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Dissertations / Theses on the topic 'Mouse skeletal muscle'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

ZHOU, TINGYANG ZHOU. "Molecular Roles of ROS in Mouse Respiratory Skeletal Muscle." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1531848449464785.

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2

Kanaan, Georges. "Mitochondrial Dysfunction: From Mouse Myotubes to Human Cardiomyocytes." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/37582.

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Mitochondrial dysfunction is a common feature in a wide range of disorders and diseases from obesity, diabetes, cancer to cardiovascular diseases. The overall goal of my doctoral research has been to investigate mitochondrial metabolic dysfunction in skeletal and cardiac muscles in the context of chronic disease development. Perinatal nutrition is well known to affect risk for insulin resistance, obesity, and cardiovascular disease during adulthood. The underlying mechanisms however, are poorly understood. Previous research from our lab showed that the in utero maternal undernutrition mouse

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3

Zhao, Wanfeng. "Development and differentiation of oesophageal muscle in mouse." Thesis, Royal Veterinary College (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367759.

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4

Williams, James Lyndon. "Cellular and molecular mechanisms of angiogenesis in mouse skeletal muscle." Thesis, University of Birmingham, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433638.

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5

McArdle, Anne. "Mechanisms skeletal muscle damage in the dystrophin-deficient MDX mouse." Thesis, University of Liverpool, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385144.

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6

Shah, Sameer Bhrugu. "Structural and functional roles of desmin in mouse skeletal muscle /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2002. http://wwwlib.umi.com/cr/ucsd/fullcit?p3055800.

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7

Amoasii, Leonela. "In vivo functional studies of myotubularin in mouse skeletal muscle." Thesis, Strasbourg, 2012. http://www.theses.fr/2012STRAJ037.

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La Myotubularine (MTM1) est une 3-phosphatase à phosphoinositides (PI) mutée dans la myopathie centronucléaire liée au chromosome X (XLCNM), caractérisée par une faiblesse musculaire et un positionnement anormal des noyaux dans les fibres musculaires. MTM1 définit une grande famille de phosphatases, exprimées dans tous les tissus, et qui englobent des phosphatases catalytiquement actives et inactives. Les myotubularines actives dephosphorylent le phosphatidylinositol 3 monophosphate [PtdIns3P] et le 3,5-bisphosphate [PtdIns(3,5)P2] en PtdIns et PtdIns5P, respectivement. Le rôle de MTM1 et son

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8

Voelker, Kevin Andrew. "Leucine and exercise improve skeletal muscle function in the mdx mouse." Diss., Virginia Tech, 2010. http://hdl.handle.net/10919/37303.

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Duchene muscular dystrophy (DMD) is a lethal X-linked disease that afflicts approximately 1 in 3500 newborn males. Boys with DMD will become progressively weaker causing wheelchair dependence by their early teens and death by their mid to late twenties. Currently there is no cure for DMD, the exact mechanism of disease action remains elusive, and treatments to improve quality of life are limited. Two areas of DMD research that could begin to fill this void and provide simple, cost effective therapy aimed to improve quality of life are neutriceutical and exercise therapies. We hypothesized

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9

Ho, Tiffany. "Consequences of IRF2BP2 Loss of Function in Mouse Development and Skeletal Muscle Regeneration." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/34611.

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IRF2BP2 is a corepressor of IRF2, a transcription factor involved in the immune response. IRF2BP2 is also a coactivator of the VGLL4/TEAD4 complex in muscle. Given its functional duality, we asked how IRF2BP2 deletion would affect mouse development and adult muscle regeneration. Most Irf2bp2-/- mice die prior to birth, those that survive develop lymphoma in adulthood. Microarray profiling of Irf2bp2 knockout liver, heart, and skeletal muscle revealed a shared program of upregulated genes involved in inflammation and immunity. The function of IRF2BP2 in adult skeletal muscle recovery from car

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10

Fisher, Ivan Brian. "Glucocorticoid-induced changes in the skeletal muscle of the dystrophic MDX mouse." Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407223.

