Relevant bibliographies by topics / Muscle apoptosis

Academic literature on the topic 'Muscle apoptosis'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Muscle apoptosis"

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Otrocka-Domagała, I. "Sensitivity of skeletal muscle to pro-apoptotic factors." Polish Journal of Veterinary Sciences 14, no. 4 (December 1, 2011): 683–94. http://dx.doi.org/10.2478/v10181-011-0104-x.

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Sensitivity of skeletal muscle to pro-apoptotic factors In mononuclear cells, apoptosis leads to DNA fragmentation and cell destruction, regardless of the activated pathway. As regards multinuclear cells, e.g. skeletal muscle fibers, apoptosis rarely induces the death of the entire cell, and it generally affects single nuclei. This process, referred to as nuclear apoptosis, has a negative effect on the expression of genes in the myonuclear domain. Apoptosis may be initiated in muscle cells by external stimuli which activate cell membrane death receptors as well as by internal stimuli which stimulate the mitochondrial release of pro-apoptotic proteins. Reactive oxygen species also play an important role in the initiation of apoptosis. In muscle cells, ROS are produced in response to extracellular reactions or by cell mitochondria. It is, therefore, believed that mitochondria play a central role in apoptosis within skeletal muscle. Skeletal muscles have a well-developed system that protects them against oxidative damage. Myogenic stem cells are an integral part of multinucleated myofibers, and they are critically important for the maintenance of normal muscle mass, muscle growth, regeneration and hypertrophy. The latest research results indicate that myogenic cells are more sensitive to oxidative stress and pro-apoptotic factors than well-differentiated cells, such as myotubes. The complex structure and activity of skeletal muscle prompted research into the role of apoptosis and its intensity under various physiological and pathological conditions. This review summarizes the results of research investigating control mechanisms and the apoptosis process in skeletal muscle fibers, and indicates unresearched areas where further work is required.
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Siu, Parco M., and Stephen E. Alway. "Age-related apoptotic responses to stretch-induced hypertrophy in quail slow-tonic skeletal muscle." American Journal of Physiology-Cell Physiology 289, no. 5 (November 2005): C1105—C1113. http://dx.doi.org/10.1152/ajpcell.00154.2005.

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In the present study, we examined the responses of apoptosis and apoptotic regulatory factors to muscle hypertrophy induced by stretch overload in quail slow-tonic muscles. The wings from one side of young and aged Japanese quails were loaded by attaching a tube weight corresponding to 12% of the bird's body weight for 7 or 21 days. Muscle from the contralateral side served as the intraanimal control. Relative to the intraanimal contralateral control side, the muscle wet weight increased by 96% in young birds, whereas the muscle weight gain in aged birds was not significant after 7 days of loading. After 21 days of loading, muscle weight significantly increased by 179% and 102% in young and aged birds, respectively. Heat shock protein (HSP)72 and HSP27 protein contents in the loaded sides were higher than on the control sides exclusively in young birds after 7 days of loading. Compared with the contralateral control muscle, the extent of apoptotic DNA fragmentation and the total cytosolic apoptosis-inducing factor protein content were reduced in all loaded muscles except for the 7-day-loaded muscles from the aged birds. Bax protein content was diminished in the loaded muscle relative to the control side from all groups, whereas Bcl-2 protein content was reduced in the young and aged muscles after 21 days of loading. The total cytosolic cytochrome c protein content was decreased and the X chromosome-linked inhibitor of apoptosis protein content was elevated in 7- and 21-day-loaded muscles relative to the intraanimal control muscle from young birds. Furthermore, after 7 days of loading the muscles of aged birds, H2O2 content and the total cytosolic protein content of second mitochondrial activator of caspases/direct inhibitor of apoptosis-binding protein with low isoelectric point were elevated compared with the intraanimal control side. These data suggest that stretch overload-induced muscle hypertrophy is associated with changes in apoptosis in slow-tonic skeletal muscle. Moreover, discrepant apoptotic responses to muscle overload in young and aged muscles may account in part for the age-related decline in the capability for muscle hypertrophy.
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Yasuhara, Shingo, Mary-Ellen Perez, Emi Kanakubo, Yoko Yasuhara, Yong-Sup Shin, Masao Kaneki, Toshiro Fujita, and J. A. Jeevendra Martyn. "Skeletal muscle apoptosis after burns is associated with activation of proapoptotic signals." American Journal of Physiology-Endocrinology and Metabolism 279, no. 5 (November 1, 2000): E1114—E1121. http://dx.doi.org/10.1152/ajpendo.2000.279.5.e1114.

