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Souza, Alyson Matheus de Carvalho. "Investigando a compress?o da percep??o de dist?ncia em ambientes virtuais atrav?s da compara??o entre dispositivos de visualiza??o." Universidade Federal do Rio Grande do Norte, 2014. http://repositorio.ufrn.br/handle/123456789/19664.
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A percep??o correta de dist?ncias ? importante para a execu??o de diversas tarefas interativas, como navega??o, sele??o e manipula??o. ? sabido, no entanto, que, em geral, existe uma significativa compress?o das dist?ncias percebidas em ambientes virtuais, principalmente quando h? a utiliza??o de Head-Mounted Displays - HMDs. Essa compress?o de dist?ncias percebidas pode trazer ? aplica??o diversos problemas e at? afetar negativamente a utilidade de aplica??es que dependem desse julgamento correto. A comunidade cient?fica, at? o presente, n?o conseguiu determinar as causas do fen?meno da compress?o da percep??o de dist?ncia em ambientes virtuais. Por esse motivo, foi o objetivo desse trabalho buscar, atrav?s de experimentos com usu?rios, encontrar pistas sobre a influ?ncia do field-of-view - FoV - e dos m?todos para estimativas de dist?ncias nessa compress?o percebida. Para tal, foi feita uma compara??o experimental entre o my3D e o HMD, utilizando 32 participantes, a fim de encontrar pistas sobre as causas da percep??o comprimida. Os resultados indicaram que o my3D possui capacidades inferiores ao HMD, produzindo estimativas piores, em m?dia, em ambos os m?todos de estimativa testados. As causas apontadas para tal foram o est?mulo incorreto da vis?o perif?rica, o FoV inferior e a menor imers?o, segundo descrito pelos participantes do experimento
The correct distance perception is important for executing various interactive tasks such as navigation, selection and manipulation. It is known, however, that, in general, there is a significant distance perception compression in virtual environments, mainly when using Head-Mounted Displays - HMDs. This perceived distance compression may bring various problems to the applications and even affect in a negative way the utility of those applications that depends on the correct judgment of distances. The scientific community, so far, have not been able to determine the causes of the distance perception compression in virtual environments. For this reason, it was the objective of this work to investigate, through experiments with users, the influence of both the field-of-view - FoV - and the distance estimation methods on this perceived compression. For that, an experimental comparison between the my3D device and a HMD, using 32 participants, seeking to find information on the causes of the compressed perception, was executed. The results showed that the my3D has inferior capabilities when compared to the HMD, resulting in worst estimations, on average, in both the tested estimation methods. The causes of that are believed to be the incorrect stimulus of the peripheral vision of the user, the smaller FoV and the smaller immersion sense, as described by the participants of the experiment.
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Xiao, Lei. "Transcriptional Regulation of the Xenopus MyoD Gene." Diss., lmu, 2003. http://nbn-resolving.de/urn:nbn:de:bvb:19-11960.
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Brunelli, Roberta de Matos 1985. "Os efeitos do laser de baixa potência no processo de reparo muscular após criolesão em ratos = The effects of low-level laser therapy on muscle healing process after cryolesion." [s.n.], 2013. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308777.
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Orientadores: Daniela Cristina Carvalho de Abreu, Alberto Cliquet JuniorDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: O objetivo deste estudo foi verificar os efeitos da laserterapia de baixa potência no comprimento de onda ?=780nm entre diferentes períodos de tratamento 7, 14 e 21 dias e verificar a dose (10J/cm2 ou 50J/cm2) que promove melhor reparo muscular através das análises histopatológicas e imunohistoquímicas. Foram utilizados 54 ratos machos divididos em 3 grupos: GC: grupo controle (criolesão, sem tratamento); G10: criolesão do músculo tibial anterior (TA) e tratados com laser dose 10J/cm² e G50: criolesão do músculo TA e tratados com laser dose 50J/cm² que foram subdivididos em 3 subgrupos (n=6): 7, 14 e 21 dias de tratamento. Os achados histopatológicos revelaram maior organização das fibras musculares dos grupos tratados com laser 10J/cm² e 50J/cm² durante os períodos 7 e 14 dias em relação ao grupo controle; no período 21 dias os grupos apresentaram semelhanças na reparação tecidual. Em relação à área da lesão os grupos tratados com laser 10J/cm² e 50J/cm² durante 7 dias obtiveram diminuição significativa (p ? 0.05) da área da lesão em relação ao grupo controle, sendo que os grupos 14 e 21 dias não apresentaram diferenças significativas entre eles. Na contagem dos vasos o grupo tratado com laser 10J/cm² no 14° dia apresentou aumento dos vasos em relação ao grupo tratado com dose 50J/cm², mas não em relação ao grupo controle. Nos tempos de 7 e 21 dias os grupos não apresentaram diferença significativa entre si. Com relação às análises imunohistoquímicas da myoD no período de 7 dias os grupos tratados com laser 10J/cm² e 50J/cm² apresentaram maior imunomarcação comparada com o grupo controle, no período 14 e 21 dias a imunomarcação estava ausente. A imunomarcação da miogenina estava presente de forma semelhante nos períodos 7 e 14 dias para os três grupos analisados e no período 21 dias a imunomarcação da miogenina estava ausente em todos os grupos experimentais. Os resultados mostraram que o laser possui efeitos positivos no reparo muscular
Abstract: The objective of this study was to assess the effects of 780nm low-level laser therapy at different periods of 7, 14 and 21 days after cryolesion, including the dose (10 or 50J/cm2) to promote a better muscle repair evidenced by histopathological and immumohistochemical analyses. Fifty-four male rats were divided into three groups: injured control group (CG) - injured animals without any treatment; injured 780nm laser treated group, at 10 J/cm² (G10) and injured 780nm laser treated group, at 50 J/cm² (G50). Each group was divided into 3 subgroups (n=6): 7, 14 and 21 days post-injury. Histopathological findings revealed better-organized muscle fibers in the G10 and G50 during the periods of 7 and 14 days compared to CG. The G10 and G50 during 7 days showed a significant reduction (p? 0.05) of lesion area compared to CG, without differences between groups treated for 14 and 21 days. The G10 showed an increase of the amount of vessels after 14 days compared to the G50, but not in relation to controls. With regard to the immumohistochemical analyses of the MyoD factor, The G10 and G50 during 7 days showed higher concentrations of immunomarkers than controls. Myogenin immunomarkers were similarly observed at days 7 and 14 in all three groups analyzed, whereas immunomarkers were found in none of the groups after 21 days of laser therapy. The results showed that laser has positive effects on muscle repair
Mestrado
Fisiopatologia Cirúrgica
Mestra em Ciências
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Armour, Christine. "Regulation of MyoD induced myogenesis in P19 cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/mq26299.pdf.
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Maguire, Richard John. "Identifying targets of MyoD in myogenic stem cells." Thesis, University of York, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.516609.
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Musgrove, Nicholas James. "Land use and vegetation change on the Long Mynd." Thesis, University of Wolverhampton, 2009. http://hdl.handle.net/2436/84479.
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The plant communities of the Long Mynd plateau are the culmination of over 3000 years of human intervention that largely deforested the uplands, and subsequently maintained the generally treeless heath and grassland communities now extant. The capacity of these communities to respond to directional change is well known, indeed the traditional mode of heathland management, burning, depends on the regenerative capacity of the target species, generally heather (Calluna vulgaris), for its success. However, changes in post WW2 stocking practice; the loss of ponies followed by an increase in the numbers of sheep and a change to them being overwintered on the hill, led to excessive grazing and damage to the heath. This coincided with the spread over the hill by bracken (Pteridium aquilinum) and other changes in the distribution and nature of the vegetation. A sequence of vegetation surveys made by various individuals and organisations over the past 75 years or so has been analysed in an attempt to delineate spatial and temporal changes in the vegetation. This demonstrated the need for a standardised survey methodology to allow consistent monitoring. The analysis showed that bracken had been infiltrating most of the communities from its origins outside the lower limits of the Common as well as from some of the valley sides. Within the last decade, this expansion has apparently been contained in line with the current management plan for control. A survey of 730 quadrats in some 30 stands was made to characterise the variation of the vegetation on the plateau, and to relate it to some of the associated environmental factors. Classification, unconstrained ordination and ordination constrained by the abiotic environmental variables, showed that, a) the strongest trend in the vegetation distinguished water-flushed communities, b) non-wetland communities differentiate between heathland and grassland, c) this trend can be only partly be attributed to the measured abiotic environmental variables, d) the amount of pure Pteridietum [U20] is limited, although much of the heathland and grassland has bracken within it. There are indications that invasion by bracken often correlates with a loss of dominance of Calluna in favour of Deschampsia flexuosa and Vaccinium myrtillus. Difficulties in associating these trends with measured abiotic variables suggests, other factors probably management processes, are critical in driving this trend. Distribution of ‘heathland’ bryophytes was found to be associated more with the structure of their ‘host’ vascular communities rather than with abiotic factors. Finally, this investigation considers the practical implications with regard to the future encouragement of heather and the control of bracken. Cutting rather than burning appears to be the ecologically most suitable method for heather regeneration and bracken control.
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Thompson, Elizabeth Claire. "Studies on SET and MYND domain proteins in Drosophila." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612456.
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Wang, Jianyu. "Effects of mechanical overload and aging on MyoD and effects of oxandrolone treatment and overload on IGF-1 and MyoD in old rats /." The Ohio State University, 1998. http://rave.ohiolink.edu/etdc/view?acc_num=osu1488186329501203.
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Scionti, Isabella. "Epigenetic Regulation of Skeletal Muscle Differentiation." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSEN084/document.
