共查询到20条相似文献,搜索用时 15 毫秒
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Corti S Salani S Del Bo R Torrente Y Strazzer S Belicchi M Paganoni S Li Z Comi GP Bresolin N Paulin D Scarlato G 《Cellular and molecular life sciences : CMLS》2001,58(1):135-140
The generation of human myogenic cell lines could potentially provide a valuable source for cell transplantation in myopathies. The dysregulation of proliferative-differentiative signals by viral oncogenes can result in the induction of apoptosis. Whether apoptosis occurred in myogenic cells expressing large T antigen (Tag) from SV40 upon differentiation was unknown. Human muscle satellite cells were transfected with two different constructs, containing either an origin-defective SV40 genome or Tag under vimentin promoter control. When differentiation was triggered, Tag expression reduced the formation of myotubes and dead cells showing apoptotic features were present. However, the cells expressing SV40 Tag under vimentin promoter control retained their capacity to form myotubes and expressed the myofibrillar proteins as myosin heavy chain and dystrophin when Tag expression was silent. Their apoptotic rate was similar to that of untransfected cells. The observation that apoptosis can be prevented by the down-regulation of Tag suggests that the programmed cell death induced in transformed cells can be reversed, and confirms the regulatory efficiency of the human vimentin promoter. 相似文献
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Yara Bou Saada Vlada Zakharova Boris Chernyak Carla Dib Gilles Carnac Svetlana Dokudovskaya Yegor S. Vassetzky 《Cellular and molecular life sciences : CMLS》2017,74(19):3439-3449
Skeletal muscle is a highly oxygen-consuming tissue that ensures body support and movement, as well as nutrient and temperature regulation. DNA damage induced by reactive oxygen species is present in muscles and tends to accumulate with age. Here, we present a summary of data obtained on DNA damage and its implication in muscle homeostasis, myogenic differentiation and neuromuscular disorders. Controlled and transient DNA damage appears to be essential for muscular homeostasis and differentiation while uncontrolled and chronic DNA damage negatively affects muscle health. 相似文献
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Temperature is known to affect fish growth, and in Atlantic salmon there is an influence on muscle cellularity. Primary muscle cell culture makes it possible to investigate direct effects of temperature on myogenic cells. Salmon myosatellite cells were cultured for the first time in this study. The cells were cultured at either 5°C or 11°C. Increased temperature led to an increase in differentiation rate and especially hypertrophic growth (Q10=4.0). No nuclear proliferation was evident in the satellite cell population isolated at either temperature. This may be due to the presence of different subpopulations of myogenic cells at different developmental ages or the presence of indirect factors in vivo. 相似文献
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Marina El Haddad Cécile Notarnicola Brendan Evano Nour El Khatib Marine Blaquière Anne Bonnieu Shahragim Tajbakhsh Gérald Hugon Barbara Vernus Jacques Mercier Gilles Carnac 《Cellular and molecular life sciences : CMLS》2017,74(10):1923-1936
Muscle satellite cells are resistant to cytotoxic agents, and they express several genes that confer resistance to stress, thus allowing efficient dystrophic muscle regeneration after transplantation. However, once they are activated, this capacity to resist to aggressive agents is diminished resulting in massive death of transplanted cells. Although cell immaturity represents a survival advantage, the signalling pathways involved in the control of the immature state remain to be explored. Here, we show that incubation of human myoblasts with retinoic acid impairs skeletal muscle differentiation through activation of the retinoic-acid receptor family of nuclear receptor. Conversely, pharmacologic or genetic inactivation of endogenous retinoic-acid receptors improved myoblast differentiation. Retinoic acid inhibits the expression of early and late muscle differentiation markers and enhances the expression of myogenic specification genes, such as PAX7 and PAX3. These