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11

Leyland, Deborah Mary. "The expression of glycogen phosphorylase in normal and abnormal mouse skeletal muscle." Thesis, University of Liverpool, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.237523.

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12

Chen, Ting. "LKB1 Regulation of High-Fat Diet-induced Adaptation in Mouse Skeletal Muscle." BYU ScholarsArchive, 2017. https://scholarsarchive.byu.edu/etd/6682.

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Ad libitum high-fat diet (HFD)-induced obesity leads to insulin resistance in skeletal muscle, altered gene expression, and altered growth signaling, all of which contributes to pathological changes in metabolism. Liver kinase B1 (LKB1) is an important metabolism regulator. The purpose of this dissertation was to understand how knocking out LKB1 influences HFD induced adaptations in mouse skeletal muscle. To do so, control and skeletal muscle LKB1 knock-out (LKB1-KO) mice were put on either standard diet (STD) or HFD for 1 week or 14 weeks, or put on the HFD for 14 weeks and then switched to S

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13

Brathwaite, Ricky Christopher. "Mechanical Stretch and Electrical Stimulation in Mouse Skeletal Muscle in Vivo: Initiation of Hypertrophic Signaling." Thesis, Available online, Georgia Institute of Technology, 2004:, 2004. http://etd.gatech.edu/theses/available/etd-07092004-171152/unrestricted/Brathwaite%5FRicky%5FC%5F200407%5FMS.pdf.

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Thesis (M.S.)--School of Bioengineering, Georgia Institute of Technology, 2005. Directed by Thomas Burkholder.<br>Thomas Burkholder, Committee Chair ; Cheng Zhu, Committee Member ; Grace Pavlath, Committee Member. Includes bibliographical references.

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14

Mänttäri, S. (Satu). "Dihydropyridine receptors in skeletal muscle with comparative reference to muscle development and exercise in mouse and salmon." Doctoral thesis, University of Oulu, 2005. http://urn.fi/urn:isbn:9514277201.

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Abstract The dihydropyridine receptor (DHPR) in the skeletal muscle plasma membrane functions as a voltage sensor for excitation-contraction coupling. In the present work the expression and special features of DHPR were studied under various conditions. In order to localize and visualize the DHPRs, a method using fluorophore-conjugated dihydropyridine molecules as a probe was developed. In addition, different laboratory assays and electrophysiological measurements were used to study the expression of the myofibrillar proteins, force production of the muscle and conduction velocity of the plasm

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15

Gali, Ramamoorthy Thanuja. "Role of PGC-1β and TIF2 co-regulators in mouse skeletal muscle function". Thesis, Strasbourg, 2013. http://www.theses.fr/2013STRAJ095.

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Le muscle squelettique (MS) est un tissu métabolique important. L'objectif de ma thèse était de caractériser le rôle des corégulateurs de la transcription, PGC-1β (transcriptional coactivator peroxisome proliferator-activated receptor-gammacoactivator 1beta) et TIF2 (Transcriptional Intermediary Factor 2) dans ce tissu. Mon travail a démontré que PGC-1β limite le stress oxydatif est crucial dans le maintien de la structure et de la fonction mitochondriale, via le contrôle de l’expression de gènes impliqués dans les voies de signalisation liées à l’énergie, à la dynamique mitochondriale et à la

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16

Smith, Cody Don. "Characterization of the LKB1-MO25-STRAD AMPKK Complex in Adult Mouse Skeletal Muscle." BYU ScholarsArchive, 2010. https://scholarsarchive.byu.edu/etd/2803.

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In liver tissue, the AMP-activated protein kinase kinase (AMPKK) complex was identified as the association of LKB1, MO25α/β, and STRADα/β proteins; however, this complex has yet to be characterized in skeletal muscle. In this report, we demonstrate the expression of the LKB1-MO25-STRAD AMPKK complex in adult skeletal muscle, confirm the absence of mRNA splice variants, and report the relative mRNA expression levels of these complex-forming proteins. To facilitate this characterization we used control (ctrl) and muscle-specific LKB1 knockout (LKB1-/-) mice. LKB1 detection in untreated ctrl and

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17

Farshidfar, Farnaz. "Effects of creatine supplementation on muscle metabolism in an Alzheimer mouse model." IOS Press, 2016. http://hdl.handle.net/1993/31212.