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LSD1 et PHF2 sont des déméthylases de lysines capables de déméthyler à la fois les protéines histones qui influencent l’expression génique et les protéines non histones en affectant leurs activités ou stabilités. Des approches fonctionnelles d’inactivation de Lsd1 ou Phf2 chez la souris ont démontré l’implication de ces enzymes dans l'engagement des cellules progénitrices au cours de la différenciation. La myogenèse est l'un des exemples les mieux caractérisés sur la façon dont les cellules progénitrices se multiplient et se différencient pour former un organe fonctionnel. Elle est initiée par une expression temporelle spécifique des gènes régulateurs cibles. Parmi ces facteurs, MYOD est un régulateur clé de l'engagement dans la différenciation des cellules progénitrices musculaires. Bien que l’action de MYOD au cours de la différenciation cellulaire ait été largement étudiée, peu de chose sont connus sur les événements de remodelage de la chromatine associés à l'activation de l'expression de MyoD. Parmi les régions régulatrices de l'expression de MyoD, la région Core Enhancer (CE) qui est transcrite en ARN activateur non codant (CEeRNA) a été démontrée pour contrôler l'initiation de l'expression de MyoD au cours de l'engagement de myoblastes dans la différenciation.Nous avons identifié LSD1 et PHF2 comme des activateurs clés du CE de MyoD. L'invalidation in vitro et in vivo de LSD1 ou l'inhibition de l'activité enzymatique de LSD1 empêche le recrutement de l'ARN PolII sur le CE, empêchant l’expression du CEeRNA. D’après nos résultats, l'expression forcée du CEeRNA restaure efficacement l'expression de MyoD et la fusion myoblastique en l'absence de LSD1. De plus, PHF2 interagit avec LSD1 en régulant sa stabilité protéique.En effet, l'ablation in vitro de PHF2 entraîne une dégradation massive de LSD1 et donc une absence d'expression du CEeRNA. Cependant, toutes les modifications d'histones qui ont lieu dans la région du CE lors de l'activation de la différenciation ne peuvent pas être directement attribuées à l'activité enzymatique de LSD1 ou PHF2. Ces résultats soulèvent la question de l'identité des partenaires de LSD1 et PHF2, qui co-participeraient à l'expression du CEeRNA et donc à l'engagement des myoblastes dans la différenciation cellulaireLSD1 and PHF2 are lysine de-methylases that can de-methylate both histone proteins, influencing gene expression and non-histone proteins, affecting their activity or stability. Functional approaches using Lsd1 or Phf2 inactivation in mouse have demonstrated the involvement of these enzymes in the engagement of progenitor cells into differentiation. One of the best-characterized examples of how progenitor cells multiply and differentiate to form functional organ is myogenesis. It is initiated by the specific timing expression of the specific regulatory genes; among these factors, MYOD is a key regulator of the engagement into differentiation of muscle progenitor cells. Although the action of MYOD during muscle differentiation has been extensively studied, still little is known about the chromatin remodeling events associated with the activation of MyoD expression. Among the regulatory regions of MyoD expression, the Core Enhancer region (CE), which transcribes for a non-coding enhancer RNA (CEeRNA), has been demonstrated to control the initiation of MyoD expression during myoblast commitment. We identified LSD1 and PHF2 as key activators of the MyoD CE. In vitro and in vivo ablation of LSD1 or inhibition of LSD1 enzymatic activity impaired the recruitment of RNA PolII on the CE, resulting in a failed expression of the CEeRNA. According to our results, forced expression of the CEeRNA efficiently rescue MyoD expression and myoblast fusion in the absence of LSD1. Moreover PHF2 interacts with LSD1 regulating its protein stability. Indeed in vitro ablation of PHF2 results in a massive LSD1 degradation and thus absence of CEeRNA expression. However, all the histone modifications occurring on the CE region upon activation cannot be directly attributed to LSD1 or PHF2 enzymatic activity. These results raise the question of the identity of LSD1 and PHF2 partners, which co-participate to CEeRNA expression and thus to the engagement of myoblast cells into differentiation
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Gerber, Anthony Nicholas. "MyoD induces chromatin remodeling : implications for lineage determination and tumorigenesis /." Thesis, Connect to this title online; UW restricted, 1997. http://hdl.handle.net/1773/6342.
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Harford, Terri J. "Regulation of Apoptosis by the Muscle Regulatory Transcription Factor MyoD." Cleveland State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=csu1265812933.
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Hamed, Munerah. "Effect of p300 HAT Activity on Myogenic Differentiation." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/23707.
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Skeletal muscle specification and differentiation programs are regulated by the myogenic regulatory factors which include Myf5, MyoD, myogenin and Mrf4. Upstream of the MRFs, the transcription co-activators and other intracellular and extracellular signals play crucial roles in regulating skeletal myogenesis. Histone acetyltransferase activity of p300 is required for Myf5 and MyoD expression. Furthermore, the MyoD core enhancer region is indispensable for MyoD expression. However, the mechanism by which p300 activates MyoD gene expression is to be determined. The histone acetyltransferase activity of p300 can be inhibited by small molecule inhibitors such as curcumin. Thus, using the inhibitor approach on stem cells is useful to investigate the role of p300 in activating MyoD expression during myogenesis. We here show that curcumin was able to inhibit stem cell determination and differentiation into skeletal myocytes. We also show that p300 is present, and histone acetylation is high at the core enhancer region. Therefore, we provide evidence that p300 is directly involved in MyoD gene expression during skeletal myogenesis.
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Stuelsatz, Pascal. "Implication de la protéase calpaïne 3 dans la régulation de l’activité transcriptionnelle du facteur MyoD au cours du processus de myogénèse." Thesis, Bordeaux 1, 2008. http://www.theses.fr/2008BOR13748/document.
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Calpaïne 3 est une cystéine protéase retrouvée principalement au niveau du tissu musculaire. Cette enzyme joue un rôle clef dans le maintient de l’intégrité des fibres musculaires. En effet, des mutations au niveau du gène de calpaïne 3 ont été identifiées comme étant responsables d’une dystrophie musculaire autosomale récessive, la LGMD2A (Limb-girdle muscular dystrophy type 2A), caractérisée par une atrophie progressive des muscles des ceintures scapulaires et pelviennes. Nos travaux montrent que calpaïne 3 inhibe l’activité transcriptionnelle de MyoD. Ce facteur de transcription myogénique (MRF) joue un rôle central dans le contrôle de la myogenèse aussi bien au cours du développement embryonnaire que chez un individu adulte au cours du processus de régénération musculaire. Cette diminution d’activité transcriptionnelle a lieu aussi bien dans des cellules myoblastiques (C2C12) que fibroblastiques (C3H10T1/2). Par contre calpaïne 3 ne modifie pas l’activité transcriptionnelle des autres MRFs (Myf5, myogénine ou MRF4). Nous avons pu montrer que calpaïne 3 affecte spécifiquement l’activité transcriptionnelle de MyoD en entraînant une diminution de son niveau protéique (Western-blot, microscopie confocale), sans affecter son niveau d’ARNm (RT-QPCR). De plus, des expériences de détermination de la demi-vie protéique ont pu montrer que calpaïne 3 intervenait sur la dégradation protéique de MyoD. Des expériences sont en cours afin de déterminer si calpaïne 3 hydrolyse directement ou non le facteur MyoD. Nos travaux montrent que l’hydrolyse de MyoD induite par calpaïne 3 représente une voie parallèle à celle du système protéolytique protéasome ubiquitine-dépendant connu pour être impliqué dans sa dégradation. Nous avons également montré qu’une modification de l’expression de calpaïne 3, soit par surexpression soit par inhibition avec des siRNA spécifiques, entraîne une perturbation du processus de différenciation myogénique. Cet effet a été plus particulièrement étudié au sein d’une sous-population de cellules qui reste indifférenciée dans les cellules C2C12 induites en différenciation. Ces cellules, appelées cellules de réserve, s’apparentent aux cellules satellites intervenant dans la régénération musculaire. Nous avons montré que calpaïne 3 participe à la régulation du nombre des cellules de réserve au cours de la différenciation des cellules C2C12. Ce rôle de calpaïne 3 pourrait être lié à son intervention dans la dégradation du facteur MyoD. L’ensemble de ces résultats suggère ainsi que calpaïne 3 pourrait jouer un rôle in vivo dans le maintien d’un stock de cellules satellites au cours de la régénération musculaireCalpain 3 (CAPN3) is a calcium-dependent cysteine protease mainly expressed in skeletal muscle. This protease plays a key role in maintaining the integrity of muscular fibers. Indeed, mutations in CAPN3 encoding gene cause limb-girdle muscular dystrophy type 2A, an autosomal recessive muscular dystrophy characterized by progressive atrophy and weakness of the proximal limb muscles. Our work reveals an inhibitory effect of CAPN3 directed against the myogenic regulatory factor (MRF), MyoD. We have shown that CAPN3 inhibits the transcriptional activity of MyoD either in myoblastic cells (C2C12 cells) or in fibroblastic ones (C3H10T1/2 cells). On the contrary, no variation in the transcriptional activity of the other members of the MRFs family (Myf5, myogenin, or MRF4) was observed. CAPN3 affects the transcriptional activity of MyoD by decreasing the quantity of the endogenous protein MyoD (Western-blots, confocal microscopy experiments), without affecting its mRNA level (RT-QPCR). Moreover, half-life determination experiments showed that CAPN3 induce MyoD degradation acts on MyoD by a proteic degradation. Experiments are in progress to determine whether CAPN3 acts directly or not on MyoD. Furthermore, the inhibitory effect of CAPN3 on MyoD is independent of the ubiquitin-proteasome proteolytic pathway that is known to play a role during MyoD degradation. Indeed, MyoD mutants resistant to proteolytic degradation by the proteasome are sensitive to CAPN3 action. Interestingly, we have shown that modifications in CAPN3 expression, induced by overexpression or downregulation (siRNA), cause perturbations in myogenic differentiation. CAPN3 appears as a regulator of myogenic differentiation by modulating the quantity of MyoD available for progressing in differentiation. In addition, we have highlighted a potential role of CAPN3 in maintaining a pool of reserve cells along C2C12 cells differentiation. These cells share numbers of similarities with satellite cells present in the adult muscles. In conclusion, we have shown that CAPN3 acts as a regulatory molecule on myogenic differentiation, and probably have implications in the area of regeneration
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Odeh, Rula S. "Thymopoietin and MyoD : their effects on the muscle nicotinic acetylcholine receptor." Thesis, McGill University, 1993. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=68233.
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The present study was done to determine whether the muscle nicotinic acetylcholine receptor (nAChR) function and expression could be regulated by two different factors: (a) thymopoietin (TPO)$ sp *$, a nicotinic antagonist and (b) MyoD, a myogenic transcription factor.Exposure of rat neonatal muscle cells in culture to TPO on a long-term (days) and short-term (minutes) basis resulted in the inhibition of $ sp{125}$I-$ alpha$-bungarotoxin (BGT) binding. Short-term pretreatment with TPO also led to a decrease in carbachol-stimulated $ sp{22}$Na uptake; however, long-term exposure resulted in an enhanced carbachol-stimulated uptake. Chronic treatment also resulted in greater muscle cell morphological development. These results suggest that TPO regulates the nAChR and exerts trophic effects on myotube morphology.
As another approach to study factors that affect nAChR expression, non-muscle cells were transfected with MyoD cDNA. After transfection, saturable, high affinity $ sp{125}$I-$ alpha$-BGT binding was readily detectable, as was carbachol-stimulated $ sp{22}$Na uptake. Both these parameters developed in parallel over time and were inhibited by nicotinic antagonists. These results suggest that the transfection of a non-muscle cell line with MyoD cDNA results in the expression, at the cell surface, of a functional muscle-type nAChR.
This work shows that the nAChR function and expression can be regulated through (a) the chronic interaction of TPO at the nAChR at the cell surface and (b) the action of MyoD at the gene level. ftn$ sp *$ As stated in the addendum to this thesis, recent work by Quik et al. 1993a has shown that the preparation presumed to be TPO, contained $ alpha$-cobratoxin; the effects observed in the present thesis must therefore now be attributed to the presence of $ alpha$-cobratoxin contaminant.
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Berkes, Charlotte Amelia. "Elucidating the mechanisms by which MyoD establishes muscle-specific gene expression /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/5071.
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Ma, Philip Chun-Ming. "Structural studies on the basic-helix-loop-helix region from MyoD." Thesis, Massachusetts Institute of Technology, 1994. http://hdl.handle.net/1721.1/28070.