results suggest that the retinoic-acid-signalling pathway might maintain myoblasts in an undifferentiated/immature stage. To determine the relevance of these observations, we characterised the retinoic-acid-signalling pathways in freshly isolated satellite cells in mice and in siMYOD immature human myoblasts. Our analysis reveals that the immature state of muscle progenitors is correlated with high expression of several genes of the retinoic-acid-signalling pathway both in mice and in human. Taken together, our data provide evidences for an important role of the retinoic-acid-signalling pathway in the regulation of the immature state of muscle progenitors. 相似文献
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K. R. Jennings R. W. Steele A. N. Starratt 《Cellular and molecular life sciences : CMLS》1984,40(5):456-458
Summary The effects of the calcium antagonist diltiazem on nerve and muscle in the cockroachPeriplaneta americana were examined. Diltiazem was observed to inhibit myogenic and glutamate-induced contractions of the visceral muscle while having either a potentiating, an inhibiting or a biphasic effect against proctolin-induced contractions. Against the isolated nervous system, diltiazem induced an increase in spontaneous discharge activity, followed by nerve block. Injection of diltiazem into cockroaches produced behavioral and toxic effects.Acknowledgments. The expert technical assistance of Miss Susan Auffarth is gratefully acknowledged. Bioresmethrin was provided by Dr. G.J.P. Singh. We would like to thank Nordic Laboratories for the gift of diltiazem. 相似文献
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Elisabetta Meacci Francesca Bini Chiara Sassoli Maria Martinesi Roberta Squecco Flaminia Chellini Sandra Zecchi-Orlandini Fabio Francini Lucia Formigli 《Cellular and molecular life sciences : CMLS》2010,67(24):4269-4285
We recently demonstrated that skeletal muscle differentiation induced by sphingosine 1-phosphate (S1P) requires gap junctions
and transient receptor potential canonical 1 (TRPC1) channels. Here, we searched for the signaling pathway linking the channel
activity with Cx43 expression/function, investigating the involvement of the Ca2+-sensitive protease, m-calpain, and its targets in S1P-induced C2C12 myoblast differentiation. Gene silencing and pharmacological inhibition of
TRPC1 significantly reduced Cx43 up-regulation and Cx43/cytoskeletal interaction elicited by S1P. TRPC1-dependent functions
were also required for the transient increase of m-calpain activity/expression and the subsequent decrease of PKCα levels. Remarkably, Cx43 expression in S1P-treated myoblasts
was reduced by m-calpain-siRNA and enhanced by pharmacological inhibition of classical PKCs, stressing the relevance for calpain/PKCα axis
in Cx43 protein remodeling. The contribution of this pathway in myogenesis was also investigated. In conclusion, these findings
provide novel mechanisms by which S1P regulates myoblast differentiation and offer interesting therapeutic options to improve
skeletal muscle regeneration. 相似文献
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Ellis JA 《Cellular and molecular life sciences : CMLS》2006,63(23):2702-2709
Emery-Dreifuss muscular dystrophy (EDMD) is a neuromuscular degenerative condition with an associated dilated cardiomyopathy
and cardiac conduction defect. It can be inherited in either an X-linked or autosomal manner by mutations in the nuclear proteins
emerin and lamin A/C, respectively. Traditionally muscular dystrophies were associated with defects in sarcolemma-associated
proteins and, therefore, a nuclear connection suggested the existence of novel signalling pathways associated with this group
of diseases. Subsequently, other mutations in the lamin A/C gene were attributed to a range of tissue-specific degenerative
conditions, collectively known as the ‘laminopathies’. Therefore, any proposed hypothesis underlying the molecular mechanism
of EDMD needs to include this anomaly. As we celebrate the 10th anniversary of the identification of emerin as a component
of the nuclear envelope, I discuss here the available evidence that currently implicates EDMD as arising from perturbations
in myogenic regulatory pathways, causing temporal delays in both cell cycle progression and muscle regeneration.