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Critical illness is associated with muscle wasting and muscle weakness. Using burn injury as a model of local and systemic inflammatory response, we tested the hypothesis that thermal injury causes apoptosis in muscle. After a 40% body surface area burn to rats, abdominal muscles beneath the burn and limb muscles distant from the burn were examined for apoptosis at varying times after burn. Ladder assay, ELISA, and histological methods showed evidence of apoptosis in the abdominal muscles within 4–12 h with peak changes occurring at 3–7 days. Maximal apoptosis was also evident at distant limb muscles at 3–7 days. Investigation of proapoptotic pathways indicated mitochondrial membrane potential to be altered by 1 h after burn. Starting at 15 min after burn, cytochrome c was released from the mitochondria into the cytosol, followed by increased activity of caspase-3, starting at 6 h after burn. These studies suggest that mitochondria and caspase-mediated apoptotic pathways may be an additional mechanism of muscle weight loss in burns and may be potential therapeutic targets for prevention of muscle wasting.
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McMillan, Elliott M., and Joe Quadrilatero. "Differential apoptosis-related protein expression, mitochondrial properties, proteolytic enzyme activity, and DNA fragmentation between skeletal muscles." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 300, no. 3 (March 2011): R531—R543. http://dx.doi.org/10.1152/ajpregu.00488.2010.

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Increased skeletal muscle apoptosis has been associated with a number of conditions including aging, disuse, and cardiovascular disease. Skeletal muscle is a complex tissue comprised of several fiber types with unique properties. To date, no report has specifically examined apoptotic differences across muscles or fiber types. Therefore, we measured several apoptotic indices in healthy rat red (RG) and white gastrocnemius (WG) muscle, as well as examined the expression of several key proteins across fiber types in a mixed muscle (mixed gastrocnemius). The protein content of apoptosis-inducing factor (AIF), apoptosis repressor with caspase recruitment domain (ARC), Bax, Bcl-2, cytochrome c, heat shock protein 70 (Hsp70), and second mitochondria-derived activator of caspases (Smac) were significantly ( P < 0.05) higher in RG vs. WG muscle. Cytosolic AIF, cytochrome c, and Smac as well as nuclear AIF were also significantly ( P < 0.05) higher in RG compared with WG muscle. In addition, ARC protein expression was related to muscle fiber type and found to be highest ( P < 0.001) in type I fibers. Similarly, AIF protein expression was differentially expressed across fibers; however, AIF was correlated to oxidative potential ( P < 0.001). Caspase-3, -8, and -9 activity, calpain activity, and DNA fragmentation (a hallmark of apoptosis) were also significantly higher ( P < 0.05) in RG compared with WG muscle. Furthermore, total muscle reactive oxygen species generation, as well as Ca2+-induced permeability transition pore opening and loss of membrane potential in isolated mitochondria were greater in RG muscle. Collectively, these data suggest that a number of apoptosis-related indices differ between muscles and fiber types. Given these findings, muscle and fiber-type differences in apoptotic protein expression, signaling, and susceptibility should be considered when studying cell death processes in skeletal muscle.
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Tidball, J. G., D. E. Albrecht, B. E. Lokensgard, and M. J. Spencer. "Apoptosis precedes necrosis of dystrophin-deficient muscle." Journal of Cell Science 108, no. 6 (June 1, 1995): 2197–204. http://dx.doi.org/10.1242/jcs.108.6.2197.