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Borensztein, Maud. "Rôle des gènes Myod et Igf2 dans le développement embryonnaire murin." Paris 6, 2010. http://www.theses.fr/2010PA066374.
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Le développement du muscle squelettique murin s’effectue sous le contrôle de plusieurs facteurs de transcription tels que Myod et Myf5. Les facteurs de croissance IGF (Igf1 et Igf2) sont également impliqués. Pour étudier les interactions entre Myod et Igf2, un modèle murin d’invalidation de ces gènes a été obtenu. Bien que les animaux simples mutants soient viables, les souris Myod-/- Igf2-/- présentent une létalité périnatale, due à une insuffisance respiratoire. Des analyses histologiques, à 18,5 dpc, ont montré une atrophie importante du diaphragme ainsi qu’une hypertrophie du tissu adipeux brun des doubles mutants en comparaison aux contrôles. Etonnamment, l’atrophie musculaire est spécifique du diaphragme et s’explique par un nombre réduit de fibres. De plus, une désorganisation importante des sarcomères a été mise en évidence et la capacité contractile du diaphragme est sévèrement réduite en comparaison aux diaphragmes contrôles. Enfin, les interactions moléculaires ont été étudiées dans le diaphragme et les muscles des cuisses à 18,5 dpc. Nous avons pu montrer l’existence d’une boucle de rétrocontrôle négative entre Myod et Igf2, au niveau transcriptionnel, ainsi qu’un contrôle de l’expression de Myod et Myf5 par Igf2, de façon spécifique au diaphragme. Des expériences de ChIP ont mis en évidence une fixation du facteur de transcription Myod au niveau d’une séquence activatrice contrôlant l’expression du locus Igf2/H19, spécifiquement dans les tissus mésodermiques. Enfin, une expérience de 3C a permis de corroborer l’interaction de cette séquence activatrice du mésoderme avec le promoteur H19, permettant l’introduction d’un nouvel acteur dans la myogenèse.
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AURADE, FREDERIC. "Fonctions et regulations de l'expression de genes de la famille myod." Paris 7, 1997. http://www.theses.fr/1997PA077166.
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Les genes de la famille myod (myf-5, myod, myogenine et mrf4) sont des facteurs de transcription specifiques du muscle squelettique. Ils controlent le processus de myogenese dans ce tissu, depuis le recrutement des cellules precurseurs jusqu'a la differenciation de ces cellules et l'etablissement du phenotype mature. De plus, ces genes semblent intervenir dans la regeneration du muscle blesse. Nous avons etudie, au moyen de modeles cellulaires, plusieurs aspects du fonctionnement de ces 4 genes : - le role des membres de la famille myod dans la mise en place du programme myogenique, ainsi que l'implication de mrf4 dans le controle de la maturation. Cette etude, basee sur la conversion des fibroblastes de la lignee c3h10t1/2, a permis de conclure que, si chaque gene permet la convertion myogenique, sa capacite a accomplir un programme myogenique complet varie. De plus, les proprietes d'auto-activation et d'activation croisee de ces genes evoquees dans la litterature ne semblent pas une regle generale. Enfin, la surexpression de mrf4 n'a pu etre correlee avec l'apparition de l'expression de genes specifiques du muscle mature. - le lien entre les somatomedines et les facteurs myogeniques. L'insuline et les facteurs insulino-mimetiques (igfs) sont des activateurs puissants de la differenciation musculaire. Par une approche de molecules d'arn anti-sens, nous avons mis en evidence l'existence d'une boucle de regulation positive entre igfs et myod qui prepare les myoblastes a la differenciation. Cette etude a permis une avancee dans la comprehension des mecanismes reliant des facteurs a specificite tissulaire, comme les genes de la famille myod, et des facteurs ubiquitairement exprimes comme les igfs. - la regulation de l'expression de myf5. Nous avons montre que des evenements transductionnels mobilises par l'usage simultane de la dexamethasone, un glucocorticoide, et de l'anisomycine, un agoniste de voies de transduction du stress, permettent une forte stimulation de l'expression de myf5. Le role de ce mecanisme reste indetermine, mais pourrait intervenir dans le processus de regeneration.
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Feldmann, Jamie Marie. "Analysis of Myogenin Function in Rhabdomyosarcoma Cells." OpenSIUC, 2009. https://opensiuc.lib.siu.edu/theses/7.
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Rhabdomyosarcomas (RMS) are the most common soft tissue cancer among children and are characterized by their expression of the myogenic regulatory factors MyoD and myogenin. Yet RMS cells cannot undergo normal myogenesis and are caught between the proliferation program and the terminal differentiation program. Many questions still remain about the defects present in rhabdomyosarcoma cells. In this work, we set out to understand the role of myogenin in these cells. To begin, we found that myogenin and its co-factors were present in rhabdomyosarcoma cells at levels that should support terminal differentiation. We examined the expression profile of several myogenin target genes in rhabdomyosarcoma cells and then assayed for myogenin activity using luciferase reporter constructs that contain myogenin dependent promoters to test for myogenin function. Many myogenin target genes were down regulated in RMS cells but that the target promoters on the luciferase constructs were activated. Terminal differentiation is a complicated process that involves many proteins. In cancer cells, it is important to compare the levels proteins with known functions to those levels in wild-type cells at the protein and RNA levels. Establishing the defect of rhabdomyosarcoma cells can lead to further insights into normal myogenesis, and may also lead to new therapeutic approaches in the treatment of this childhood cancer.
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Crutzen, Helene Sabine Giovanna. "Cis-regulation of MyoD : a systems analysis of a fate master regulator." Thesis, University College London (University of London), 2009. http://discovery.ucl.ac.uk/17977/.
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Myogenesis is highly regulated and its activation in the embryo is controlled by a series of complex transcriptional regulatory networks that ultimately result in the expression of myogenic regulatory factors (MRFs). The MRFS, particularly MyoD and Myf5, are responsible, in concert with a vast range of cofactors, for directing the expression of genes responsible for muscle formation and activity. Several candidate proteins have emerged as being responsible for MRF expression, as well as numerous downstream effectors involved in muscle formation in vivo. Several cis-regulatory elements have been identified for MyoD, but only a handful of factors have been identified that bind these elements. In addition, knockout experiments of these regions do not result in a complete loss of MyoD expression, suggesting a certain level of redundancy and the existence of other yet unidentified cis-regulatory modules. In this study, novel potential regulatory regions within the MyoD upstream genomic locus were identified by comparative genomics. These regions, named ReMos 9, 10 and 11, were conserved in mammals, chick and fish. Reporter assays in C2C12 cells using these regions cloned upstream of the MyoD promoter revealed that they positively enhanced the promoter activity. A synergy was uncovered between ReMo 9 and 10, which have a strong positive effect on promoter activity, but none individually; ReMo 11 seemed to disrupt this synergy. In addition, ReMos 9+10 and the CER enhancer were shown, by double fluorescent RNA in situ hybridisations, to be transcribed and possess cryptic promoter activity. This suggested that these elements acted as alternative promoters and encoded RNAs that regulated MyoD gene expression. Furthermore, the use of a newly engineered database generated predictions of DNA-binding factors interacting with the cis-regulatory regions, as well as protein interaction networks involved in MyoD regulation. These predictions were refined and constrained with biological input data derived by microarrays of single-cells transiently expressing relevant constructs. A list of candidate muscle-specific binding factors was then tested in vitro by siRNA knockdown experiments, and showed that MyoD disrupts the positive synergistic effect of ReMos 9 and 10 on the PRR. In conclusion, this study identified a number of regions that seem to be involved in MyoD regulation, and candidate factors binding to the MyoD cis-regulatory regions. Further in vivo validation will identify their function in MyoD spatio-temporal gene expression.
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B, Huot Nicolas. "Un adenovirus exprimant MyoD induit la myogenèse des cellules souches embryonnaires humaines." Thesis, Université Laval, 2009. http://www.theses.ulaval.ca/2009/26054/26054.pdf.
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B-Huot, Nicolas. "Un adenovirus exprimant MyoD induit la myogenèse des cellules souches embryonnaires humaines." Master's thesis, Université Laval, 2009. http://hdl.handle.net/20.500.11794/20682.
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Avec leurs caractéristiques d'auto-renouvellement illimité et de pluripotence, les cellules souches embryonnaires humaines (hESC) représentent une source infinie de cellules pour la thérapie cellulaire de maladies, telle que la dystrophie musculaire de Duchenne. Des études ont démontré que les hESC pouvaient être différenciées en cellules musculaires squelettiques, mais les techniques employées sont longues et inefficaces. Ce mémoire décrit un nouveau protocole de différenciation des hESC en cellules musculaires squelettiques à l'aide d'un adénovirus exprimant le gène MyoD sous le contrôle du promoteur CAO (Ad.CAO-MyoD). L'efficacité de ce virus pour induire la myogenèse des hESC a été mise en évidence par la présence de divers marqueurs myogéniques. Ensuite, le potentiel de fusion de ces cellules a été illustré par le marquage de la MyHC et par l'observation de quelques myotubes. Ces résultats préliminaires semblent indiquer que l'Ad.CAO-MyoD est un outil prometteur pour différencier les hESC en cellules musculaires squelettiques.
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Kuroda, Kazuki. "Delta-induced notch signaling mediated by RBP-J inhibits MyoD expression and myognesis." Kyoto University, 1999. http://hdl.handle.net/2433/181742.
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Daou, Nissrine. "Étude de l’intéraction MyoD/NFATc2 au cours de la myogenèse chez la souris." Thesis, Paris 5, 2013. http://www.theses.fr/2013PA05T013/document.
