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Ashok Kumar - One of the best experts on this subject based on the ideXlab platform.
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the tweak fn14 system is a critical regulator of denervation induced Skeletal Muscle Atrophy in mice
Journal of Cell Biology, 2010Co-Authors: Ashwani Mittal, Shephali Bhatnagar, Estelle Lachtrifilieff, Sandrine Wauters, Denys Y Makonchuk, David J Glass, Hong Li, Akhilesh Kumar, Ashok KumarAbstract:Skeletal Muscle Atrophy occurs in a variety of clinical settings, including cachexia, disuse, and denervation. Inflammatory cytokines have been shown to be mediators of cancer cachexia; however, the role of cytokines in denervation- and immobilization-induced Skeletal Muscle loss remains unknown. In this study, we demonstrate that a single cytokine, TNF-like weak inducer of apoptosis (TWEAK), mediates Skeletal Muscle Atrophy that occurs under denervation conditions. Transgenic expression of TWEAK induces Atrophy, fibrosis, fiber-type switching, and the degradation of Muscle proteins. Importantly, genetic ablation of TWEAK decreases the loss of Muscle proteins and spared fiber cross-sectional area, Muscle mass, and strength after denervation. Expression of the TWEAK receptor Fn14 (fibroblast growth factor–inducible receptor 14) and not the cytokine is significantly increased in Muscle upon denervation, demonstrating an unexpected inside-out signaling pathway; the receptor up-regulation allows for TWEAK activation of nuclear factor κB, causing an increase in the expression of the E3 ubiquitin ligase MuRF1. This study reveals a novel mediator of Skeletal Muscle Atrophy and indicates that the TWEAK–Fn14 system is an important target for preventing Skeletal Muscle wasting.
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The TWEAK–Fn14 system is a critical regulator of denervation-induced Skeletal Muscle Atrophy in mice
The Journal of cell biology, 2010Co-Authors: Ashwani Mittal, Shephali Bhatnagar, Sandrine Wauters, Denys Y Makonchuk, David J Glass, Akhilesh Kumar, Estelle Lach-trifilieff, Ashok KumarAbstract:Skeletal Muscle Atrophy occurs in a variety of clinical settings, including cachexia, disuse, and denervation. Inflammatory cytokines have been shown to be mediators of cancer cachexia; however, the role of cytokines in denervation- and immobilization-induced Skeletal Muscle loss remains unknown. In this study, we demonstrate that a single cytokine, TNF-like weak inducer of apoptosis (TWEAK), mediates Skeletal Muscle Atrophy that occurs under denervation conditions. Transgenic expression of TWEAK induces Atrophy, fibrosis, fiber-type switching, and the degradation of Muscle proteins. Importantly, genetic ablation of TWEAK decreases the loss of Muscle proteins and spared fiber cross-sectional area, Muscle mass, and strength after denervation. Expression of the TWEAK receptor Fn14 (fibroblast growth factor–inducible receptor 14) and not the cytokine is significantly increased in Muscle upon denervation, demonstrating an unexpected inside-out signaling pathway; the receptor up-regulation allows for TWEAK activation of nuclear factor κB, causing an increase in the expression of the E3 ubiquitin ligase MuRF1. This study reveals a novel mediator of Skeletal Muscle Atrophy and indicates that the TWEAK–Fn14 system is an important target for preventing Skeletal Muscle wasting.
Ashwani Mittal - One of the best experts on this subject based on the ideXlab platform.
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Tinospora cordifolia protects from Skeletal Muscle Atrophy by alleviating oxidative stress and inflammation induced by sciatic denervation.
Journal of ethnopharmacology, 2020Co-Authors: Bhawana Sharma, Ashwani Mittal, Vikas Dutt, Nirmaljeet Kaur, Rajesh DaburAbstract:Abstract Ethanopharmacological relevance Tinospora cordifolia (TC) is widely being used as immunomodulatory and re-juvenile drug and well described in Indian Ayurveda system of medicine. Rejuvenation also means the fine tuning of the Skeletal Muscles. Skeletal Muscle related disorder, i.e. Atrophy is major problem which arise due to cachexia, sarcopenia and immobilization. However, despite of the great efforts, there is scarcity of FDA approved drugs in the market to treat Skeletal Muscle Atrophy. Aim of the study The current study was aimed to explore the in-vitro and in-vivo efficacy and mechanism of TC in myogenic differentiation and Skeletal Muscle Atrophy to establish the possibility of its usage to counteract Skeletal Muscle Atrophy. Materials and methods C2C12 cell lines were used to determine myogenic potential and anti-atrophic effects of T. cordifolia water extract (TCE). Its in-vitro efficacy was re-validated in vivo by supplementation of TCE at a dose of 200 mg/kg/p.o. for 30 days in denervated mice model of Skeletal Muscle Atrophy. Effects of TCE administration on levels of oxidative stress, inflammatory markers and proteolysis were determined. Results TCE supplementation displayed increased lymphocyte proliferation and induced myogenic differentiation of C2C12 myoblasts by significantly increasing myocytes length and thickness, in comparison to control (p Conclusion TCE supplementation promotes myogenic differentiation in C2C12 cell lines and prevents denervation induced Skeletal Muscle Atrophy by antagonizing the proteolytic systems (calpain and UPS) and maintaining the oxidative defense mechanism of the cell. Hence, TCE can be used as a protective agent against Muscle Atrophy.