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Alzheimer’s disease (AD), the most common form of dementia in the elderly, is a global issue affecting about 24 million individuals. Because AD is a systemic pathology, dementia is not the only leading factor contributing to loss of independence in AD patients. AD may also impair skeletal muscle metabolism and function. Creatine (CR) supplementation may enhance skeletal muscle hypertrophy/mass and function in sarcopenia and muscular dystrophies, but has yet to be studied in AD. This study examined the effect of oral CR on muscle metabolism in a triple-transgenic (3xTg) AD mouse model. Twenty-f

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18

Hesse, Erik. "Effects of Carbohydrate Availability on Fatigue and Fatigue Pre-Conditioning in Mouse FDB Muscle." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/39528.

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To prevent damaging ATP depletion during periods of intense activity‚ intrinsic mechanisms within skeletal muscle are activated and lead to myoprotection; a process known as muscle fatigue. It has been proposed that the primary mechanism of fatigue is a submaximal sarcoplasmic reticulum Ca2+ release and decreased force generation‚ however‚ what triggers this mechanism remains controversial. It is possible that glycogen may act as a trigger as studies have repeatedly shown a direct correlation between glycogen content at the beginning of activity and time to fatigue. In previous studies‚ a fati

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19

Thomas, Lisa Beth. "EFFECT OF DYSTROPHIN DEFICIENCY ON SELECTED INTRINSIC LARYNGEAL MUSCLES OF THE mdx MOUSE." UKnowledge, 2008. http://uknowledge.uky.edu/gradschool_diss/591.

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The intrinsic laryngeal muscles are recognized as a highly specialized allotype of skeletal muscle. To date, much of the research examining the properties of this muscle group has been conducted on 2 primary muscles: the thyroarytenoid and posterior cricoarytenoid. Consequently, it is unknown whether the remaining intrinsic laryngeal muscles evidence this highly refined phenotype or if they retain a phenotype more similar to prototypical skeletal muscle. The purpose of this study was to further define the biologic properties of the interarytenoid (IA) and cricothyroid (CT) muscles of the laryn

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20

Wang, Jennifer Jin. "Gene expression and isoform structure-function relationship of mouse fast skeletal muscle troponin T." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq24706.pdf.

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21

Russell, Paul. "Membrane properties and calcium ion activity in skeletal muscle fibres of the dystrophic mouse." Thesis, University of Central Lancashire, 1993. http://clok.uclan.ac.uk/20630/.

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The ReJI29 murine model of muscular dystrophy was employed to investigate the properties of skeletal muscle plasmalemma and calcium ion movements during muscle wastage, with the intention of determining the route of calcium influx, and the efficacy of calcium ion blockers in preventing this influx. Electrophysiological parameters (Resting membrane potential [RMP] and input resistance) reached adult magnitude in normal soleus and extensor digitorum longus (EDL) by 4 weeks and 3 weeks respectively. Electrophysiological parameters in dystrophic soleus developed in a similar maimer to normal muscl

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22

Scott, Kyle. "Loss of KATP Channel Activity in Mouse FDB Leads to an Impairment in Energy Metabolism During Fatigue." Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/22839.

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Recently, it has been postulated that fatigue is a mechanism to protect the muscle fiber from deleterious ATP depletion and cell death. The ATP-sensitive potassium (KATP) channel is believed to play a major role in this mechanism. Under metabolic stress, the channels open, reducing membrane excitability, Ca2+ release and force production. This alleviates energy demand within the fiber, as activation of the channel reduces ATP consumption from cellular ATPases. Loss of KATP channel activity during fatigue results in excessive intracellular Ca2+ ([Ca2+]i) levels, likely entering the fiber throug

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23

Struthers, Kyle Remington. "ISCHEMIA IMPAIRS VASODILATION IN SKELETAL MUSCLE RESISTANCE ARTERY." DigitalCommons@CalPoly, 2011. https://digitalcommons.calpoly.edu/theses/546.