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La voie de signalisation calcineurine/NFAT (Nuclear Factor of Activated T-cells) est très largement impliquée dans plusieurs aspects du développement et des pathologies du muscle squelettique. De nombreuses études ont souligné son implication dans la spécification des fibres musculaires adultes. Cependant, son rôle dans l’établissement du phénotype musculaire au cours de l’embryogenèse reste peu connu. Il faut noter que certains travaux suggèrent une implication de NFATc3 dans le nombre de fibres musculaires alors que l’isoforme NFATc2 pourrait être impliquée dans la taille des fibres musculaires. Les facteurs myogéniques (MRF) de la famille MyoD (incluant MyoD, Myf5, MRF4 et la myogénine) sont des facteurs de transcription à domaine bHLH (basic-Helix-Loop-Helix) clés pour la myogenèse squelettique. L’étude de leurs partenaires protéiques est essentielle pour bien comprendre la régulation de l’expression des gènes musculaires. Un nouveau paradigme de la transcription a été démontré (Armand et al. 2008), où une protéine NFAT pourrait coopérer spécifiquement avec un MRF : en effet, l’isoforme, NFATc3, coopère avec MyoD pour activer l’expression de la myogénine au cours de la somitogenèse. Ce rôle est spécifique du complexe NFATc3/MyoD puisque les souris mutantes myod (-/-) ; nfatc2 (-/-) ne présentent aucune modification de l’expression de la myogénine au cours de la somitogenèse. L’objectif de ce travail est d’étudier l’implication du complexe NFATc2/MyoD dans la myogenèse chez la souris. Nous montrons que l’isoforme NFATc2 coopère avec MyoD pour induire spécifiquement l’expression de la chaine lourde néonatale la myosine (MHCneo), in vitro aussi bien qu’in vivo. Cette coopération est spécifique et cruciale puisque les souris double mutantes myod (-/-) ; nfatc2 (-/-) meurent à la naissance avec une réduction spectaculaire de l’expression de la MHCneo, principale isoforme de la myosine exprimée à la naissance, alors que l’expression de cette chaine lourde de la myosine n’est pas affectée chez les simples mutants. Par des analyses d’immunoprécipitation de la chromatine et de retard sur gels, nous avons montré que les isoformes NFATc1 et NFATc3 se lient de manière préférentielle au gène codant la chaine lourde embryonnaire de la myosine (MHC emb). Ce travail, qui met en évidence pour la première fois le rôle de la voie de signalisation calcineurine/NFAT dans la construction précoce de la fibre musculaire au cours de l’embryogenèse, montre aussi l’implication spécifique du complexe NFATc2/MyoD dans le contrôle du nombre de fibres musculaires au cours de l’embryogenèseCell biology
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Lima, Amanda de Paula. "EFEITOS DA SUPLEMENTAÇÃO COMBINADA DE LISINA E METIONINA NO DESEMPENHO E EXPRESSÃO DE GENES RELACIONADOS AO CRESCIMENTO MUSCULAR DE ALEVINOS DE TILÁPIA DO NILO, Oreochromis niloticus." Universidade Estadual de Ponta Grossa, 2018. http://tede2.uepg.br/jspui/handle/prefix/2677.
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Fundação Araucária de Apoio ao Desenvolvimento Científico e Tecnológico do Paraná
A presente pesquisa foi realizada com o objetivo avaliar os efeitos da suplementação combinada de lisina e metionina sobre o desempenho produtivo e expressão de genes relacionados com o crescimento muscular em alevinos de tilápia do Nilo revertidos sexualmente. Trezentos e trinta e seis alevinos de tilápia do Nilo (peso inicial 0,90 ± 0,01 g) foram distribuídos em 24 aquários de 70L com sistema contínuo de fluxo de água (2,0 L/min), em um delineamento inteiramente casualizado com quatro tratamentos e seis repetições. Foram elaboradas quatro dietas isoproteicas (~330,50 g/kg de proteína bruta) e isocalóricas (~18,59 MJ/kg) sem suplementação de lisina e metionina (Controle), suplementada com lisina (Lys), suplementada com metionina (Met) e suplementada com lisina e metionina (Lys+Met) durante oito semanas. Os peixes foram alimentados manualmente, quatro vezes por dia até saciedade aparente. Peixes tratados com as dietas Lys e Met apresentaram maior peso corporal e taxa de crescimento específico em relação aos peixes mantidos com as demais dietas. Peixes tratados com dieta Lys apresentaram maior taxa de eficiência proteica em comparação aos peixes mantidos com as outras dietas. O índice hepatostomático e a gordura corporal foram menores nos peixes alimentados com as dietas Met e Lys+Met em comparação aos peixes tratados com a dieta controle. O consumo, sobrevivência, umidade, proteína bruta, cinzas corporais e a expressão do mRNA da miostatina não foram influenciados pelas dietas. Peixes que receberam dieta Lys+Met apresentaram maior nível de expressão de mRNA da MyoD em comparação aos peixes que receberam a dieta controle, mas nenhum efeito da suplementação isolada de lisina e metionina foi observada. Em conclusão, a suplementação combinada de lisina e metionina melhora o desempenho produtivo e aumenta a expressão de mRNA de MyoD e miogenina e reduz conteúdo de gordura corporal de alevinos de tilápias do Nilo.
This work was carried out with the objective of evaluating the effects of the combination of lysine and methionine on the performance of growth and expression of genes related to muscle growth in sexually reversed Nile tilapia fingerlings. Fish (n = 336, initial weight 0.90 ± 0.01 g) were randomly distributed into 24 70 L aquaria with a continuous water flow system in an entirely randomized design with four treatments and six replicates. Four isoproteic (~330.50 g/kg crude protein) and isocaloric (~ 18.59 MJ / kg) diets without lysine or methionine supplementation (Control), or supplemented with lysine (Lys), methionine (Met) and lysine and methionine (Lys + Met) were elaborated. Fish were hand fed until apparent satiety. Fish fed diets Lys+Met and Met showed higher final body weight and specific growth ratio compared to fish fed other diets. The protein efficiency ratio was higher in fish diet Lys compared to fish fed other diets. Fish fed Met and Lys+Met diets showed lower hepatosomatic index and whole-body fat compared to fish fed the control diet. Feed intake, survival and whole-body moisture, crude protein, ash and mRNA expression of myostatin of fish were not affected by diets. Fish fed diet Lys+Met demonstrated higher mRNA expression level of MyoD compared to those fed the control diet. In conclusion, Nile tilapia fingerlings fed combined lysine and methionine demonstrates improved growth performance in line to higher mRNA expression of MyoD and myogenin, and also reduced body fat contents
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Jones, Gwawr Eleri. "Ei phwer ni phaid : gwragedd ym myd baledi'r 19eg ganrif." Thesis, Bangor University, 2010. https://research.bangor.ac.uk/portal/en/theses/ei-phwer-ni-phaid-gwragedd-ym-myd-baledir-19eg-ganrif(cdd79e55-862a-4103-bce6-e921e0a7a267).html.
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Zhang, Meiling. "MOLECULAR DEFECTS OF MEF2 FAMILY PROTEINS AND NAC PROTEINS THAT BLOCK MYOGENESIS AND PROMOTE TUMORIGENESIS IN RHABDOMYOSARCOMA." OpenSIUC, 2015. https://opensiuc.lib.siu.edu/dissertations/1079.
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Rhabdomyosarcoma (RMS) is a highly malignant pediatric cancer that is the most common form of soft tissue tumors in children. RMS cells have many features of skeletal muscle cells, yet do not differentiate. Thus, our studies have focused on the molecular defects present in these cells that block myogenesis. We have found MEF2D is absent in RMS cell lines representing both major subtypes of RMS and primary cells derived from an embryonal RMS mice model. We have shown that the down regulation of MEF2D is a major cause for the failure of RMS cells to differentiate. We find MEF2D cannot bind to muscle specific gene promoters. Exogenous expression of MEF2D activates muscle specific luciferase constructs, upregulates p21 expression and increases muscle specific gene expression including the expression of myosin heavy chain, a marker for skeletal muscle differentiation. Restoring expression of MEF2D also inhibits proliferation, cell motility, anchorage independent growth in vitro, and tumor growth in vivo by xenograft assay. We also have found MEF2C is deregulated in rhabdomyosarcoma with the aberrant alternative splicing. We have shown that exon α in MEF2C is aberrantly alternatively spliced in RMS cells, with the ratio of α2/α1 being highly downregulated in RMS cells compared with normal myoblasts. We find that MEF2Cα1 is the ubiquitously expressed isoform which exhibits no myogenic activity and that MEF2Cα2, the muscle specific MEF2C isoform, is required for efficient differentiation. Compared with MEF2Cα2, MEF2Cα1 more strongly interacts with and recruits HDAC5 to myogenic gene promoters to repress muscle specific genes. Overexpression of the MEF2Cα2 isoform in RMS cells increases myogenic activity and promotes differentiation in RMS cells. We have also identified a serine protein kinase, SRPK3, which is downregulated in RMS cells and found that expression of SRPK3 promoted the splicing of the MEF2Cα2 isoform and induced differentiation. Restoration of either MEF2Cα2 or SPRK3 inhibited both proliferation and anchorage independent growth of RMS cells. The NAC complex performs many diverse biological functions, and the deregulation of its subunits has been correlated with many cancers. We sought to understand the function of the NAC complex in normal myogenesis and tumor progression in rhabdomyosarcoma cells. We found that the muscle specific subunit of the NAC complex, skNAC, which is the alternatively spliced isoform of NACα, was induced in normal cells and downregulated in RMS cells, while BTF3, also known as NACβ, was induced in normal cells and severely downregulated in RMS cells. We also showed that skNAC associated with muscle specific promoters together with BTF3 in differentiated normal cells, and this association was dependent on the expression of BTF3. We further investigated the involvement of skNAC in RMS progression. We found that the muscle specific expressed methyltransferase Smyd1 was nuclear localized in RMS cells and its interaction partner skNAC was switched with corepressors (HDAC1 and TBX2). We also confirmed the expression of skNAC was regulated by the splicing factor kinase SRPK3 and overexpression of SPRK3 induced skNAC expression and muscle differentiation in RMS cells. We also confirmed the overexpression of BTF3 in patient RMS tumors and depletion of BTF3 induced apoptosis in RMS cells and decrease RMS cell survival. BTF3 depletion also sensitized TRAIL induced cell apoptosis in RMS cells. However, BTF3 played a different role in normal cells. Deletion of BTF3 in C2C12 cells does not induce cell apoptosis, which suggests BTF3 functions as an anti-apoptosis factor in RMS cells and could be used as a cancer specific therapeutic target in RMS cells.
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Lagirand-Cantaloube, Julie. "MyoD et eIF3f : cibles majeures du complexe ubiquitine-ligase SCFMAFbx au cours de l'atrophie musculaire." Paris 11, 2008. http://www.theses.fr/2008PA11T020.
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Vandromme, Marie. "Caractérisation fonctionnelle de deux régulateurs transcriptionnels, MyoD et p67SRF, impliqués dans la différenciation musculaire squelettique." Montpellier 1, 1993. http://www.theses.fr/1993MON1T030.
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Delfini, Marie-Claire. "Etude des facteurs myogéniques Myf5 et MyoD au cours du développement embryonnaire chez le poulet." Paris 7, 2003. http://www.theses.fr/2003PA077244.
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Batonnet-Pichon, Sabrina. "Régulation et contrôle des fonctions du facteur de transcription musculaire myod par ubiquitylation et phosphorylations." Paris 5, 2005. http://www.theses.fr/2005PA05S013.