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The current view that death of dystrophin-deficient muscle fibers is a necrotic process relies primarily upon the histological appearance of the tissue after the degenerative process is well advanced. Here, we tested this view by examining the possibility that apoptosis is a component of dystrophin-deficient muscle cell death. Three assays for apoptosis were employed in analyzing prenecrotic, peak necrotic and regenerated hindlimb muscle of mdx mice: (1) terminal deoxynucleotidyl transferase (TdT) mediated end-labeling of DNA in nuclei in tissue sections; (2) assays for DNA ladders; and (3) electron microscopic assays for the presence of organelles undergoing structural changes characteristic of apoptosis. At all ages sampled, mdx muscle contained apoptotic nuclei, according to TdT-mediated dUTP labeling of tissue sections. Nuclei in regenerated mdx muscle fibers did not display apoptosis. dUTP-labeled nuclei in control C57 muscles were rare or absent at all ages sampled. DNA from 4-week-old mdx mice was found to be cleaved into fragments indicative of preferential cleavage at internucleosomal sites. Electron microscopic analysis showed that organelle structural changes indicating apoptosis appear before pathological changes diagnostic of necrosis. For example, condensed mitochondria, fragmented sarcoplasmic reticulum and nuclei with chromatin condensations resembling apoptosis appear in fibers that otherwise possess normal morphology. Together, the findings show that apoptosis precedes any detectable necrotic change in mdx muscle, and that apoptotic events continue into the stage of dystrophic pathology that is currently viewed as necrosis. Thus, apoptosis characterizes the onset of pathology in dystrophin-deficient muscle which is followed secondarily by necrotic processes.
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dalla Libera, Luciano, Roberta Zennaro, Marco Sandri, Giovanni Battista Ambrosio, and Giorgio Vescovo. "Apoptosis and atrophy in rat slow skeletal muscles in chronic heart failure." American Journal of Physiology-Cell Physiology 277, no. 5 (November 1, 1999): C982—C986. http://dx.doi.org/10.1152/ajpcell.1999.277.5.c982.

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Congestive heart failure is characterized by a skeletal muscle myopathy with muscle bulk loss. The mechanisms responsible for these changes are not clear at present. We have investigated the role of apoptosis in the rat “slow” soleus muscle during the development of heart failure, which was induced by injection of monocrotaline (30 mg/kg). We looked at the time course of apoptosis by studying six animals at each of the following time points: 0, 17, 24, and 30 days. We found a decreased expression of the antiapoptotic protein Bcl-2, which was accompanied by a rise of proapoptotic caspase-3. Ubiquitin levels did not change. DNA nick-end labeling showed an increased number of apoptotic nuclei both in myofibers and interstitial cells when heart failure occurred. At variance with previous observations in the fast-twitch tibialis anterior muscle in the same animals, in which tumor necrosis factor-α (TNF-α) increased at the time that apoptosis occurred, the magnitude of apoptosis is lower in soleus muscle and there is no appearance of muscle atrophy. In soleus muscle, apoptosis is accompanied by activation of the caspase-3 system. There is no activation of the TNF-α- and ubiquitin-dependent protein waste. In conclusion, slow muscles are less prone to develop apoptosis than fast muscles. Muscle atrophy appears earlier in these latter ones.
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Siu, Parco M., Emidio E. Pistilli, and Stephen E. Alway. "Apoptotic responses to hindlimb suspension in gastrocnemius muscles from young adult and aged rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 289, no. 4 (October 2005): R1015—R1026. http://dx.doi.org/10.1152/ajpregu.00198.2005.

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Although apoptosis has been demonstrated in soleus during hindlimb suspension (HS), it is not known whether apoptosis is also involved in the loss of muscles dominated by mixed fibers. Therefore, we examined the apoptotic responses in gastrocnemius muscles of young adult and aged Fischer 344 × Brown Norway rats after 14 days of HS. The medial gastrocnemius muscle wet weight significantly decreased by 30 and 32%, and muscle wet weight normalized to the animal body weight decreased by 11 and 15% in young adult and aged animals, respectively, after HS. The extent of apoptotic DNA fragmentation increased by 119 and 61% in suspended muscles from young and aged rats, respectively. Bax mRNA increased by 73% in young muscles after HS. Bax and Bcl-2 protein levels were greater in suspended muscles relative to control muscles in both age groups. The level of cytosolic mitochondria-housed apoptotic factor cytochrome c was significantly increased in the mitochondria-free cytosol of suspended muscles from young and aged rats. In contrast, the release/accumulation of AIF, a caspase-independent apoptogenic factor, was exclusively expressed in the suspended muscles from aged rats. Our data also show that aging favors the proapoptotic signaling in skeletal muscle by altering the contents of Bax, Bcl-2, Apaf-1, AIF, caspases, XIAP, Smac/DIABLO, and cytochrome c. Furthermore, these results indicate that apoptosis occurs not only in slow-twitch soleus muscle but also in the mixed-fiber (predominately fast fibered) gastrocnemius muscle. Our data are consistent with the hypothesis that apoptotic signaling differs in young adult and aged gastrocnemius muscles during HS.
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Nguyen, Hanh T., Francesca Voza, Nader Ezzeddine, and Manfred Frasch. "Drosophila mind bomb2 is required for maintaining muscle integrity and survival." Journal of Cell Biology 179, no. 2 (October 22, 2007): 219–27. http://dx.doi.org/10.1083/jcb.200708135.