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the tweak fn14 system is a critical regulator of denervation induced Skeletal Muscle Atrophy in mice
Journal of Cell Biology, 2010Co-Authors: Ashwani Mittal, Shephali Bhatnagar, Estelle Lachtrifilieff, Sandrine Wauters, Denys Y Makonchuk, David J Glass, Hong Li, Akhilesh Kumar, Ashok KumarAbstract:Skeletal Muscle Atrophy occurs in a variety of clinical settings, including cachexia, disuse, and denervation. Inflammatory cytokines have been shown to be mediators of cancer cachexia; however, the role of cytokines in denervation- and immobilization-induced Skeletal Muscle loss remains unknown. In this study, we demonstrate that a single cytokine, TNF-like weak inducer of apoptosis (TWEAK), mediates Skeletal Muscle Atrophy that occurs under denervation conditions. Transgenic expression of TWEAK induces Atrophy, fibrosis, fiber-type switching, and the degradation of Muscle proteins. Importantly, genetic ablation of TWEAK decreases the loss of Muscle proteins and spared fiber cross-sectional area, Muscle mass, and strength after denervation. Expression of the TWEAK receptor Fn14 (fibroblast growth factor–inducible receptor 14) and not the cytokine is significantly increased in Muscle upon denervation, demonstrating an unexpected inside-out signaling pathway; the receptor up-regulation allows for TWEAK activation of nuclear factor κB, causing an increase in the expression of the E3 ubiquitin ligase MuRF1. This study reveals a novel mediator of Skeletal Muscle Atrophy and indicates that the TWEAK–Fn14 system is an important target for preventing Skeletal Muscle wasting.
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The TWEAK–Fn14 system is a critical regulator of denervation-induced Skeletal Muscle Atrophy in mice
The Journal of cell biology, 2010Co-Authors: Ashwani Mittal, Shephali Bhatnagar, Sandrine Wauters, Denys Y Makonchuk, David J Glass, Akhilesh Kumar, Estelle Lach-trifilieff, Ashok KumarAbstract:Skeletal Muscle Atrophy occurs in a variety of clinical settings, including cachexia, disuse, and denervation. Inflammatory cytokines have been shown to be mediators of cancer cachexia; however, the role of cytokines in denervation- and immobilization-induced Skeletal Muscle loss remains unknown. In this study, we demonstrate that a single cytokine, TNF-like weak inducer of apoptosis (TWEAK), mediates Skeletal Muscle Atrophy that occurs under denervation conditions. Transgenic expression of TWEAK induces Atrophy, fibrosis, fiber-type switching, and the degradation of Muscle proteins. Importantly, genetic ablation of TWEAK decreases the loss of Muscle proteins and spared fiber cross-sectional area, Muscle mass, and strength after denervation. Expression of the TWEAK receptor Fn14 (fibroblast growth factor–inducible receptor 14) and not the cytokine is significantly increased in Muscle upon denervation, demonstrating an unexpected inside-out signaling pathway; the receptor up-regulation allows for TWEAK activation of nuclear factor κB, causing an increase in the expression of the E3 ubiquitin ligase MuRF1. This study reveals a novel mediator of Skeletal Muscle Atrophy and indicates that the TWEAK–Fn14 system is an important target for preventing Skeletal Muscle wasting.
David J Glass - One of the best experts on this subject based on the ideXlab platform.