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La régulation du taux d'expression de MyoD, un facteur de transcription spécifique du muscle squelettique strié, apparaît indispensable à l'arrêt de la prolifération et à l'activation de gènes musculaires nécessaires au déclenchement de la différenciation myogénique. Dans les myoblastes normaux, MyoD est exprimé en phase G1 et en fin de phase G2 où son activité transcriptionnelle et son niveau d'expression sont régulés par différentes modifications post-traductionnelles. Dans la première partie de notre projet, nous avons mis en évidence le mécanisme majeur conduisant à la dégradation nucléaire de MyoD. Ainsi, nous montrons que l'ubiquitylation de MyoD se réalise majoritairement sur sa Lysine 133, et semble également impliquée dans son activité myogénique. La seconde partie de notre étude aborde la régulation de MyoD lors de la transition G2/M. Ainsi, nous montrons que MyoD est partiellement dégradé en fin de phase G2 indépendamment de son motif D-box et du complexe ubiquitine ligase APCcdc20/cdh1. Cette dégradation est uniquement dépendante de la phosphorylation de sa sérine 200. Enfin, nous avons également déterminé que la double phosphorylation de MyoD a pour rôle majeur son inactivation transcriptionnelle, via une baisse de son affinité pour l'ADN d'où son exclusion de la chromatine mitotique. MyoD apparaît donc très finement régulé au cours du cycle cellulaire par deux mécanismes hautement spécifiques lors des transitions G1/S et G2/M. Ainsi, notre étude participe à une meilleure compréhension des mécanismes de régulation de MyoD au cours de la phase proliférative des myoblastes, nécessaire pour identifier à l'avenir les différents mécanismes pathologiques de diverses maladies musculairesRegulation of the MyoD expression level, a skeletal muscle specific transcription factor, is dispensable to cell cycle arrest and activation of muscle gene expression required for myogenic differentiation program. In normal myoblasts, MyoD is expressed in G1 phase and end-G2 phase, where its transcriptional activity and its expression level are regulated by post-traductional modifications. In first part of our project, we have shown the major mechanism leading to the nuclear degradation of MyoD. So, we have demonstrated that the ubiquitylation of MyoD is majoritarly realized on its Lysine 133, and seems to be also implicated in its myogenic activity. The second part of our study deals with MyoD regulation during G2/M transition. Thus, we have shown that MyoD is partially degraded in the end of the G2 phase independently of its D-box motif and of the ubiquitin ligase APCcdc20/cdh1. This degradation is only dependent of Serine 200 phosphorylation. Finally, we have also demonstrated that the double-phosphorylation of MyoD plays a major role in its transcriptional inhibition through a decreased ADN affinity leading to its chromatin exclusion in mitosis. Thus, MyoD appears to be tightly regulated during cell cycle by two highly specific mechanisms during G1/S and G2/M transitions. Therefore, our study participates to the understanding of MyoD regulation during the proliferation of Myoblasts, required for identifying in the future several pathological mechanisms involved in muscular diseases
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Almeida, Fernanda Losi Alves de. "Expressão do fator de regulação miogenica MyoD, na musculatura estriada esqueletica do pacu (Piaractus mesopotamicus), durante o crescimento." [s.n.], 2007. http://repositorio.unicamp.br/jspui/handle/REPOSIP/317706.
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Orientador: Maeli Dal Pai SilvaDissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: Nos peixes, o crescimento do tecido muscular ocorre por hipertrofia e/ou hiperplasia a partir da proliferação e diferenciação de mioblastos adultos ou células miossatélites, processos regulados pela expressão diferencial dos fatores de regulação miogênica (MRFs). O objetivo desse trabalho foi avaliar os mecanismos de crescimento muscular hiperplasico e hipertrofico e a expressão do MRF MyoD, na musculatura branca do pacu (Piaractus mesopotamicus), durante o crescimento. Exemplares juvenis (n=5) e adultos (n=5) de pacu foram anestesiados, sacrificados e determinados o peso corporal (g) e o comprimento total (cm). Fragmentos musculares brancos da região dorsal de cada exemplar, em cada fase estudada, foram congelados e imersos em nhexano congelado em nitrogenio liquido. Cortes histológicos (10 µm), obtidos em criostato, foram submetidos à coloração hematoxilina-eosina para avaliação da morfologia e morfometria das fibras musculares brancas. Foi calculado o menor diametro de 100 fibras musculares brancas em cada animal de cada fase estudada. As fibras musculares foram distribuÃdas em classes, na dependência do seu diametro (<20, 20-50, >50 µm), para avaliar o grau de crescimento hipertrófico e hiperplá¡sico da musculatura. A expressão do MRF MyoD na musculatura branca foi analisada por Reação em Cadeia da Polimerase apos Transcrição Reversa (RT - PCR). Todos os produtos visualizados em gel de agarose a 1% foram clonados e sequenciados. A morfologia da musculatura dos exemplares juvenis e adultos foi semelhante, apresentando um padrão em mosaico caracterizado por fibras de diferentes diâmetros. Nos exemplares juvenis, foi observado um predomínio de fibras com diametro menor que 20 µm, caracterizando intensa hiperplasia. Nos exemplares adultos, houve o predomínio de fibras musculares com diâmetro maior que 50 µm, caracterizando intensa hipertrofia da musculatura. A expressão do RNAm para o gene MyoD foi significativamente maior na fase juvenil, se comparada com a fase adulta. Foi obtida a sequencia consenso parcial do gene MyoD (338 pares de bases) expresso na musculatura branca do pacu. Essa sequencia apresentou similaridade com as sequencias de MyoD de varias especies de vertebrados, incluindo peixes teleósteos. A expressão diferencial do MRF MyoD, observada nas fases de crescimento juvenil e adulta do pacu, possivelmente seja responsavel pelas diferenças observadas no padrão de crescimento, com a hiperplasia predominando nos juvenis e a hipertrofia, nos adultos
Abstract: Skeletal muscle growth in fish occurs by hypertrophy and hyperplasia and is dependent of the proliferation and differentiation of myogenic progenitor cells, events regulated by the diferential expression of the myogenic regulatory factors (MRFs). The aim of this study was to analyze the hyperplasia and hypertrophy processes and the MRF MyoD expression in the white muscle in pacu (Piaractus mesopotamicus) during growth. Juvenile (n=5) and adult (n=5) fishes were anaesthetized, sacrificed and the weight (g) and the total length (cm) were determined. White muscle samples from dorsal region of each sample, in each growth phase, were collected and and immersed in n- Hexane cooled in liquid nitrogen. Transverse sections (10 µm thick), obtained in a cryostat, were stained with Haematoxilin-Eosin to morphological and morphometric analysis. We calculated the smallest diameter from 100 white muscle fibres per animal in each group. White muscle fibers were grouped in three classes: <20, 20-50 and >50 µm to evaluate hypertrophy and hyperplasia in pacu white skeletal muscle. MyoD gene expression was determined by using RT-PCR. All PCR products visualized in 1% agarose gels were cloned and sequenced. Juvenile and adult pacu fish skeletal muscle showed similar morphology, with mosaic pattern characterized by fibers with different diameters. The great number of muscle fibers with diameter inferior 20 µm observed in juvenile fish confirms the active hyperplasic process. In adult fish, most fibers were over 50 µm diameter and denote the more intense muscle fiber hypertrophy. MyoD mRNA level in the juvenile fish was higher compared to adult fish. A consensus partial sequence for MyoD gene (338 bases pairs) was obtained. This sequence showed similarity with various vertebrate species, including teleost fishes. Differential expression of MyoD gene observed in white muscle of pacu possibly is related to differences in growth patterns during the phases analysed, with predominance of hyperplasia in juveniles and hypertrophy in adult fish
Mestrado
Histologia
Mestre em Biologia Celular e Estrutural
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Li, 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.
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C/EBPβ is a bZIP transcription factor known to be involved in various physiological processes, including adipogenesis, osteogenesis and liver development. Previous studies in this laboratory revealed an inhibition of myogenesis and reduced myogenic protein expression in 5-azacytidine treated mesenchymal stem cells retrovirally transduced to overexpress C/EBPβ. The goal of this thesis was to evaluate the role of C/EBPβ in myogenic differentiation by overexpression in C2C12 myoblasts and primary myoblasts. We demonstrate reduced MyoD protein expression and subsequent downregulation of myogenic proteins during differentiation following C/EBPβ overexpression. We localized C/EBPβ to the quiescent Pax7+ satellite cells associated with the muscle fiber. Upon satellite cell activation, we observed the downregulation of C/EBPβ protein expression prior to MyoD protein expression. Furthermore, the re-expression of C/EBPβ correlated with the loss of MyoD expression later in differentiation. Histological analysis of C/EBPβ-/- mice revealed smaller fibers and a reduced Pax7+ satellite cell population as compared to control animals. In this thesis, we propose that C/EBPβ is a negative regulator of skeletal muscle differentiation by inhibiting the expression of MyoD, thus impairing proper progression through the myogenic program. In addition, we propose a role for C/EBPβ in the maintenance of undifferentiatied satellite cells.
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Liu, Yubing. "The Role of Six1 in Transcriptional Regulation during Myogenesis." Thesis, Université d'Ottawa / University of Ottawa, 2017. http://hdl.handle.net/10393/35952.
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Skeletal myogenesis is under the control of a combinatorial network of transcription factors. It has been shown that the homeobox protein Six1 is required for embryonic myogenesis. Using functional genomics approaches, I determined that Six1 is required for myoblasts differentiation through direct binding to a cluster of genes that are related to muscle function and muscle structure during my Master’s studies. However, it was still not fully understood how Six1 selects its genomic targets and whether Six1 regulates the expression of Myod directly. I devoted my PhD work to study three central aspects of Six1 function: through what DNA motif it binds to DNA, how it regulates the expression of the myogenic regulatory factor MyoD, and how it might regulate chromatin structure at the enhancer regions of muscle genes. A more degenerate MEF3-like DNA sequence consensus has been identified from Six1 ChIP-on-chip experiments. This MEF3 motif was further optimized using bioinformatic methods and was proved to discover Six1 binding sites with improved specificity and sensitivity. Myod, a member of myogenic regulatory factors (MRFs), is a master regulator in the myogenic lineage. Multiple MEF3 sites were identified on the regulatory regions of Myod, including two MEF3 sites within its core enhancer region (CER). Six1 was able to bind to the CER directly through these two MEF3 sites and regulated the Myod expression in cultured primary myoblasts. Previous work has suggested that the CER is also bound by Myod in myoblasts. I demonstrated that the binding of Myod to the CER depended on the presence of Six1. Six1 was also involved in maintaining a relatively ‘open’ chromatin structure at the CER, suggesting that Six1 may play a direct or indirect role in chromatin remodeling. During my Master’s studies, I demonstrated a synergistic regulation by the Six and MRF families. This synergistic function gains potential importance by the fact that ~25% of Six1 genomic targets are also bound by Myod. I decided to study whether the co-occupancy of Six1 and Myod was essential to maintain the proper global chromatin structure at these loci. Six1 and Myod co-bound genomic regions correlated with more accessible chromatin, which was detected by the formaldehyde-assisted isolation of regulatory elements (FAIRE) assay followed by DNA deep sequencing (FAIRE-seq). When combined with small interfering RNA-mediated gene knockdown of Six1 or Myod, FAIRE-seq data suggested that Six1, but not Myod, was involved in regulating the chromatin accessibility at these co-bound DNA loci. To shed light on the mechanism by which Six1 functions, proteomics approaches were used and revealed that proteins involved in “regulation of transcription” and “chromatin organization” were enriched among Six1-bound proteins. Cdk9 and its partner cyclin T have been shown to stimulate gene expression by releasing RNA polymerase II from transcriptional pause, but they can also function at gene enhancers. I determined that Six1 and Cdk9 participated in the same protein complex, and that the Cdk9 activity appeared to mediate the effect of Six1 on the chromatin accessibility at the CER to regulate the Myod expression. Taken together, these results demonstrate that Six1 regulates the expression of Myod through its direct binding on the CER which facilitates transcriptional elongation.