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We report that the Drosophila mind bomb2 (mib2) gene is a novel regulator of muscle development. Unlike its paralogue, mib1, zygotic expression of mib2 is restricted to somatic and visceral muscle progenitors, and their respective differentiated musculatures. We demonstrate that in embryos that lack functional Mib2, muscle detachment is observed beginning in mid stage 15 and progresses rapidly, culminating in catastrophic degeneration and loss of most somatic muscles by stage 17. Notably, the degenerating muscles are positive for apoptosis markers, and inhibition of apoptosis in muscles prevents to a significant degree the muscle defects. Rescue experiments with Mib1 and Neuralized show further that these E3 ubiquitin ligases are not capable of ameliorating the muscle mutant phenotype of mib2. Our data suggest strongly that mib2 is involved in a novel Notch- and integrin-independent pathway that maintains the integrity of fully differentiated muscles and prevents their apoptotic degeneration.
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Vescovo, Giorgio, Barbara Ravara, Valerio Gobbo, Marco Sandri, Annalisa Angelini, Mila Della Barbera, Massimo Dona, et al. "l-Carnitine: a potential treatment for blocking apoptosis and preventing skeletal muscle myopathy in heart failure." American Journal of Physiology-Cell Physiology 283, no. 3 (September 1, 2002): C802—C810. http://dx.doi.org/10.1152/ajpcell.00046.2002.

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Skeletal muscle in congestive heart failure is responsible for increased fatigability and decreased exercise capacity. A specific myopathy with increased expression of fast-type myosins, myocyte atrophy, secondary to myocyte apoptosis triggered by high levels of circulating tumor necrosis factor-α (TNF-α) has been described. In an animal model of heart failure, the monocrotaline-treated rat, we have observed an increase of apoptotic skeletal muscle nuclei. Proapoptotic agents, caspase-3 and -9, were increased, as well as serum levels of TNF-α and its second messenger sphingosine. Treatment of rats withl-carnitine, known for its protective effect on muscle metabolism injuries, was found to inhibit caspases and to decrease the levels of TNF-α and sphingosine, as well as the number of apoptotic myonuclei. Staurosporine was used in in vitro experiments to induce apoptosis in skeletal muscle cells in culture. Whenl-carnitine was applied to skeletal muscle cells, before staurosporine treatment, we observed a reduction in apoptosis. These findings show that l-carnitine can prevent apoptosis of skeletal muscles cells and has a role in the treatment of congestive heart failure-associated myopathy.
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Kim, Hye Jin, and Oran Kwon. "Aerobic exercise prevents apoptosis in skeletal muscles of high-fat-fed ovariectomized rats." Physical Activity and Nutrition 26, no. 2 (June 30, 2022): 001–7. http://dx.doi.org/10.20463/pan.2022.0007.