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Functional vasodilation in arterioles is impaired with chronic ischemia. We sought to examine the impact of chronic ischemia and age on skeletal muscle resistance artery function. To examine the impact of chronic ischemia, the femoral artery was resected from young (2-3mo) and adult (6-7mo) mice and the profunda femoris artery diameter was measured at rest and following gracilis muscle contraction 14 days later using intravital microscopy. Functional vasodilation was significantly impaired in ischemic mice (14.4±4.6% vs. 137.8±14.3%, p<0.0001 n=8) and non-ischemic adult mice (103.0±9.4% vs. 13

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24

Gainer, Thomas Gregory. "Immune Response Markers are Prevalent in the mRNA Expression Profile of Maturing Dystrophic Murine Skeletal Muscle." Thesis, Virginia Tech, 2005. http://hdl.handle.net/10919/33263.

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Duchenne muscular dystrophy (DMD) is a severe and fatal muscle wasting disease characterized by a high mutation rate in the gene that encodes the membrane-associated protein dystrophin that results in absence of expressed protein. Although the primary genetic defect for DMD is known, the mechanisms that initiate the onset of DMD are not currently understood. This study tested the hypothesis that pathophysiological processes involved in DMD could be identified by the global expression of mRNA in maturing dystrophin- and utrophin-deficient mouse (mdx:utrn-/-) muscles. Two potential dystrophic o

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25

Vinnakota, Kalyan Chakravarthy. "pH dynamics, glycogenolysis and phosphoenergetics in isolated cell free reconstituted systems and in mouse skeletal muscle /." Thesis, Connect to this title online; UW restricted, 2006. http://hdl.handle.net/1773/8034.

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26

Claus, Carol L. "Inhibition of troponin C expression in C¦2C¦12 mouse skeletal muscle cells by an antisense oligodeoxyribonucleotide." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0021/MQ47318.pdf.

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27

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.

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Thesis (Ph. D.)--West Virginia University, 2001.<br>Title from document title page. Document formatted into pages; contains ix, 109 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 88-104).

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28

Bookless, Connie. "The influence of sex hormones on cardiac and skeletal muscle function in the MDX mouse model of Duchenne Muscular Dystrophy." University of Southern Queensland, Faculty of Sciences, 2006. http://eprints.usq.edu.au/archive/00003582/.

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[Abstract]: Duchenne Muscular Dystrophy (DMD) is a fatal recessive genetic human disease affecting one in 3500 live male births. DMD is progressive, there is no cure, and patients typically die of respiratory or cardiac failure intheir second decade of life. Clinical disease symptoms are exacerbated at the onset of puberty and the physiological basis of this is unknown. The mdx mouse is the preferred experimental animal model of DMD, although aspectsof the model remain poorly understood. This dissertation characterises physiological and histological features of the dystrophic mdx mouse in resp

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29

Latvanlehto, A. (Anne). "Type XIII collagen:organization of the mouse gene, generation of three genetically engineered mouse lines by homologous recombination, and biochemical studies on the molecular properties of the type XIII collagen protein." Doctoral thesis, University of Oulu, 2004. http://urn.fi/urn:isbn:9514275934.

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Abstract Genomic clones covering the entire mouse type XIII collagen gene (Col13a1) were isolated, and the complete exon-intron organization was characterized. The gene was found to be about 135 kb in size and to locate in the mouse chromosome 10. Comparison of gene structures and promoter regions between man and mouse indicated high conservation between the two species. In order to understand the biological function of type XIII collagen, a mouse line that expresses type XIII collagen with replacement of the cytosolic and transmembrane domains by a short, non-descript sequence was generated

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30

Woolf, Peter James. "Cardiac calcium handling in the mouse model of Duchenne Muscular Dystrophy." University of Southern Queensland, Faculty of Sciences, 2003. http://eprints.usq.edu.au/archive/00001525/.