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Chen, Chao-Min Amy. "Identification and characterization of I-mf, a novel myogenic repressor that interacts with MyoD family members /." Thesis, Connect to this title online; UW restricted, 1996. http://hdl.handle.net/1773/5060.
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Mathioudakis, Nikolaos. "Etudes fonctionnelles sur le composant de la voie des piRNA TDRD1." Phd thesis, Université de Grenoble, 2012. http://tel.archives-ouvertes.fr/tel-00907417.
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Les ARN interagissants avec Piwi (ARNpi) sont des petits ARN non-codants qui sont exprimes dans la ligne grrminale des animaux. Ils interagissent avec les proteines de la branche Piwi de la famille des Argonautes en formant des complexes des ribonucleproteines impliques dans le maintien de l'intégrité du génome. La region N-terminale des quelques proteines Piwi contiennent symetriquement des arginines diméthylées. Il est considere que ce status symmetrique de la dimethylation est responsable du recrutement des proteines possédant des domaines Tudor (TDRDs). Ces domaines peuvent avoir un role comme platforme pour medier les interactions entre les proteines de la voie de l'ARNpi. Nous avons mesure indivindiuellemnt l'affinite de liaison des quatres domaines etendus Tudor (TD) de la proteine murine TDRD1 pour les trois differents peptides de la protein murine Mili qui contiennent de la methyl-arginine. Les resultats montrent une preference des TD2 et TD3 pour les peptides consecutives Mili alors que TD4 et TD1 ont une affinite plus bas et plus faible respectivement pour tous les peptides. Ces observations ont ete confirmees par des experiences pull-down en utilisant des proteines Piwi endogenes et des proteines-interagissent avec Piwi. L'affinite de TD1 pour les peptides qui contiennent de la methyl-arginine peut etre restoree par une seul mutation ponctuelle dans la cage aromatique pour revenir a la sequence consensus. La structure de cristal de la proteine TD3 lie au peptide methyle Mili montre une orientation inattendue de la peptide de liaison et de la chaine latérale de l'arginine methyle dans la cage aromatique. Finalement, le model SAXS des quatres domains tandem Tudor de TDRD1 revele une forme de la proteine flexible et elongee. Globalement, les resultats montrent que la proteine TDRD1 peut accommoder des differents peptides des differentes proteines et ainsi de fonctionner comme une protéine d'échafaudage dans la voie de l'ARNpi. La proteine FKBP6 (FK506 Binding Protein) a ete recemment identifiee comme un nouvel facteur interagissent dans la voie de l'ARNpi. FKBP6 est constituee d'une domaine d'isomerase FK et une domaine de tetratricopeptide (TPR). Une perte de la Fkbp6 conduit a la de -repression des transposons et a la sterilite masculine des souris. Le domaine TPR est implique dans l'interaction avec la proteine chaperone Hsp90 et le domaine FK est une isomerase inactive qui a ete evolue a une module structurale. En effectuant des exepriences biochimiques preliminaires nous avons identifie la region N-terminal du domaine MYND de TDRD1 comme le partenaire d'interaction du domaine FK de la FKBP6. Nous proposons que la proteine TDRD1 est une plateforme moleculaire qui reconnait des marques de methylation de MILI et elle recrute FKB6 pour promouvoir la formation d'un complexe indispensable pour la fonction de la voie de l'ARNpi.
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Rana-Poussine, Vanessa. "Régulation du gène MyoD au cours de la myogenèse post-natale et du développement : et implication du modulateur d'Akt : CTMP dans la prolifération et la différenciation cellulaires." Montpellier 2, 2008. http://www.theses.fr/2008MON20007.
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Teng, Allen C. T. "Transcriptional Control of Metabolism and the Response to Ischemia in Muscle." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/20479.
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Skeletal muscle is one of the largest tissues in humans and provides many pivotal functions to support life. Abnormality in skeletal muscle functions can lead to disease. For example, insulin resistance in skeletal muscle leads to type II diabetes. The underlying mechanisms that control energy balance in skeletal muscle remain largely elusive, especially at the genetic level. Here in the second chapter, I showed that MyoD mediated the transcriptional regulation of ACSL5, a mitochondrial protein, in C2C12 myoblasts via two E-box elements. A SNP rs2419621 (T) created a de novo E-box that together with the two pre-existing proximal E-boxes strongly enhances ACSL5 expression in both CV1 and C2C12 cells. In the third chapter, I identified a novel VGLL4-interacting protein IRF2BP2 and verified the interaction with co-immunoprecipitation and mammalian two-hybrid assays. Functionally, overexpression of IRF2BP2 and transcription factor TEAD1 activates mouse VEGF-A promoter in CV1 cells and enhances the biosynthesis of VEGF-A in C2C12 myoblasts. In vivo studies showed that ischemia induced the expression of IRF2BP2 by more than three fold, suggesting that IRF2BP2 could play a pivotal role during tissue ischemia. IRF2BP2 is a nuclear protein in both mouse cardiac myocytes and C2C12 myoblasts as demonstrated by immunohistochemistry and immunocytochemistry, respectively. Therefore, I sought to delineate the mechanism for the nuclear shuttling of IRF2BP2 in the fourth chapter. With various DNA alternations, I mapped the NLS to an evolutionarily conserved sequence 354ARKRKPSP361 in IRF2BP2. Deletion of the positively charged amino acids resulted in the abolishment of the NLS signal. Next, I showed that phosphorylation of serine 360 (S360) mediates the nuclear import of the protein. Whereas an alanine substitution (S360A) at the site resulted in perinuclear accumulation of the protein, an aspartic acid substitution (S360D) forced the nuclear accumulation. Nevertheless, the forced accumulation of the S360D mutant did not enhance the activation of VEGF-A promoter in CV1 cells as did the wild-type protein. My studies revealed two novel mechanisms by which skeletal muscle could harvest energy, thus providing new insight into the energy metabolism in skeletal muscle
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Leitão, Natalia de Jesus [UNESP]. "Influência da alimentação inicial no crescimento muscular e na expressão da MyoD e Miogenina em larvas de pacu." Universidade Estadual Paulista (UNESP), 2009. http://hdl.handle.net/11449/96595.
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O objetivo deste estudo foi verificar o crescimento hipertrófico e hiperplásico das fibras musculares e avaliar a expressão diferencial dos fatores de regulação miogênica (MRFs), MyoD e Miogenina, na musculatura esquelética de larvas de pacu. Duas dietas formuladas (DC — dieta comercial e DE — dieta experimental) e alimento vivo (A) foram utilizados de acordo com os seguintes tratamentos: A: alimento vivo; DC e DE: dietas formuladas por todo período; ADC e ADE: alimento vivo por 11 dias, três dias de alimentação mista seguida pelas dietas formuladas; J: jejum. Biometrias foram realizadas aos 5, 11, 14, 23 e 31 dias para avaliação do crescimento. A taxa de sobrevivência foi determinada aos 31 dias. Análises histológicas foram realizadas para avaliação do crescimento muscular. A análise semiquantitativa da expressão gênica da MyoD e Miogenina foi realizada por reação em cadeia da polimerase após transcrição reversa (RT — PCR) nos tratamentos A, ADC e ADE. Os maiores valores médios para comprimento, peso e sobrevivência foram obtidos com alimentação à base de alimento vivo (A). Mortalidade total ocorreu no 14° dia nos tratamentos DC e J. Apesar das diferenças no crescimento, a distribuição das fibras musculares nas classes de diâmetro e a expressão dos genes da MyoD e da Miogenina foram semelhantes (p > 0,05) entre os tratamentos A, ADC e ADE. A utilização exclusiva de microdietas não constitui uma prática viável para larvicultura do pacu. A substituição do alimento vivo por microdietas induz diferenças no crescimento, porém não compromete o potencial para o desenvolvimento muscular
The aim of this study was to evaluate lhe hypertrophic and hyperplasic growth of muscle fibers and the differential expression of myogenic regulatory factors (MRFs), MyoD e Myogenin, in the skeletal musculature of pacu larvae. Two formulated diets (DC - commercial diet and DE - experimental diet) and live prey (A) were used according to lhe following treatments: A: exclusively live prey; DC and DE: formulated diets for the entire period; ADC and ADE: live prey for 11 days, three days of co-feeding and the following days of lhe experimental period with lhe formulated diets; J: starvation. Biometries were carried after 5, 11, 14, 23 and 31 days. Survival was detemined at day 31. Histological analyses were nade to evaluate the muscle growth. MyoD and Miogenina gene expression were determined by RT — PCR semiquantitative in A, ADC and ADE treatments. The highest means values for weight, length and survival were obtained when feeding with tive prey (A). Total nriortality of larvae was observed in lhe 14th day in DC and J treatments. Contrary to growth results, muscle fibers distributions in diameter classes and MyoD and Miogenina gene expression were similar (p > 0.05) in A, ADC e ADE treatments. The exclusive feeding with microdiets does not constitute a viable food schedule for pacu larviculture. The substitution of live prey for microdiets induces differences in growth, but does not commit the potential for muscle development
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Leitão, Natalia de Jesus. "Influência da alimentação inicial no crescimento muscular e na expressão da MyoD e Miogenina em larvas de pacu /." Jaboticabal : [s.n.], 2009. http://hdl.handle.net/11449/96595.
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Orientador: Maria Célia PortellaCoorientador: Maeli Dal Pai Silva
Banca: Selma Maria Michelin Matheus
Banca: Rosângela Kiyoko Jomori Bonichelli
Resumo: O objetivo deste estudo foi verificar o crescimento hipertrófico e hiperplásico das fibras musculares e avaliar a expressão diferencial dos fatores de regulação miogênica (MRFs), MyoD e Miogenina, na musculatura esquelética de larvas de pacu. Duas dietas formuladas (DC - dieta comercial e DE - dieta experimental) e alimento vivo (A) foram utilizados de acordo com os seguintes tratamentos: A: alimento vivo; DC e DE: dietas formuladas por todo período; ADC e ADE: alimento vivo por 11 dias, três dias de alimentação mista seguida pelas dietas formuladas; J: jejum. Biometrias foram realizadas aos 5, 11, 14, 23 e 31 dias para avaliação do crescimento. A taxa de sobrevivência foi determinada aos 31 dias. Análises histológicas foram realizadas para avaliação do crescimento muscular. A análise semiquantitativa da expressão gênica da MyoD e Miogenina foi realizada por reação em cadeia da polimerase após transcrição reversa (RT - PCR) nos tratamentos A, ADC e ADE. Os maiores valores médios para comprimento, peso e sobrevivência foram obtidos com alimentação à base de alimento vivo (A). Mortalidade total ocorreu no 14° dia nos tratamentos DC e J. Apesar das diferenças no crescimento, a distribuição das fibras musculares nas classes de diâmetro e a expressão dos genes da MyoD e da Miogenina foram semelhantes (p > 0,05) entre os tratamentos A, ADC e ADE. A utilização exclusiva de microdietas não constitui uma prática viável para larvicultura do pacu. A substituição do alimento vivo por microdietas induz diferenças no crescimento, porém não compromete o potencial para o desenvolvimento muscular
Abstract: The aim of this study was to evaluate lhe hypertrophic and hyperplasic growth of muscle fibers and the differential expression of myogenic regulatory factors (MRFs), MyoD e Myogenin, in the skeletal musculature of pacu larvae. Two formulated diets (DC - commercial diet and DE - experimental diet) and live prey (A) were used according to lhe following treatments: A: exclusively live prey; DC and DE: formulated diets for the entire period; ADC and ADE: live prey for 11 days, three days of co-feeding and the following days of lhe experimental period with lhe formulated diets; J: starvation. Biometries were carried after 5, 11, 14, 23 and 31 days. Survival was detemined at day 31. Histological analyses were nade to evaluate the muscle growth. MyoD and Miogenina gene expression were determined by RT - PCR semiquantitative in A, ADC and ADE treatments. The highest means values for weight, length and survival were obtained when feeding with tive prey (A). Total nriortality of larvae was observed in lhe 14th day in DC and J treatments. Contrary to growth results, muscle fibers distributions in diameter classes and MyoD and Miogenina gene expression were similar (p > 0.05) in A, ADC e ADE treatments. The exclusive feeding with microdiets does not constitute a viable food schedule for pacu larviculture. The substitution of live prey for microdiets induces differences in growth, but does not commit the potential for muscle development
Mestre
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L'Honoré, Aurore. "Régulations transcriptionnelles du facteur myogénique MyoD au cours des phases prolifératives et différenciées de la myogénèse squelettique adulte." Montpellier 1, 2003. http://www.theses.fr/2003MON1T014.
