Academic literature on the topic 'Cellules musculaires squelettiques'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Contents
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Cellules musculaires squelettiques.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Journal articles on the topic "Cellules musculaires squelettiques"
Florin, A., C. Lambert, C. Sanchez, J. Zappia, and Y. Henrotin. "Mise au point d’un modèle de culture original de cellules musculaires squelettiques à partir de biopsies musculaires humaines." Revue du Rhumatisme 87 (December 2020): A242—A243. http://dx.doi.org/10.1016/j.rhum.2020.10.433.
Full textMouzou, A. P., S. Titrikou, B. Constantin, S. Sebille, C. Cognard, M. Gbeassor, and G. Raymond. "Effets du décocté de Biophytum petersianum (Oxalidaceae) sur la libération du calcium du réticulum sarcoplasmique des cellules musculaires squelettiques." Phytothérapie 8, no. 4 (August 2010): 231–35. http://dx.doi.org/10.1007/s10298-010-0563-8.
Full textIdoux, Romane, Sandrine Bretaud, Christine Berthier, Vincent Jacquemond, Florence Ruggiero, and Bruno Allard. "Étude physiopathologique de la myopathie de Bethlem à l’aide d’un modèle de poisson zèbre." médecine/sciences 35 (November 2019): 39–42. http://dx.doi.org/10.1051/medsci/2019182.
Full textDéguénonvo, GNC, A. Sow, and CMM Dial. "C86: Rhabdomyosarcomes de localisations inhabituelles : A propos de deux cas colligés au laboratoire d'Anatomie Pathologique à l'Hôpital Général Idrissa Pouye." African Journal of Oncology 2, no. 1 Supplement (March 1, 2022): S35—S36. http://dx.doi.org/10.54266/ajo.2.1s.c86.ioqi5122.
Full textChazaud, Bénédicte. "Cellules satellites et cellules souches musculaires." Les Cahiers de Myologie, no. 17 (June 2018): 11–14. http://dx.doi.org/10.1051/myolog/201817003.
Full textBenoît, R. "Analyse génétique et physiologique." Revue d'Orthopédie Dento-Faciale 52, no. 4 (October 2018): 351–72. http://dx.doi.org/10.1051/odf/2018029.
Full textRaoufi, Mohammed, Mohamed Oukabli, Abdelhamid Biyi, Hanane Elouazzani, Ismail Abderrahman Rhorfi, and Ahmed Abid. "Métastases musculaires squelettique asymptomatique d’un cancer bronchique non à petites cellules." Pan African Medical Journal 22 (2015). http://dx.doi.org/10.11604/pamj.2015.22.181.7994.
Full textDissertations / Theses on the topic "Cellules musculaires squelettiques"
Mougeolle, Alexis. "Effet du stress oxydant sur les cavéoles dans les cellules musculaires squelettiques." Thesis, Bordeaux, 2014. http://www.theses.fr/2014BORD0298/document.
Full textSarcopenia is an age-related degenerative disease which is characterized by a progressive and involuntary loss of muscle mass and strength. It is accompanied by an impairment of muscle regeneration and accumulation of reactive oxygen species. Caveolae are invaginations of the plasma membrane. In muscle, they play a role in the differentiation of satellite cells and in maintaining the contractile unit of the differentiated skeletal muscle. Some myopathies are resulting from the absence of caveolae in muscle. Caveolae are also involved in mediating signals related to the regulation of oxidative stress. To better understand the mechanisms involved in the development of sarcopenia, we investigated here the relationship between oxidative stress and caveolae. Mouse muscle cells were treated with H2O2 and decreased levels of caveolin-1 and -3 were demonstrated in myoblasts and myotubes, respectively. It therefore appears that caveolae constituent proteins are actually sensitive to oxidative stress in muscle cells. In the presence of H2O2, caveolae functions (endocytosis and resistance to mechanical stress) were also significantly degraded in myoblasts. Altogether, these data suggest that oxidative stress would affect caveolae, which could have consequences on regeneration and maintenance of muscle integrity during aging
Croissant, Coralie. "Le rôle des Annexines dans la réparation membranaire des cellules musculaires squelettiques humaines." Thesis, Bordeaux, 2019. http://www.theses.fr/2019BORD0316/document.
