for mitochondrial deoxyuridine triphosphate nucleotidohydrolase against oxidative stress-induced apoptosis in mouse myoblasts." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=95249.
Full textL'ischémie cardiaque provoque la mort des cellules myocardiques en partie en raison de l'apoptose. Des thérapies géniques basées sur l'introduction directe des gènes anti-apoptotiques dans l'infarctus du myocarde sont actuellement en train d'êtres évalués à leur capacité de limiter la mort cellulaire programmée après une crise cardiaque. En dépit du progrès de la génétique humaine, le répertoire complet des gènes cardiaques anti-apoptotiques reste peu connu. Afin d'accroître notre compréhension de l'apoptose cardiaque, il est essentiel d'identifier et caractériser le répertoire des gènes anti-apoptotiques dans le cur humain. En effet, il a été prouvé que le mécanisme moleculaire de l'apoptose est conservé le long de l'évolution entre les métazoaires et la levure. En examinant les effets anti-apoptotiques d'une banque d'ADNc cardiaque dans des cellules de levure exprimant conditionnellement le pro-apoptotique Bax des mammifères, notre laboratoire a identifié plus de 60 clones capables de prévenir les effets délétères de Bax chez la levure. Le présent travail montre également les effets potentiels anti-apoptotiques de ces gènes chez des cellules mammaliennes. Nos resulats ont prouvé aussi que la protéine désoxyuridine triphosphate nucleotidohydrolase (dUTPase) a un effet anti-apoptotique en prévenant le processus apoptotique induite par le stress oxydatif dans les myoblastes mammaliennes C2C12. Ces résultats servent à illustrer les similitudes entre le processus anti-apoptotique chez la levure et les cellules humaines et, indiquent que la dUTPase pourrait avoir un intérêt thérapeutique afin de limiter la mort cellulaire dans les infarctus cardiaques. fr
Penton, Christopher M., Vasudeo Badarinarayana, Joy Prisco, Elaine Powers, Mark Pincus, Ronald E. Allen, and Paul R. August. "Laminin 521 maintains differentiation potential of mouse and human satellite cell-derived myoblasts during long-term culture expansion." BIOMED CENTRAL LTD, 2016. http://hdl.handle.net/10150/622727.
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