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The dystrophinopathies are a group of disorders characterised by cellular absence of the membrane stabilising protein, dystrophin. Duchenne muscular dystrophy is the most severe disorder clinically. The deficiency of dystrophin, in the muscular dystrophy X-linked (mdx) mouse causes an elevation in intracellular calcium in cardiac myocytes. Potential mechanisms contributing to increased calcium include enhanced influx, sarcoplasmic reticular calcium release and\or reduced sequestration or sarcolemmal efflux. This dissertation examined the potential mechanisms that may contribute to an intracell

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31

Do, Andrew. "The Effects of Growth Hormone and Thyroxine Treatment on the Insulin Signaling of Female Ames Dwarf Mouse Skeletal Muscle Tissue." Honors in the Major Thesis, University of Central Florida, 2013. http://digital.library.ucf.edu/cdm/ref/collection/ETH/id/941.

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Ames dwarf (df/df) mice are deficient in anterior pituitary hormones: growth hormone (GH), thyroid stimulating hormone (TSH), and prolactin (PRL) due to a spontaneous, homozygous mutation of prop1[superscript df] gene. These dwarf mice exhibit characteristics such as delayed growth and development coupled with delayed aging, increased lifespan, overall increased insulin sensitivity, as well as resistance to certain diseases and cancers. The mutant mice possess low blood glucose, low serum insulin, and lower body temperature. Their enhanced longevity (about 40-60% longer lifespan than normal mi

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32

Julien, Anaïs. "Rôle du muscle au cours de la régénération osseuse : étude fonctionnelle de la contribution cellulaire et impact des traumatismes musculosquelettiques Periosteum contains skeletal stem cells with high bone regenerative potential controlled by Periostin Role of muscle stem cells during skeletal regeneration Muscle-‐derived profibrotic progenitors impair bone healing in musculoskeletal trauma." Thesis, Sorbonne Paris Cité, 2018. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=2170&f=15825.

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33

Kosterina, Natalia. "Muscular force production during non-isometric contractions : towards numerical muscle modeling /." Licentiate thesis, Stockholm : Skolan för teknikvetenskap, Kungliga Tekniska högskolan, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-10672.

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34

Haramizu, Satoshi. "Verification of the senescence-accelerated mouse as a model of aging-related physical performance decline and beneficial effects of catechins on physical performance." Kyoto University, 2014. http://hdl.handle.net/2433/193549.

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35

Desypris, George. "The role of the motor neuron in the maintenance of contractile properties and myosin expression in skeletal muscle of the mouse." Thesis, University of Ottawa (Canada), 1992. http://hdl.handle.net/10393/7801.

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This study was undertaken to further elucidate the relative contributions of activity and myotrophic influences in maintaining certain contractile and histochemical properties of skeletal muscle. Four month old male C57BL mice were subjected to unilateral hindlimb denervation for either 10 days of 6 weeks. The denervation-induced changes in contractile properties as well as fiber-type distribution and myosin isoforms of the soleus (SOL) and extensor digitorum longus (EDL) muscles were investigated. To determine whether the denervation-induced alterations seen were due to withdrawal of putative

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36

Burke, Steven Russell Alan. "Assessment of In Vivo Muscle Force in the R6/2 Mouse Model of Huntington's Disease Using Newly Designed Force Rig." Wright State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=wright1610360658382723.

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37

Richter, Jennifer Jo. "Gene expression during skeletal muscle development affect of in ovo IGF-1 administration on broiler embryogenesis and postnatal myogenesis in the mouse /." Morgantown, W. Va. : [West Virginia University Libraries], 2002. http://etd.wvu.edu/templates/showETD.cfm?recnum=2517.

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Thesis (Ph. D.)--West Virginia University, 2002.<br>Title from document title page. Document formatted into pages; contains xii, 118 p. : ill. (some col.). Includes abstract. Includes bibliographical references.

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38

Hauck, James Spencer. "Mineralocorticoid Receptor Signaling in Acute and Chronic Muscle Injury." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1565089935933727.

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39

Sperringer, Justin Edward. "Chronic Dietary Supplementation of Branched-Chain Amino Acids Does Not Attenuate Muscle Torque Loss in a Mouse Model of Duchenne Muscular Dystrophy." Diss., Virginia Tech, 2019. http://hdl.handle.net/10919/93577.