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[Purpose] Aging and obesity are associated with skeletal muscle atrophy-related signaling pathways, including apoptosis. Many studies have shown that menopause is associated with an increased risk of skeletal muscle atrophy. There is an increasing need to develop strategies that will improve the risk of skeletal muscle atrophy through exercise interventions. However, the effect of exercise on estrogen deficiency-induced apoptosis in skeletal muscles is poorly understood. Therefore, we examined the effects of low-intensity exercise on ovariectomy (OVX)-induced apoptosis of the soleus and plantaris muscles.[Methods] The ovaries of all female Sprague-Dawley rats aged 8 weeks, were surgically removed to induce postmenopausal status. The rats were randomly divided into three treatment groups: (1) NSV (normal-dietsedentary-OVX); (2) HSV (high-fat-diet-sedentary-OVX); and (3) HEV (high-fat-diet-exercise-OVX). The exercise groups were regularly running for 30-40 min/day at 15-18 m/minute, five times/week, for eight weeks.[Results] The mRNA levels of Bax significantly decreased in the exercised soleus muscle, and caspase-3 decreased in the plantaris. The skeletal muscle TUNEL-positive apoptotic cells in the high-fat-diet-sedentary OVX rats improved in the treadmill exercise group. Additionally, nuclear caspase-3 levels decreased in the treadmill exercise group compared to those in both sedentary groups. These results suggest that low-intensity treadmill exercise prevents skeletal muscle apoptosis in HFD-fed OVX rats.[Conclusion] Induction of HFD in estrogen-deficient mice increased apoptosis in skeletal muscle, which could also be alleviated by low-intensity aerobic exercise. These results may indicate a crucial therapeutic effect of treadmill exercise in preventing skeletal muscle apoptosis in menopausal or post-menopausal women.
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Dissertations / Theses on the topic "Muscle apoptosis"

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Siu, Parco Ming-fai. "The role of apoptosis in muscle remodeling." Morgantown, W. Va. : [West Virginia University Libraries], 2005. https://etd.wvu.edu/etd/controller.jsp?moduleName=documentdata&jsp%5FetdId=4040.

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Thesis (Ph. D.)--West Virginia University, 2005.
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Fellows, Adam Lee. "FOXO3a in vascular smooth muscle cell apoptosis." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/275687.

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FOXO3a is a pro-apoptotic transcription factor which shows increased activation in vascular smooth muscle cells (VSMCs) of advanced atherosclerotic plaques, specifically within the intimal layer. Since VSMC apoptosis plays a crucial role in the pathophysiology of atherosclerosis, we investigated the mechanisms underlying FOXO3a-mediated cell death in this particular cell type. We aimed to characterise a novel VSMC system (FOXO3aA3ERTM) and use these cells to validate MMP-13 and TIMP3 as new FOXO3a target genes. Also, we sought to determine the mechanisms of FOXO3aA3ERTM-mediated VSMC apoptosis, particularly regarding MMP-13 and TIMP3, potential MMP-13 substrates in the extracellular matrix and the precise apoptotic signalling involved. Furthermore, we aimed to investigate whether VSMC-specific activation of FOXO3aA3ERTM in mouse affects vascular remodelling during injury and whether this is reliant on MMP-13. Lastly, we aimed to address if endogenous FOXO3a upregulates MMP-13 in mouse and human VSMCs. Our laboratory has created a transgenic rat VSMC line which stably expresses an inducible FOXO3a mutant allele known as FOXO3aA3ERTM and previous microarray experiments identified matrix metalloproteinase 13 (MMP-13) as a potential novel FOXO3a target gene. Initially, we described several key features of the FOXO3aA3ERTM VSMCs used throughout this thesis, and subsequently demonstrated that MMP-13 is a bona fide target whose expression is rapidly upregulated upon FOXO3a activation, leading to markedly higher levels of protein, cleavage and proteolytic capacity. This induction of MMP-13 was responsible for the vast majority of FOXO3a-mediated apoptosis which was accompanied by prominent degradation of fibronectin, a glycoprotein found in the extracellular matrix. However, we could not identify a terminal apoptotic pathway. FOXO3a also downregulated the endogenous MMP inhibitor TIMP3, the recombinant protein of which reduced both MMP-13 proteolysis and FOXO3a-mediated apoptosis. Activation of FOXO3aA3ERTM in the VSMCs of medium and large arteries in mice resulted in heightened expression of MMP-13 in the vessel wall, which contributed to enhanced neointimal formation during carotid ligation. Finally, endogenous FOXO3a activation leads to increased MMP-13 expression in human VSMCs, but not mouse. Overall, we have shown that FOXO3a promotes VSMC apoptosis through MMP-13 both in vitro and in vivo, a novel pathway that has important implications for the pathogenesis and treatment of vascular disease.
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Sattiraju, Sandhya Ramani. "Apoptosis and necrosis drive muscle fiber loss in lipin1 deficient skeletal muscle." Wright State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=wright1598626794423032.