Full textMuscular dystrophy encompasses a group of genetic disorders which cause progressive weakness and wasting of skeletal muscle. Among them, limb girdle muscular dystrophy type 2B (LGMD2B) is characterized by mutations in the dysferlin gene leading to several dysfunctions including a failure in cell membrane repair process. Cell membrane disruption is a physiological phenomenon induced by mechanical stress, such as contraction of muscle fibers. Thus, eukaryotic cells have a repair protein machinery ensuring a rapid resealing of large cell membrane ruptures. The exhaustive list of components of the repair machinery and their interplay remain to be established.The annexin (Anx) family consists of twelve soluble proteins in mammals and share the property of binding to membranes exposing negatively charged phospholipids in a Ca2+-dependent manner. Several studies have shown the involvement of Anx (AnxA1, A2, A4, A5, A6 and A7) in membrane repair of different cell types (muscle, cancer, endothelium…) in different species (mouse, zebrafish, human…). The presence of different Anx in skeletal muscle, together with the participation of several members of the Anx family in membrane repair processes, raise the question of a collective role of these proteins in the protection and repair of sarcolemma injuries.The PhD project aimed 1) at identifying Anx that are essential for membrane repair in human skeletal muscle cells, 2) developing a correlative light and electron microscopy to study the wounded site and the Anx distribution at high resolution, 3) elucidating the function of each Anx in this process and 4) analyzing Anx in dystrophic muscle cells. Using approaches including cellular and molecular biology, fluorescence microscopy and transmission electron microscopy, we studied the behavior of Anx during sarcolemma damage.We showed that AnxA1, A2, A4, A5 and A6 are expressed in human myoblasts and myotubes, and are recruited at the disruption site within seconds after the sarcolemmal damage, forming a dense structure outside the cell, named the “cap” domain. Furthermore, we determined the relative order of Anx recruitment at the disruption site. The first Anx recruited are AnxA1, followed by AnxA6 and A5, the less sensitive to Ca2+. The last Anx recruited are the most sensitive to Ca2+, AnxA4 and A2. AnxA2 and A4 are instead rapidly recruited to intracellular vesicles present deeper in the cytosol. We also studied the ultrastructure of the disruption site at high resolution. Our results revealed that the “cap” domain correspond to a disorganized membrane structure, associated with the Anx. Thanks to our results and the literature, we have proposed a model for membrane repair involving Anx in human skeletal muscle cells. We also looked at the expression of Anx in dystrophic muscle cell lines from patients with limb girdle muscular dystrophy type 2B (dysferline deficient) and 1C (deficient in cadaveoline-3). We have thus shown that the pathological context disrupts the expression of some Anx, without altering their subcellular location.In conclusion, this work shows that several members of the Anx family are involved in membrane repair and act together to repair plasma membrane damage. The implication of Anx in other pathologies, such as preeclampsia or cancer, reinforces the interest of their study in the process of membrane repair
Yennek, Siham. "Etude des mécanismes régissant les divisions symétriques et asymétriques dans les cellules souches musculaires squelettiques." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066615.
Full textDuring muscle regeneration, muscle stem (satellite) cells proliferate symmetrically and asymmetrically. Non-random segregation of old and new template DNA strands (NRDS) is one mechanism associated with an asymmetric cell division, and this is often linked with distinct daughter cell fates. How this frequency is modulated and when during tissue remodelling are key questions that are the focus of my thesis project. To address the role of extrinsic cues in NRDS and cell fate decisions, we used micropatterns coated with extracellular matrix and designed with symmetric and asymmetric topological motifs. We show that the frequency of NRDS and transcription factors asymmetry (Pax7, stem; Myogenin, differentiated) can be modulated depending on the topology of the adhesion cues of the micropattern. Moreover, we show that a temporal switch occurs in vivo during early muscle regeneration from symmetric to asymmetric DNA segregation in a subpopulation of satellite cells. Gene expression profiling of symmetrically and asymmetrically dividing cells allowed the identification of candidate regulators that might impinge on this regulatory transition. Some candidate genes were assayed in a high throughput screen that was on 2D artificial stem-cell niches. Preliminary data show that extrinsic cues (ECM protein and substrate stiffness) combined with signalling pathways can regulate the balance between proliferation and differentiation in a context dependent manner. Taken together, this thesis project shows that the interplay between microenvironment and intracellular signalling impacts on the regulation of stem cell behaviour
Charrier, Elisabeth. "Implication de la desmine dans les propriétés mécaniques des cellules musculaires squelettiques dans le contexte des desminopathies." Paris 7, 2014. http://www.theses.fr/2014PA077170.
