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Several physiological and pathological conditions cause muscle atrophy. Muscle mass los sis associated with decreased muscle strength and mobility, which contribute to increase morbidity and mortality risk.
A great number of catabolic conditions are associated with hypercortisolism and glucocorticoids, frequently used as immunosuppressive and anti-inflammatory drugs, induce muscle atrophy. It makes therefore important to understand the mechanism of the catabolic action of the glucocorticoids with the aim to identify new tools to protect muscle mass from atrophy. Since glucocorticoid-induced muscle atrophy is associated with an induction of muscle myostatine (Mst), a negative regulator of muscle mass, and overexpression of Mst leads to muscle atrophy, Mst can be suggest to be necessary for glucocorticoids to exert their atrophic effects on muscle. If this hypothesis comes true, Mst would represent a potential attractive therapeutic target for treatment of muscle atrophy induced by glucocorticoids.
The goal of our work to investigate whether inhibition of Mst activity, during pre- and postnatal life, could prevent muscle atrophy caused by glucocorticoids.
First, we wanted to know if Mstn gene disruption could prevent muscle atrophy caused by glucocorticoids. Using an Mst KO mouse model, we have demonstrated that Mstn gene disruption protects the animal treated by glucocorticoids from muscle atrophy, through downregulation of the ubiquitin-proteosome and lysosomial proteolytic pathways.
Secondly, we blocked Mst activity during postnatal life by surexpression of follistatin, one of his carrier protein which inhibits its action. Un fortunately, the surexpression of follistatin had caused muscle inflammation, distorting our results. The presence of this inflammation did not allow us to determine whether surexpression of follistatin protects skeletal muscle mass from atrophy induced by glucocorticoids. The aim of ongoing experiments is to inhibit Mst expression by siRNA De nombreuses situations cliniques favorisent le développement d’une atrophie musculaire. Cette diminution de la masse musculaire est responsable, non seulement d’une perte de force et de mobilité, mais surtout d’une augmentation du risque de morbidité et mortalité. La physiopathologie de l’atrophie musculaire reste mal connue, ce qui constitue un frein à l’avènement de nouvelles thérapeutique.
Les glucocorticoïdes jouent incontestablement un rôle dans le développement de l’atrophie musculaire. Des observations récentes montrent que les glucocorticoïdes stimulent l’expression de la myostatine (Mst), un régulateur négatif de la croissance musculaire, dont la surexpression induit une diminution de la masse musculaire. Ces données suggèrent que la Mst puisse être nécessaire à l’effet atrophiant des glucocorticoïdes sur le muscle squelettique. Si cette hypothèse se vérifie, la Mst pourrait représenter une cible thérapeutique potentielle pour le traitement de l’atrophie musculaire dur aux glucocorticoïdes.
Le but de notre travail a donc été de déterminer si l’inhibition de l’activité de la Mst, tant en période pré-natale que post-natale, prévenant l’atrophie musculaire induite par le glucocorticoïdes.
Dans un premier temps, nous avons cherché à savoir si l’invalidation constitutive du gène de la Mst chez les souris prévenait l’atrophie musculaire due aux glucocorticoïdes. L’expérience a été réalisée chez les souris KO Mst. Nos données montrent que l’invalidation du gène de la Mst protège l’animal de l’atrophie musculaire en bloquant la stimulation de la protéolyse par les glucocorticoïdes. En effet, l’induction par les glucocorticoïdes de plusieurs « atrogènes » et de l’activité du protéasome 20S n’est pas observée chez les souris KO Mst contrairement aux souris sauvages.
Dans un second temps, nous avons cherché à savoir, si l’inhibition de la Mst durant la vie postnatale exerçait le même effet protecteur vis-à-vis de l’atrophie musculaire que celui de l’invalidation constitutive du gène. L’inhibition de la Mst a été obtenue en surexprimant par électroporation dans la muscle le gène de follistatine (FS), une protéine porteuse inhibitrice de l’activité de la Mst. La surexpression de la FS crée cependant une importante inflammation musculaire qui ne permet pas d’évaluer l’effet anti-atrophique de l’inhibition de la Mst. Pour répondre à cette question, l’inhibition de la Mst devra être réalisée par l’infusion d’anticorps monoclonaux ou l’électroporation de siRNA dirigés contre la Mst.
En conclusion, l’inhibition de la Mst prévient l’atrophie musculaire induite par les glucocorticoïdes en bloquant la protéolyse par le système ubiquitine-protéasome