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LA REGENERATION CONSTITUE L'EVENEMENT MAJEUR AFFECTANT LE MUSCLE SQUELETTIQUE POST-NATAL. ELLE REPRESENTE LA CAPACITE QU'A LE TISSU MUSCULAIRE A SE RECONSTRUIRE, CONSECUTIVEMENT A UNE LESION TRAUMATIQUE, PATHOLOGIQUE OU EXPERIMENTALE DE LA FIBRE. LES CELLULES SATELLITES, ENCORE APPELEES CELLULES SOUCHES DU MUSCLE SQUELETTIQUE ADULTE, SONT LES RESPONSABLES DE CE PROCESSUS DE REGENERATION : CELLULES MONONUCLEES, QUIESCENTES, POSITIONNEES LE LONG DE LA FIBRE, ELLES S'ACTIVENT EN REPONSE A CERTAINS STIMULI POUR REFORMER LA FIBRE LESEE, AU COURS DE DEUX ETAPES DE PROLIFERATION PUIS DE DIFFERENTIATION. AU COURS DE CE PROCESSUS, LE FACTEUR MYOGENIQUE MyoD JOUE UN ROLE CLE, PUISQUE SON ABSENCE SE TRADUIT PAR UNE PERTE DE LA CAPACITE REGENERATIVE. LA COMPREHENSION DE SES MECANISMES DE REGULATION TRANSCRIPTIONNELLE, EST DONC D'UNE IMPORTANCE MAJEURE. DANS CETTE ETUDE, NOUS AVONS MONTRE LA PRESENCE, DANS LES REGIONS REGULATRICES DU GENE MyoD, D'UNE NOUVELLE SEQUENCE HYBRIDE NECESSAIRE A LA REGULATION DU GENE MyoD AU COURS DE LA REGENERATION MUSCULAIRE. LA CARACTERISATION DE CETTE SEQUENCE A REVELE SA CAPACITE A LIER DEUX COMPLEXES MULTIPROTEIQUES DISTINCTS CONTENANT (1) LA PROTEINE SRF EN PROLIFERATION ET DIFFERENTIATION, (2) LE FACTEUR MUSCULAIRE MEF2 UNIQUEMENT EN DIFFERENTIATION. ENFIN, L'ETUDE FONCTIONNELLE DE CETTE SEQUENCE A DEMONTRE QUE SON INTERACTION AVEC LES DEUX PROTEINES SRF ET MEF2 EST SUCCESSIVEMENT NECESSAIRE A L'EXPRESSION DU GENE MyoD AU COURS DES DEUX ETAPES DE PROLIFERATION ET DE DIFFERENTIATION DE LA REGENERATION MUSCULAIRE SQUELETTIQUE.
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Perry, Robert L. S. Rudnicki Michael. "Requirement of MyoD for myogenic lineage maintenance and regulation of skeletal muscle terminal differentiation by the MAPK signaling pathway /." *McMaster only, 2003.
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Menon, Snehalatha Ramakrishna. "Ediacaran discoidal impressions and related structures from Newfoundland, Canada and the Long Mynd, Shropshire, UK : their nature and biogenicity." Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:ff1dc37f-711d-41f2-a3b8-733cd26cb571.
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The nature of the Ediacaran macrobiota (c. 580-541 Ma) remains puzzling. These first assemblages of large, complex fossils may have included early animals; giant microbial forms; and organisms representing radically different body plans that went extinct. Discoidal impressions â some forming the base of Ediacaran fronds but most found as isolated discs â dominate the Ediacaran macrobiota. However round markings may also be formed in a variety of abiogenic ways. This study investigates the nature and biogenicity of discoidal impressions from two Ediacaran successions: the c. 560-Ma upper Burway Formation, Longmyndian Supergroup, Shropshire, UK; and several sites on the Bonavista and Avalon Peninsulas, Newfoundland, Canada, ranging in age from 565âc. 560 Ma. The investigation involved fieldwork, photography, serial grinding through cross-sections, and optical and scanning electron microscopy. It concludes that several Longmyndian discoidal forms are pseudofossils formed by sediment injection resulting from small-scale fluid escape inferred to be driven by microbial mat sealing. Turning to clearly biogenic impressions, comparison of the varied morphologies of holdfast discs associated with fronds preserved under ash and sand from several Newfoundland sites leads to a generic model of their architecture as consisting of enclosed chambers, a complex construction perhaps for strength or possibly symbiosis. Detailed observations of the rayed disc Hiemalora suggest that it may have had an amoeboid lifestyle. Finally, the key Ediacaran taxon Aspidella is separated from the discs Ediacaria and Spriggia, with which it has been synonymized, and interpreted as a possible polyp-like animal capable of limited movement. This thesis thus demonstrates that the earliest reported Ediacaran discoidal impressions are abiogenic, produced by mat-influenced processes particularly relevant to the Precambrian, and proposes models and interpretations for several key Ediacaran forms that have important implications for both the nature and diversity of the Ediacaran macrobiota, and early animal evolution.
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Pedraza, González Neus. "Estudi de la regulació transcripcional del gen de la proteïna desacobladora UCP3." Doctoral thesis, Universitat de Barcelona, 2004. http://hdl.handle.net/10803/2987.
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El gen UCP3 s'expressa majoritàriament al múscul esquelètic i al TAM en rosegadors, i pràcticament de manera exclusiva al múscul esquelètic en humans. El gen s'activa en resposta a diferents estímuls, entre els quals trobem l'àcid retinoic, els àcids grassos no esterificats i les hormones tiroïdals. L'estudi de la regulació de la transcripció del gen UCP3 en cèl·lules musculars ens ha permès obtenir informació sobre els mecanismes moleculars responsables de l'expressió d'UCP3 al múscul esquelètic i de la modulació d'aquesta expressió deguda als estímuls esmentats. L'estudi de la regulació de l'expressió d'UCP3in vivo ens ha permès establir la importància d'alguns d'aquests mecanismes en un context fisiològic. D'acord amb l'expressió específica d'UCP3 al múscul, el factor de transcripció miogènic MyoD és necessari per l'activitat basal del promotor del gen UCP3. MyoD regula l'expressió del gen humà UCP3 a través d'unes seqüències semblants a Ebox properes al lloc d'inici de la transcripció (-29/-9). A més a més, l'activació del promotor del gen humà UCP3 per MyoD és necessària per tal que l'àcid retinoic, els àcids grassos o les hormones tiroïdals en modulin l'activitat.
L'àcid retinoic, un conegut activador transcripcional de l'expressió dels gens UCP1 i UCP2, activa l'expressió del gen UCP3 en cèl·lules musculars diferenciades. La resposta del gen UCP3 humà a l'àcid retinoic està mitjançada pels receptors d'àcid retinoic (RAR-RXR) i l'element de resposta a hormones DR1 (AGGTTTCAGGTCA) situat a la regió proximal (-71/-59) del promotor d'UCP3.
Per altra banda, l'activació del gen UCP3 pels àcids grassos es dóna a través de PPARalfa o PPARdelta (receptors activats per proliferadors peroxisomals) i de l'element DR1, in vitro i in vivo. En ratolins PPAR-alfa-KO s'ha observat una necessitat diferencial de PPAR-alfa per regular l'expressió del gen UCP3, en funció del teixit (cor o múscul esquelètic) i de l'estadi del desenvolupament (nounats i adults).
A nivell molecular, els processos d'acetilació són importants per l'activació del promotor del gen UCP3. El coactivador p300 és capaç de coactivar la resposta dependent de lligand de PPAR-alfa en el promotor, i l'activitat acetiltransferasa de p300 és necessària per aquesta coactivació. Tant l'estat d'acetilació de les histones com de MyoD són importants per l'activació del promotor del gen UCP3.
Finalment, s'ha observat que les hormones tiroïdals activen l'expressió del gen UCP3 humà i de ratolí al múscul esquelètic in vivo i en cèl·lules musculars en cultiu. Les hormones tiroïdals activen el promotor d'UCP3 a través dels receptors d'hormones tiroïdals (TR) i la regió del DNA que conté l'element DR1.
Per tant, l'element DR1 present en la regió proximal del promotor del gen UCP3 és un element multihormonal que mitjança l'activació del gen UCP3 per l'àcid retinoic, les hormones tiroïdals i els àcids grassos. En el futur, seria interessant estudiar la relació que s'estableix entre aquestes vies de senyalització in vivo.
UCP3 gene is mainly expressed in skeletal muscle and brown adipose tissue in rodents, and almost exclusively in skeletal muscle in humans. The gene is activated in response to different stimulus, such as retinoic acid, fatty acids and thyroid hormones. In the present study we investigate the molecular mechanisms responsible for UCP3 gene expression in skeletal muscle and for the retinoic acid, fatty acids and thyroid hormones-dependent activation. Studying UCP3 gene regulation in vivo has allowed to establish the importance of some of these mechanisms in a physiological context.
In agreement with the specific expression of human UCP3 in muscle, the myogenic transcription factor MyoD is needed for UCP3 promoter basal activity. MyoD regulates the expression of the human UCP3 gene through Ebox-like sequences near the initiation transcription site (-29/-9). Moreover, MyoD is necessary for retinoic acid, fatty acid or thyroid hormone-dependent activation of the UCP3 promoter.
Retinoic acid, a transcriptional activator of UCP1 and UCP2 gene expression, activates UCP3 gene expression in differentiated skeletal muscle cells. Human UCP3 gene response to retinoic acid is mediated by retinoic acid receptors (RAR-RXR) through a hormone response element DR1 (AGGTTTcAGGTCA) located in the proximal region of the promoter (-71/-59).