Full textDesminopathies are neuromuscular genetic diseases caused by mutations in the desmin gene. They are characterized by the presence in muscles of aggregates containing desmin and by degenerative changes of the contractile apparatus. Although desminopathies have been largely studied at clinical level, the different steps that lead from a desmin gene mutation to progressive muscle weakness are stiil unclear. We investigated this problem in early stages of disease pathology and within an isogenic background, by using C2C12 myoblasts electroporated with the E413K mutant desmin. We first show that the expression of this mutant induces a large desmin network disorganization associated with important aggregate formation. We also compared the mechanical properties of wild-type C2C12 cells, cells over-expressing desmin-WT-GFP and cells expressing mutated desmin E413K-GFP. We show that the three cell types share similar visco-elastic moduli of the cortex, whereas expression of WT-desmin -but not of mutated desmin — increases the overall rigidity of cells. We finally investigated the impact of mutated desmin on the contractility of myoblasts in two different geometries, with a custom-made single cell technique, and with Traction Force Microscopy. We show that E413K-mutation significantly decreases cell contraction abilities. We thus demonstrate for the first time that the impaired contractile strength of muscles observed in desminopathies is already present at very early stage, in isolated myoblasts and at very short time of mutated desmin expression. Finally we have begun to investigate the effect of E413K mutated desmin expression on engineered microtissues made of C2C12 myoblasts
Rocheteau, Pierre. "Isolement et caractérisation d'une sous population de cellules souches musculaires squelettiques qui ségrégent de façon non aléatoire leurs brins d'ADN." Paris 6, 2011. http://www.theses.fr/2011PA066049.
Full textMetzinger, Laurent. "Effetv des glucocorticoides et des lazaroides sur la differenciation de cellules musculaires squelettiques d'un modele animal de la dystrophie musculaire de duchenne." Université Louis Pasteur (Strasbourg) (1971-2008), 1994. http://www.theses.fr/1994STR13135.
Full textDeval, Emmanuel. "Activité et expression de l'échangeur Na+/Ca2+ dans les cellules musculaires squelettiques de mammifère en culture primaire." Poitiers, 2001. http://www.theses.fr/2001POIT2259.
Full textMarchand, Eric. "Conséquences fonctionnelles d'une activation ou d'une inhibition de l'expression de la dystrophine dans des cellules musculaires squelettiques transfectées." Poitiers, 2001. http://www.theses.fr/2001POIT2280.
Full textBOURI, KHALED. "Contribution a l'etude du mecanisme d'action des glucocorticoides sur la differenciation des cellules musculaires squelettiques c2 en lignee." Université Louis Pasteur (Strasbourg) (1971-2008), 1996. http://www.theses.fr/1996STR13175.
Full textBensaid, Samir. "Mise en place de contre-mesures pour limiter la perte protéique de cellules musculaires squelettiques consécutive à l’hypoxie cellulaire." Thesis, Lille 2, 2019. http://www.theses.fr/2019LIL2S021.
Full textBackground and aims : Chronic exposure to severe hypoxia has deleterious effects on the muscular system, in particular on skeletal muscle mass. Hypoxia leads to imbalance of protein homeostasis, decreasing protein synthesis (mainly regulated through PI3K-Akt-mTOR pathway) while increasing protein degradation (mainly through autophagy and proteasomal degradation). In contrast, mechanical stimuli and nutrients, particularly the branched-chain amino acids (BCAA), induce activation of the mTOR pathway in human and rat skeletal muscle as well as and in cultured muscle cells, and decrease protein catabolism. In a model of skeletal muscle cell culture, we attempt to determine whether the combination of mechanical stimulation, nutritional supplementation and reoxygenation could reverse the deleterious effects of hypoxia on protein homeostasis.Experimental methodsWe induced a hypoxic stress on skeletal muscle murine cells differentiated into myotubes C2C12: four days after differentiation, the C2C12 myotubes were placed into a hypoxic chamber at 4% O2 for 24h. Electrical stimulation was applied to the cells using a pulse generator to provide electric pulses. Following the ES treatment, myotubes were firstly supplemented with branched-chain amino acids (BCAA: mixture of leucine, isoleucine and valine added to culture media) while placed to normoxia during 2 hours (corresponding so to a reoxygenation protocol).ResultsAfter 24 hours of hypoxia, the morphological analysis of myotubes shows a significant decrease in their diameter, translating the activation of protein degradation pathways at the expense of protein synthesis pathways. When applied separately, each treatment has little effect on the mTOR pathway and morphology of myotubes. However, the combination of electrical stimulation, supplementation BCAA and reoxygenation lead to an increase of the phosphorylation of key proteins involved in protein synthesis pathway (Akt and p70S6 kinase), thus reflecting their activation state. In addition, morphological analysis shows a significant increase in myotube diameter and fusion index (reflecting the state of differentiation), a sign of the presence of muscle hypertrophy.ConclusionOur preliminary results suggested that mTOR pathway responds to a combination of electrostimulation, nutrient supplementation and reoxygenation by phosphorylation of key regulators of protein synthesis, and could reverse the protein loss induced by hypoxia