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Duchenne Muscular Dystrophy (DMD) is an X-linked recessive, progressive muscle-wasting disease characterized by mutations in the dystrophin gene. Duchenne muscular dystrophy is the most common and most severe form of inherited muscle diseases, with an incidence of 1 in 3,500 male births1,2. Mutations in the dystrophin gene result in non-functional dystrophin or the complete absence of the protein dystrophin, resulting in necrosis and fibrosis in the muscle, loss of ambulation, cardiomyopathies, inadequate or failure of respiratory function, and decreased lifespan. Although there has been littl

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40

Croze, Marine. "Study of the insulin-sensitizing effect of myo-inositol in mouse : Evaluation of the nutritional interest of a myo-inositol supplementation." Thesis, Lyon, INSA, 2013. http://www.theses.fr/2013ISAL0139/document.

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Le diabète de type 2 constitue un enjeu majeur de santé publique et la mise au point de stratégies insulino-sensibilisantes est un défi permanent pour les scientifiques. Cette étude montre qu’un traitement chronique au myo-inositol améliore la sensibilité à l’insuline, réduit l’accrétion adipeuse et augmente la capacité de survie des souris au paraquat. L’effet insulino-sensibilisant semble passer, au moins en partie, par un effet direct sur la voie de signalisation insuline (éventuelle implication de médiateurs de type inositol glycanes). La diminution de l’accrétion adipeuse semble, quant à

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41

Watanabe, Miki. "Development of DNA aptamer as a HMGA inhibitor for cancer therapy and NMR-based metabonomics studies in human/mouse cell lines." Miami University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=miami1322753081.

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42

Nakano, Masako. "α2 isoform-specific activation of 5' adenosine monophosphate-activated protein kinase by 5-aminoimidazole-4-carboxamide-1-β-D-ribonucleoside at a physiological level activates glucose transport and increases glucose transporter 4 in mouse skeletal muscle". Kyoto University, 2008. http://hdl.handle.net/2433/135919.

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43

Cerveró, Cebrià Clàudia. "Atròfia muscular espinal: mecanismes patogènics i estratègies terapèutiques en models murins de la malaltia." Doctoral thesis, Universitat de Lleida, 2016. http://hdl.handle.net/10803/399028.

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L’atròfia muscular espinal (AME) és una malaltia genètica que cursa amb mort de motoneurones espinals i atròfia muscular. S’ha caracteritzat un model murí d’AME, l’Smn2B/-, amb una clínica menys severa que la mostrada per altres models més extensament utilitzats. S’ha evidenciat una alteració multisistèmica acompanyant a la clàssicament coneguda del sistema neuromuscular. S’han estudiat les sinapsis colinèrgiques tipus C en l’AME i testat el paper del PRE-084 (agonista del receptor sigma-1 present en aquestes) com a possible teràpia en els models SMNΔ7 i Smn2B/-. Malgrat no conferir neuropro

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44

Parente, Alexis. "Dualités fonctionnelles de GASP-1 et GASP-2, deux protéines multi-domaines antagonistes de la myostatine." Thesis, Limoges, 2019. http://www.theses.fr/2019LIMO0028.

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GASP-1 et GASP-2 sont deux protéines très proches structuralement caractérisées par plusieurs modules inhibiteurs de protéases et identifiés comme des inhibiteurs de plusieurs membres de la famille TGF-ß tel que la myostatine ou GDF-11, respectivement régulateurs négatifs de la myogenèse et de l’ostéogénèse. Malgré l’organisation structurale commune des protéines GASPs, leurs profils d’expression différents laissent supposer des rôles physiologiques distincts. C’est pourquoi, nous avons généré des modèles souris Tg(Gasp-1) et Tg(Gasp-2) surexprimant Gasp-1 ou Gasp-2 afin de mieux appréhender l

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45

Dudley, Roy W. R. "Oxidativenitrosative stress, contractile dysfunction and gene replacement studies in skeletal muscles in mouse models of neuromuscular disease." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85905.