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Smith, Sierra Marie. "FoxO1 Induces Apoptosis in Skeletal Myotubes." University of Toledo / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1270334870.

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PESSINA, PATRIZIA. "Necdin enhances muscle reconstitution of dystrophic muscle by mesoangioblast cells." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2009. http://hdl.handle.net/10281/7594.

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Improving stem cell therapy is a major goal for the treatment of muscle diseases, where physiological muscle regeneration is progressively exhausted. Mesoangioblasts are vessel-associated stem cells that appear to be the most promising cell type for the cell therapy for muscular dystrophies because of their significant contribution to restoration of muscle structure and function in different muscular dystrophy model. Here we report that MAGE protein Necdin enhances muscle differentiation and regeneration by mesoangioblasts. Indeed, when Necdin is constitutively overexpressed, it accelerates their differentiation and fusion in vitro and it increases their efficacy to restore dystrophic phenotype of α-sarcoglycan mutant mouse. Moreover, Necdin confers a enhanced survival ability when mesoangioblasts are exposed to cytotoxic stimuli that mimic inflammatory dystrophic environment. Taken together, these data demonstrate the pivotal role of Necdin in muscle reconstitution from which we could take advantage to boost therapeutic applications of mesoangioblasts.
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Koutsouki, Evgenia. "The role of cadherins in vascular smooth muscle cell apoptosis." Thesis, University of Bristol, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.420910.

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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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Storbeck, Christopher J. "Effects of the myotonic dystrophy mutation in muscle differentiation and apoptosis." Thesis, University of Ottawa (Canada), 2002. http://hdl.handle.net/10393/6194.

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Myotonic dystrophy (DM) is the most common inherited neuromuscular disorder of adult life. The genetic defect for DM was identified as an unstable CTG trinucleotide repeat found in the 3' untranslated region (UTR) of a serine threonine p&barbelow;rotein k&barbelow;inase, DMPK. Normal individuals possess 5--35 CTG repeats, typical adult DM patients have repeat sizes ranging from 80 to 1000 while cDM patients have from 1000 to several thousand CTG repeats. This discovery provided a molecular basis to account for large variability of penetrance and age of onset in DM. Work in our laboratory progressed from ascertaining mRNA levels in patient tissues to testing the hypothesis that overexpression of DMPK might cause features of DM. Transgenic mice expressed the human DMPK mRNA and protein in the appropriate tissues and had many features of DM including type I fibre atrophy, central nuclei and ringed fibres. Induction of expression resulted in about three fold higher levels of CTG 99 mRNA over CTG 11 mRNA at 48 hours post induction. Levels of cell death were assayed following induction and CTG 99 cell lines showed a marked level of cell death while CTG 11 cell lines did not. The presence of CTG repeats within mRNA therefore appears to be very problematic for the cell. Furthermore, we found that patient amniocytes and myoblasts are susceptible to staurosporine induced cell death. Taken together, this data suggests that myoblasts expressing the DMPK 3' UTR are prone to cell death in an expression level and repeat length dependent manner. In addition, patient cells were found to be susceptible in much the same way. These experiments also revealed that myogenin levels in vivo were reduced in transgenic embryos compared with wild type embryos suggesting that expression of the DMPK 3' UTR in vivo inhibits accumulation of myogenin and perhaps myogenesis. In adult mice there was consistent muscle atrophy in CTG 91 but not in CTG 11 mice despite much lower expression levels of the CTG 91 transgene. Together, these results indicate that expression of the DMPK 3' UTR by itself may inhibit myogenesis in vivo and contribute to pathological features of DM-like muscle atrophy. (Abstract shortened by UMI.)
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Leskinen, Markus. "Mast cell-mediated apoptosis of smooth muscle cells and endothelial cells." Helsinki : University of Helsinki, 2003. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/leskinen/.

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Pistilli, Emidio E. "The extrinsic apoptotic pathway in aged skeletal muscle roles of tumor necrosis factor-[alpha] and interleukin-15 /." Morgantown, W. Va. : [West Virginia University Libraries], 2006. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=4912.