Received 25 May 2006; received after revision 22 June 2006; accepted 22 August 2006 相似文献
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Koleva M Kappler R Vogler M Herwig A Fulda S Hahn H 《Cellular and molecular life sciences : CMLS》2005,62(16):1863-1870
Muscle satellite cells are believed to form a stable, self-renewing pool of stem cells in adult muscle where they function in tissue growth and repair. A regulatory disruption of growth and differentiation of these cells is assumed to result in tumor formation. Here we provide for the first time evidence that sonic hedgehog (Shh) regulates the cell fate of adult muscle satellite cells in mammals. Shh promotes cell division of satellite cells (and of the related model C2C12 cells) and prevents their differentiation into multinucleated myotubes. In addition, Shh inhibits caspase-3 activation and apoptosis induced by serum deprivation. These effects of Shh are reversed by simultaneous administration of cyclopamine, a specific inhibitor of the Shh pathway. Taken together, Shh acts as a proliferation and survival factor of satellite cells in the adult muscle. Our results support the hypothesis of the rhabdomyosarcoma origin from satellite cells and suggest a role for Shh in this process.Received 23 February 2005; received after revision 2 May 2005; accepted 9 June 2005 相似文献
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J. F. Barker 《Cellular and molecular life sciences : CMLS》1979,35(4):552-554
Summary In the imported fire antSolenopsis invicta, wing casting and flight muscle histolysis are blocked by allatectomy. Treatment of alate allatectomized females with a synthetic mixture with high juvenile hormone activity induced wing casting and flight muscle histolysis. Apparently, wing casting and flight muscle histolysis in the fire ant are part of postemergence developmental program regulated, directly or indirectly, by the corpora allata.The author thanks the Entomology Department of the University of Georgia for postdoctoral support and Dr A.O. Lea for the use of his facilities. 相似文献
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dng1 is a Dictyostelium homologue of the mammalian tumor suppressor ING gene. DNG1 protein localizes in the nucleus, and has a highly conserved PHD finger domain found in chromatin-remodeling proteins. Both dng1 disruption and overexpression impaired cell proliferation. In dng1-null cells, the progression of differentiation was delayed in a cell-density-dependent manner, and many tiny aggregates were formed. Exogenously applied cAMP pulses reversed the inhibitory effect caused by dng1 disruption on the aggregation during early development, but formation of tiny aggregates was not restored. dng1-overexpressing cells acquired the ability to undergo chemotaxis to cAMP earlier and exhibited enhanced differentiation. These phenotypes were found to be coupled with altered expressions of early genes such as cAMP receptor 1 (car1) and contact site A (csA). Furthermore, disordered histone modifications were demonstrated in dng1-null cells. These results suggest a regulatory role of dng1 in the transition of cells from growth to differentiation.Received 29 December 2004; received after revision 24 May 2005; accepted 26 May 2005 相似文献
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Brink C 《Cellular and molecular life sciences : CMLS》2003,60(6):1033-1048
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Williams AE 《Cellular and molecular life sciences : CMLS》2008,65(4):545-562
MicroRNAs (miRNAs) are a recently discovered family of small regulatory molecules that function by modulating protein production.
There are approximately 500 known mammalian miRNA genes, and each miRNA may regulate hundreds of different protein-coding
genes. Mature miRNAs bind to target mRNAs in a protein complex known as the miRNA-induced silencing complex (miRISC), sometimes
referred to as the miRNP (miRNA-containing ribonucleoprotein particles), where mRNA translation is inhibited or mRNA is degraded.
These actions of miRNAs have been shown to regulate several developmental and physiological processes including stem cell
differentiation, haematopoiesis, cardiac and skeletal muscle development, neurogenesis, insulin secretion, cholesterol metabolism
and the immune response. Furthermore, aberrant expression has been implicated in a number of diseases including cancer and
heart disease. The role of miRNAs in these developmental, physiological and pathological processes will be reviewed.
Received 3 August 2007; received after revision 3 October 2007; accepted 5 October 2007 相似文献
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The turnover of adenosine triphosphate (ATP) in vertebrate skeletal muscle can increase more than a hundredfold during high-intensity exercise while the content of ATP in muscle may remain virtually unchanged. This requires that the rates of ATP hydrolysis and ATP synthesis are exactly balanced despite large fluctuations in reaction rates. ATP is regenerated initially at the expense of phosphocreatine (PCr) and then mainly through glycolysis from muscle glycogen. The increased ATP turnover in contracting muscle will cause an increase in the contents of adenosine diphosphate (ADP), adenosine monophosphate (AMP) and inorganic phosphate (Pi), metabolites that are substrates and activators of regulatory enzymes such as glycogen phosphorylase and phosphofructokinase. An intracellular metabolic feedback mechanism is thus activated by muscle contraction. How muscle metabolism is integrated in the intact body under physiological conditions is not fully understood. Common frogs are suitable experimental animals for the study of this problem because they can readily be induced to change from rest to high-intensity exercise, in the form of swimming. The changes in metabolites and effectors in gastrocnemius muscle were followed during exercise, post-exercise recovery and repeated exercise. The results suggest that glycolytic flux in muscle is modulated by signals from outside the muscle and that fructose 2,6-bisphosphate is a key signal in this process. 相似文献