In addition, UCP3 gene activation by fatty acids is achieved by PPAR-alpha or PPAR-delta (peroxisome proliferator activated receptor) through the previously described DR1, in vitro and in vivo. Studies in PPAR-alpha-KO mice has revealed that PPAR-alpha is differentially required for UCP3 gene expression, depending on tissues (heart or skeletal muscle) and development stages (newborns and adults).
Finally, thyroid hormones activate human and mouse UCP3 gene expression in vivo and in vitro. This activation is mediated by thyroid hormone receptor (TR) through the DNA region that contains the DR1 element, in both human and mouse UCP3 promoter.
In conclusion, the DR1 element located in the proximal region of UCP3 gene promoter is a multihormonal response element able to mediate retinoic acid, thyroid hormone and fatty acid-dependent activation of UCP3 gene. In the future, it should be interesting to study the relationship between these signalling pathways in vivo.
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Ribeiro, Jacira Souza. "O ultrassom pulsado de baixa intensidade na regeneração do músculo tibial anterior de rato: análise morfológica, organização e deposição de colágeno e expressão de fatores regulatórios miogênicos." Universidade Nove de Julho, 2015. http://bibliotecatede.uninove.br/handle/tede/1808.
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The low-intensity pulsed ultrasound (LIPUS) has been used to promote muscle repair with better quality and in shorter time, however, there is no standardization for the parameters used in clinical practice. Thus, the aim of this study was to evaluate the effect of USPBI on the repair of skeletal muscle of rats after cryoinjury. Male Wistar rats (n=45) were divided into 3 groups: control; only injury; Injured and treated with LIPUS. The LIPUS application was performed daily, using the stationary mode, pulse 1: 4, 1 MHz frequency, intensity 0.4 W / cm2 for 3 minutes. The injured groups were euthanized at 1, 2, 3 and 7 days following injury induction. The tibialis anterior muscle (TA) was removed for morphological analysis and collagen remodeling, and the muscle sections stained with H&E and Picrosirus Red, respectively. Then, the slides were photographed and quantified using the program "Image J". The analysis of MyoD and myogenin gene expression was performed using real time PCR. The results showed that the USPBI promoted modulation of inflammatory responses with a decrease of inflammatory infiltrates after 1, 2, 3 and 7 days, and reduction of myonecrosis after 7 days, followed by an increase in the number of immature fibers after 3 and 7 days, and increase of blood vessels on days 2, 3 and 7 days. Regarding the deposition of collagen, the results showed better organization of the fibers in all experimental periods, and increased deposition of collagen fibers in the injured group and treated after 2 and 3 days. In addition, treatment with LIPUS promoted increased gene expression of MyoD reduction after 3 days and after 7 days. Regarding myogenin expression, the treated group showed increased expression after 7 days. In conclusion, the LIPUS induced positive effects on muscle repair process leading to reduced inflammation and myonecrosis, increased in the immature fibers and mature blood vessels, as well as modulation of Myod and miogenin in different periods.
O ultrassom pulsado de baixa intensidade (USPBI) tem sido utilizado por promover um reparo muscular de melhor qualidade e menor duração, porém, não há padronização quanto aos parâmetros utilizados na prática clínica. O objetivo deste estudo foi avaliar o efeito do USPBI sobre o reparo do músculo esquelético de rato após criolesão. Foram utilizados 45 ratos Wistar, machos, divididos em 3 grupos experimentais: controle; somente lesão; lesionado tratado com USPBI. A aplicação de USPBI foi realizada diariamente após indução da lesão, modo estacionário, pulsado 1:4, frequência 1 MHz, intensidade 0,4 W/cm2, durante 3 minutos. Os grupos lesionados foram eutanasiados após 1, 2, 3 e 7 dias da indução da lesão. O músculo tibial anterior (TA) foi removido para análise morfológica e de remodelamento do colágeno, sendo os cortes corados com H&E e Picrosirius Red, respectivamente. As lâminas foram fotografadas e quantificadas com auxílio do programa “Image J”. A expressão gênica de MyoD e miogenina foi obtida por PCR em tempo real. Os resultados evidenciaram que o USPBI promoveu modulação da resposta inflamatória, havendo redução do infiltrado inflamatório após 1, 2, 3 e 7 dias, e redução da mionecrose após 7 dias, seguido pelo aumento no número de fibras imaturas após 3 e 7 dias, e aumento dos vasos sanguíneos nos dias 2, 3 e 7 dias. Em relação à deposição de colágeno, os resultados evidenciaram melhor organização das fibras em todos os períodos experimentais, além de aumento da deposição de fibras colágenas no grupo lesionado e tratado após 2 e 3 dias. Além disso, o tratamento com USPBI promoveu aumento da expressão gênica de MyoD após 3 dias e redução após 7 dias. Em relação a expressão de miogenina, o grupo tratado demonstrou aumento da expressão após 7 dias. Em conclusão, o USPBI nos parâmetros utilizados induziu efeitos positivos ao processo de reparo muscular causando redução do processo inflamatório e mionecrose, aumento de fibras jovens vasos sanguíneos maduros, além de modulação de MyoD e miogenina nos diferentes períodos avaliados.
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Kitzmann, Magali. "Régulations du facteur myogénique MyoD au cours du cycle cellulaire et de la transition prolifération-différenciation des cellules musculaires squelettiques." Montpellier 1, 1999. http://www.theses.fr/1999MON1T006.
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Ross, Jason Allen. "Basal Signaling Through Death Receptor 5 and Caspase 3 Activates p38 Kinase to Regulate Serum Response Factor – Mediated MyoD Transcription." Cleveland State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=csu160915772455676.
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Junior, Erivan Schnaider Ramos. "Expressão e localização de fatores regulatórios miogênicos (MyoD e Miogenina) em músculos somíticos de ratos reinervados pela técnica de tubulização." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/25/25142/tde-03072009-101927/.
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As lesões dos nervos periféricos, que inervam os músculos esqueléticos, evoluem para perdas da propriocepção e alterações na morfologia e função das fibras musculares, causando um impacto negativo na qualidade de vidas dos indivíduos. Tais lesões implicam em alteração na expressão de genes específicos do músculo, como por exemplo, na MyoD e Miogenina, atuantes na ativação de células satélites e reguladores da massa muscular A técnica cirúrgica de tubulização é um recurso empregado na prática clínica para tratamento de músculos que sofreram desnervação. O objetivo do presente estudo foi analisar se a técnica de tubulização com o preenchimento de gordura altera a expressão de Myod e Miogenina, a morfometria do músculo sóleo de ratos e localização da Myod e Miogenina. Para isso, 57 ratos Wistar foram separados em grupos: controle inicial (GCI); final 45 (GCF45), final 150 (GCF150), desnervado 45 dias (GD45), desnervado 150 dias (GCD150) e grupos experimentais com veia vazia 45 dias (GESP45) e 150 dias (GESP150) e com veia preenchida de gordura 45 dias (GEG45) e 150 dias (GEG150). Para os procedimentos cirúrgicos de desnervação e reinervação e coleta do músculo os animais foram profundamente anestesiados. Após os devidos tempos experimentais, os animais foram sacrificados, o músculo sóleo foi dissecado, envolvido em meio de criopreservação e estocado a -80°C. A quantificação de mRNA do MyoD e Miogenina foi realizada por amplificação por reação em cadeia de polimerase (PCR) em tempo real (RealTimePCR) e a localização da produção de Myod e Miogenina foi realizada por microscopia confocal a laser e imunofluorescência. A morfometria foi realizada em lâminas coradas com HE, observadas em microscópio ótico e calculadas pelo software Image Pro-Plus 6.2. Os resultados do presente estudo mostraram que houve aumento da expressão do Myod e Miogenina nos grupos experimentais 45 dias quando comparados ao grupo controle inicial e um decréscimo da expressão de Myod e Miogenina para os grupos experimentais com 150 dias. A área da secção transversa nos grupos experimentais com 45 dias (GESP45 e GEG45) não apresentaram diferença estatística, quando comparado com grupo desnervado 45 dias (GCD45), enquanto que o grupo experimental com preenchimento de gordura 150 dias (GEG150) obteve os melhores resultados na medida da área da secção transversal do músculo sóleo. As lâminas observadas no microscópio confocal mostram a MyoD e Miogen localizadas no mionúcleo. Concluiu-se que o uso da gordura na técnica de tubulização do nervo ciático de ratos, interfere na regeneração do músculo sóleo.Peripheral nerve injuries can result in the loss of propioception, morphological and functional alterations of muscle fibers which causes a negative impact on the quality of life. These injuries elicit an alteration on the expression of muscle specific genes, like MyoD and Myogenin, involved in the satellite cell activation and muscle mass regulation. The vein graft tubulization is a well known technique for treatment of denervated muscle. The aim of this work was to investigate if vein graf tubulization filled with fat tissue changes the expression and localization of MyoD and Myogenin and to study if it can modify the morphometry of soleus muscle. Fifty seven Wistar rats were divided in initial control group (ICG), final control group 45 days and 150 days (FCG45; FCG150), denervated 45 days and 150 days (D45; D150) and experimental groups with vein graft 45 days and 150 days (VG45; VG150). and vein graft filled with fat tissue 45 days and 150 days (VF45; VF150). For denervation and reinervation procedures and muscle biopsy the animals were submitted to anaesthesia and after the experimental time they were euthanized. Soleus muscle was dissected, involved in criopreservation medium and stored at -80oC. It was performed RealTime polymerase chain reaction (RealTimePCR) for MyoD and Myogenin mRNA quantification. The localization of its production was analysed by laser confocal microscopy and immunofluorescence staining. The morphometric analysis were done by Hematoxilin-Eosin staining and examined at optical microscopy using the Image ProPlus 6.2 software. There was an upregulation on the expression of MyoD and Myogenin for the experimental groups at 45 days when compared to the initial control group. On the other hand, we found a downregulation on the MyoD and Myogenin expression in the same groups with 150 days. The area of transversal section in the 45 days experimental groups (VF45, VG45) did not show statistical difference compared with denervated group with 45 days (D45). Moreover, the group filled with fat tissue at 150 days (VF150) presented the best results in the transversal section area of soleus muscle. In addition, the slides analysed under confocal microscopy showed the localization of MyoD and Myogenin in the mionuclei. In conclusion, the application of vein graft filled fat tissue improves the soleus muscle regeneration.
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Barrett, Brianna L. "MOLECULAR DISTINCTIONS REGULATING THE TEMPORAL EXPRESSION OF THE MYOD-RESPONSIVE GENES PUMA (RESPONSIBLE FOR APOPTOSIS) AND MYOGENIN (RESPONSIBLE FOR DIFFERENTIATION)." Cleveland State University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=csu1557264097566887.
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Penn, Bennett H. "Promoter-specific restriction of MyoD binding and feed-forward regulation cooperate to produce a multi-staged transcriptional program during skeletal myogenesis /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/4993.
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