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Thesis (Ph. D.)--West Virginia University, 2006.
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Books on the topic "Muscle apoptosis"

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Mitchell, Lylieth Paula-Ann. Vascular endothelial and smooth muscle cell apoptosis in vivo and in vitro. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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Vasconsuelo, Andrea A., ed. Sex Steroids and Apoptosis In Skeletal Muscle: Molecular Mechanisms. BENTHAM SCIENCE PUBLISHERS, 2019. http://dx.doi.org/10.2174/97898114123631190101.

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Vasconsuelo, Andrea A. Sex Steroids and Apoptosis in Skeletal Muscle: Molecular Mechanisms. Bentham Science Publishers, 2019.

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Dirks, Amie J. The role of apoptosis in sarcopenia: The effects of age and caloric restriction on skeletal muscle apoptosis. 2002.

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Merklinger, Sandra Lea. Progression and regression of pulmonary vascular disease related to smooth muscle cell apoptosis, S100A4/Mts1 and fibulin-5. 2005.

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Marco, Crescenzi, ed. Reactivation of the cell cycle in terminally differentiated cells. Georgetown, Tex: Landes Bioscience, 2002.

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Crescenzi, Marco. Reactivation of the Cell Cycle in Terminally Differentiated Cells (Molecular Biology Intelligence Unit, 17). Springer, 2003.

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Book chapters on the topic "Muscle apoptosis"

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Alway, Stephen E., and Parco M. Siu. "Nuclear Apoptosis and Sarcopenia." In Sarcopenia – Age-Related Muscle Wasting and Weakness, 173–206. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9713-2_9.

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Bauriedel, Gerhard, Sven Schluckebier, Randolph Hutter, Ulrich Welsch, and Berndt Lüderitz. "Post-Angioplasty Smooth Muscle Cell Apoptosis." In Arterial Remodeling: A Critical Factor in Restenosis, 181–98. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-6079-1_10.

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LaBelle, Edward F., Ken Wilson, and Cyril Pilane. "Apoptosis In Vascular Smooth Muscle Accompanied By Increases In Arachidonic Acid." In Advances in Experimental Medicine and Biology, 433–37. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0193-0_67.

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Eickelberg, Oliver, and Fotini M. Kouri. "Biochemistry and Cellular Mechanisms of Apoptosis in Vascular Smooth Muscle and Endothelial Cells." In Textbook of Pulmonary Vascular Disease, 347–56. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-0-387-87429-6_22.

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Juan, Shu-Hui, and Lee-Young Chau. "Induction of Apoptosis in Vascular Smooth Muscle Cells by Heme Oxygenase-1-Derived Carbon Monoxide." In Heme Oxygenase in Biology and Medicine, 449–57. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0741-3_40.

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Miyashita, Yoh, Takeyoshi Murano, Hitoshi Watanabe, Yoshiaki Itoh, Mitsuya Totsuka, and Kohji Shirai. "PDGF Enhanced 7-Ketocholesterol-induced Apoptosis of Vascular Smooth Muscle Cell, accompaning with c-myc Expression." In Lipoprotein Metabolism and Atherogenesis, 266–68. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-68424-4_57.

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Li, Chun Jiang, Yu Feng Zheng, Chao Li, and Lian Cheng Zhao. "The Studies on Biocompatibility of Self-Expanding NiTi Stent and Apoptosis of Smooth Muscle Cells after Stenting." In Advanced Biomaterials VI, 587–90. Stafa: Trans Tech Publications Ltd., 2005. http://dx.doi.org/10.4028/0-87849-967-9.587.

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Liang, Weiwei, Qunhui Yang, Gaofeng Wu, Shumei Lin, Jiancheng Yang, Ying Feng, and Jianmin Hu. "Effects of Taurine and l-Arginine on the Apoptosis of Vascular Smooth Muscle Cells in Insulin Resistance Hypertensive Rats." In Advances in Experimental Medicine and Biology, 813–19. Dordrecht: Springer Netherlands, 2017. http://dx.doi.org/10.1007/978-94-024-1079-2_63.

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Alway, Stephen. "Apoptosis in Skeletal Muscle Health and Conditions of Muscle Wasting." In Apoptosis, 167–81. Science Publishers, 2010. http://dx.doi.org/10.1201/9781439845431-14.