Muscular Atrophy --- Glucocorticoids --- Growth differentiation factor 8 --- Mice, Knockout

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Saccharomyces cerevisiae --- Yeast --- Cell differentiation --- Saccharomyces cerevisiae --- Levure --- Cellules --- Différenciation

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This is the second of three planned volumes in the Methods in Enzymology series on the topic of stem cells. This volume is a unique anthology of stem cell techniques focusing on adult stem cells, and written by experts from the top laboratories in the world. The contributors not only have hands-on experience in the field but often have developed the original approaches that they share with great attention to detail. The chapters provide a brief review of each field followed by a "cookbook? and handy illustrations. The collection of protocols includes the isolation and maintenance of ste

Adult Stem Cells. --- Cell differentiation. --- Physiology. --- Stem Cells. --- Stem Cells --- Cell Physiological Processes --- Cell Physiological Phenomena --- Cells --- Anatomy --- Phenomena and Processes --- Adult Stem Cells --- Cell Differentiation --- Human Anatomy & Physiology --- Health & Biological Sciences --- Animal Biochemistry --- Stem cells --- Stem cells. --- Colony-forming units (Cells) --- Mother cells --- Progenitor cells --- Cell fate specification --- Cell specification --- Differentiation of cells --- Fate specification of cells --- Specification of cells --- Differentiation --- Fate specification --- Specification --- Morphogenesis

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It is now known that the adult mammalian brain undergoes repair and renewal from pools of stem cells and that cell cycle alteration may cause a variety of neurological disorders ranging from autism to brain tumors. In The Cell Cycle in the Central Nervous System, prominent researchers, physicians, engineers, and pharmacologists join forces to delineate how the brain is a complex organ composed of widely varying cell types, including blood vessels, and what its cellular-based disorders may be. Topics covered range from the cell cycle during the prenatal development of the mammalian central nervous system (CNS) to future directions in postnatal neurogenesis through gene transfer, electrical stimulation, and stem cell introduction. Additional chapters examine the postnatal development of neurons and glia, the regulation of cell cycle in glia, and how that regulation may fail in pretumor conditions or following a nonneoplastic CNS response to injury. Highlights include treatments of the effects of deep brain stimulation on brain development and repair; the connection between the electrophysiological properties of neuroglia, cell cycle, and tumor progression; and the varied immunological responses and their regulation by cell cycle. State-of-the-art and readily understandable, The Cell Cycle in the Central Nervous System illuminates our understanding of how brain development, disease, renewal, and repair may be mediated by vasculogenesis, neurogenesis, and the immune system, and offers an exciting variety of new research opportunities for all those investigating brain tumors, neurodevelopment, and neurological disorders.

Central nervous system --- Cell cycle. --- Growth. --- Differentiation. --- Nervous system, Central --- Nervous system --- Mitotic cycle --- Nuclear cycle (Cytology) --- Biological rhythms --- Neurosciences. --- Neural sciences --- Neurological sciences --- Neuroscience --- Medical sciences

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A thorough appreciation of the cellular, molecular and tissue changes which precede the birth of an animal is a fundamental requirement for understanding normal structural development and also abnormal processes which result in congenital defects. This textbook provides information relevant to many subjects taught in preclinical, paraclinical and clinical years. Early chapters describe and explain sequential events relating to the division, growth and differentiation of cells and to the formation of foetal membranes, implantation and placentation. Succeeding chapters trace the origin, growth,

Animal embryology and growth --- Veterinary medicine --- Veterinary embryology. --- Animals, Domestic --- Cell Differentiation. --- Embryonic Development. --- embryology. --- Veterinary embryology --- Embryology. --- Embryonic and fetal development --- Organogenesis