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Amyotrophic lateral sclerosis (ALS) and Duchenne muscular dystrophy (DMD) are two fatal neuromuscular disorders for which there is no effective treatment. Furthermore, the exact pathogenic mechanisms of these diseases have not been precisely determined. Oxidative/nitrosative stress has been implicated in the skeletal muscle dysfunction in both cases. A subset of ALS patients (~2%) have mutations in the antioxidant enzyme SOD1, and transgenic mice overexpressing these mutant enzymes develop motor neuron disease. ALS primarily affects motor neurons, but recent evidence suggests skeletal m

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46

Lescroart, Fabienne. "Recruitment of progenitor cells at the poles of the mouse heart : clonal analyses reveal common origins with a subset of skeletal muscles." Paris 6, 2011. http://www.theses.fr/2011PA066339.

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Le développement cardiaque implique deux lignages cellulaires, dont un correspond au second champ cardiaque qui contribue aux pôles veineux et artériel du coeur. De manière intéressante, une partie des muscles squelettiques antérieurs, non-somitiques, a un développement proche à celui du second champ cardiaque. Nous avons d’abord montré que les muscles de la tête, qui dérivent du premier arc branchial, sont clonalement reliés au ventricule droit alors que les muscles de la tête, pour l’expression, dérivant du deuxième arc branchial, sont clonalement reliés au myocarde à la base des grandes art

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47

Yao, Guoying. "Effect of LPL activity on fatty acid composition in mouse plasma, liver, skeletal and cardiac muscles, adipose and brain tissues." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0019/MQ53989.pdf.

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Tiger, Carl-Fredrik. "Cellular Interactions with Extracellular Matrix During Development and in Muscle Disease." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis, 2002. http://publications.uu.se/theses/91-554-5328-7/.

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49

Hovhannisyan, Yeranuhi. "Modélisation cardiaque des myopathies myofibrillaires à l'aide de cellules souches pluripotentes induites pour explorer la pathogenèse cardiaque Polyacrylamide Hydrogels with Rigidity-Independent Surface Chemistry Show Limited Long-Term Maintenance of Pluripotency of Human Induced Pluripotent Stem Cells on Soft Substrates Modéliser la myopathie myofibrillaire pour élucider la pathogenèse cardiaque Synemin-related skeletal and cardiac myopathies: an overview of pathogenic variants Desmin prevents muscle wasting, exaggerated weakness and fragility, and fatigue in dystrophic mdx mouse Effects of the selective inhibition of proteasome caspase-like activity by CLi a derivative of nor-cerpegin in dystrophic mdx mice." Thesis, Sorbonne université, 2020. http://www.theses.fr/2020SORUS095.

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La myopathie myofibrillaire est une maladie neuromusculaire à évolution lente caractérisée par de graves troubles musculaires causés par des mutations dans le gène codant pour des protéines du cytosquelette. L'un des gènes affectés en relation avec le développement de la MFM est DES. Des mutations dans le gène de la desmine entraînent des myopathies des muscles squelettiques et cardiaques. Cependant, les évènements qu'elles entraînent et qui sont à l’origine des phénotypes pathologiques cardiaques restent mal connus. Mon objectif est de créer un modèle in vitro de MFM basé sur des cellules sou

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Perrier, Antoine. "Conception et évaluation d’un modèle biomécanique, éléments finis, patient-spécifique, du pied humain. Applications en podologie, orthopédie et diabétologie : applications en podologie, orthopédie et diabétologie." Thesis, Université Grenoble Alpes (ComUE), 2016. http://www.theses.fr/2016GREAS035/document.

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Conception et évaluation d’un modèle biomécanique, éléments finis, patient-spécifique, du pied humainApplications en podologie, orthopédie et diabétologieLe pied est une des structures les plus complexes du corps humain. Avec 28 os, 33 articulations et une centaine de structures ligamentaires, cette entité poly articulée est le résultat d’une hyperspécialisation ayant contribué à faire de l’homme l’unique primate totalement bipède. Quelque soit le relief, quelque soit le mouvement en cours, le pied transmet au tibia le bon vecteur force afin de finaliser le geste de la manière la plus précise

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