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"Apoptosis in Skeletal Muscle Health and Conditions of Muscle Wasting." In Apoptosis, 177–92. CRC Press, 2010. http://dx.doi.org/10.1201/9781439845431-15.

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Conference papers on the topic "Muscle apoptosis"

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Suzuki, YJ, L. Liu, and A. Park. "Differential Mechanisms of Apoptosis in Pulmonary Artery Smooth Muscle Cells and in Cardiac Muscle Cells." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5359.

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Yao, Dong, Bo Xiao, Lixia Hou, Lihong Yang, and Biwen Mo. "The effect of Icaritin on airway smooth muscle cells proliferation and apoptosis." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa4204.

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Hartman, William R., Lucas W. Meuchel, Dan F. Smelter, Michael A. Thompson, Christina M. Pabelick, and Y. S. Prakash. "Brain Derived Neurotrophic Factor Prevents Apoptosis In Human Pulmonary Artery Smooth Muscle Cells." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3400.

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Kute, Stephanie M., and David A. Vorp. "Regional Association of Biological and Hemodynamic Parameters in Distal End-to-Side Vascular Anastomoses Perfused Ex Vivo." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32513.

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Abstract:
Vascular bypass graft failure is a significant clinical problem and is frequently due to the formation of intimal hyperplasia (IH) [1–3]. IH is characterized by the accumulation of smooth muscle cells (SMC) and extracellular matrix in the intima of the vessel, which occurs when the normal balance between vascular cell proliferation and apoptosis (regulated cell death) is altered [4]. The disturbed flow present at the anastomosis has been implicated in the formation of IH and the link between hemodynamics and graft failure is via a complex cascade of events whereby biomechanical forces cause biological responses [5, 6]. For example, immediate early genes (IEG) such as c-fos, c-jun and egr-1 are involved in the signaling pathways for proliferation and apoptosis. When extracellular biomechanical stimuli (e.g. shear stress) cause the expression of IEG, their protein products translocate to the nucleus. These proteins regulate the expression of a number of genes implicated in cardiovascular disease including growth factors, adhesion molecules, proapoptotic substrates and coagulation factors [7–9]. Because IEG are involved in both proliferation and apoptosis, their expression may upset the normal balance between cell proliferation and apoptosis and could play a vital role in the IH formation in vascular bypass grafts.
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Faraoni, María, Lorena Milanesi, Darío Lincor, Florencia Musso, and Andrea Vasconsuelo. "EXTRACTS FROM Nicotiana glauca INDUCE APOPTOSIS THROUGH CASPASES IN SKELETAL MUSCLE CELLS." In The 21st International Electronic Conference on Synthetic Organic Chemistry. Basel, Switzerland: MDPI, 2017. http://dx.doi.org/10.3390/ecsoc-21-04784.

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Yin, Huijuan, Xiaoyuan Li, Hong Lin, Jianzhong Liu, and Hongkui Yu. "The apoptosis induced by HMME-based photodynamic therapy in rabbit vascular smooth muscle cells." In Biomedical Optics (BiOS) 2007, edited by David Kessel. SPIE, 2007. http://dx.doi.org/10.1117/12.702042.

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Jalali, Samuel, Guru Kumar Kollongod Ramanathan, Prasanna Tamarapu Parthasarathy, Salman Aljubran, Ruan Cox Jr, Richard Lockey, and Narasaiah Kolliputi. "Role Of Microrna 206 In Human Pulmonary Artery Smooth Muscle Cell Proliferation And Apoptosis." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4838.

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Zhang, Meiling, and Judith Davie. "Abstract 28: Deregulation of NAC complex inhibits muscle differentiation and blocks apoptosis in rhabdomyosarcoma cells." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-28.

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Chettimada, Sukrutha U., Robert Kobelja, rakhee S. Gupte, and sachin A. gupte. "Role Of Glucose-6-Phosphate Dehydrogenase In Pulmonary Artery Smooth Muscle Cell Proliferation & Apoptosis." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3457.

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James, J., M. Valuparampil Varghese, M. Niihori, M. Zemskova, P. R. Langlais, O. Rafikova, and R. Rafikov. "The NFU1 G206C Mutation Metabolically Reprograms Pulmonary Artery Smooth Muscle Cells, Promotes Proliferation and Apoptosis Resistance." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2500.

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