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the tweak fn14 system is a critical regulator of denervation induced Skeletal Muscle Atrophy in mice
Journal of Cell Biology, 2010Co-Authors: Ashwani Mittal, Shephali Bhatnagar, Estelle Lachtrifilieff, Sandrine Wauters, Denys Y Makonchuk, David J Glass, Hong Li, Akhilesh Kumar, Ashok KumarAbstract:Skeletal Muscle Atrophy occurs in a variety of clinical settings, including cachexia, disuse, and denervation. Inflammatory cytokines have been shown to be mediators of cancer cachexia; however, the role of cytokines in denervation- and immobilization-induced Skeletal Muscle loss remains unknown. In this study, we demonstrate that a single cytokine, TNF-like weak inducer of apoptosis (TWEAK), mediates Skeletal Muscle Atrophy that occurs under denervation conditions. Transgenic expression of TWEAK induces Atrophy, fibrosis, fiber-type switching, and the degradation of Muscle proteins. Importantly, genetic ablation of TWEAK decreases the loss of Muscle proteins and spared fiber cross-sectional area, Muscle mass, and strength after denervation. Expression of the TWEAK receptor Fn14 (fibroblast growth factor–inducible receptor 14) and not the cytokine is significantly increased in Muscle upon denervation, demonstrating an unexpected inside-out signaling pathway; the receptor up-regulation allows for TWEAK activation of nuclear factor κB, causing an increase in the expression of the E3 ubiquitin ligase MuRF1. This study reveals a novel mediator of Skeletal Muscle Atrophy and indicates that the TWEAK–Fn14 system is an important target for preventing Skeletal Muscle wasting.
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The TWEAK–Fn14 system is a critical regulator of denervation-induced Skeletal Muscle Atrophy in mice
The Journal of cell biology, 2010Co-Authors: Ashwani Mittal, Shephali Bhatnagar, Sandrine Wauters, Denys Y Makonchuk, David J Glass, Akhilesh Kumar, Estelle Lach-trifilieff, Ashok KumarAbstract:Skeletal Muscle Atrophy occurs in a variety of clinical settings, including cachexia, disuse, and denervation. Inflammatory cytokines have been shown to be mediators of cancer cachexia; however, the role of cytokines in denervation- and immobilization-induced Skeletal Muscle loss remains unknown. In this study, we demonstrate that a single cytokine, TNF-like weak inducer of apoptosis (TWEAK), mediates Skeletal Muscle Atrophy that occurs under denervation conditions. Transgenic expression of TWEAK induces Atrophy, fibrosis, fiber-type switching, and the degradation of Muscle proteins. Importantly, genetic ablation of TWEAK decreases the loss of Muscle proteins and spared fiber cross-sectional area, Muscle mass, and strength after denervation. Expression of the TWEAK receptor Fn14 (fibroblast growth factor–inducible receptor 14) and not the cytokine is significantly increased in Muscle upon denervation, demonstrating an unexpected inside-out signaling pathway; the receptor up-regulation allows for TWEAK activation of nuclear factor κB, causing an increase in the expression of the E3 ubiquitin ligase MuRF1. This study reveals a novel mediator of Skeletal Muscle Atrophy and indicates that the TWEAK–Fn14 system is an important target for preventing Skeletal Muscle wasting.
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A signaling role for dystrophin: Inhibiting Skeletal Muscle Atrophy pathways
Cancer cell, 2005Co-Authors: David J GlassAbstract:Skeletal Muscle Atrophy is a common comorbidity of cancer. The cellular signaling mechanisms that regulate Muscle size constitute a balance of the protein breakdown pathways upregulated during Atrophy, and the protein synthesis pathways that are activated during Skeletal Muscle hypertrophy. In this issue of Cancer Cell, Acharyya et al. demonstrate a new and surprising regulatory axis that is centered around dystrophin, the protein that is mutated in settings of muscular dystrophy. These data reposition dystrophin as a signaling protein and connect an important cellular complex required for the structural integrity of Muscle to the pathways that modulate Muscle size.
Suresh C. Tyagi - One of the best experts on this subject based on the ideXlab platform.
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TFAM overexpression diminishes Skeletal Muscle Atrophy after hindlimb suspension in mice.
Archives of biochemistry and biophysics, 2018Co-Authors: Nicholas T. Theilen, Nevena Jeremic, Gregory J. Weber, Suresh C. TyagiAbstract:Abstract The present study aims to investigate if overexpressing the mitochondrial transcription factor A (TFAM) gene in a transgenic mouse model diminishes soleus and gastrocnemius Atrophy occurring during hindlimb suspension (HLS). Additionally, we aim to observe if combining exercise training in TFAM transgenic mice prior to HLS has a synergistic effect in preventing Skeletal Muscle Atrophy. Male C57BL/6J-based transgenic mice (12–14 weeks old) overexpressing TFAM were assigned to a control (T-Control), 7-day HLS (T-HLS), and 2-week exercise training prior to 7-day HLS (T-Ex + HLS) groups. These groups were compared to male C57BL/6J wild-type (WT) mice (12–14 weeks old) assigned to Control, 7-day HLS (HLS), 2-week exercise training prior to 7-day HLS (Ex + HLS), and 2-week exercise training (Ex). Overexpressing TFAM results in a decrease of 8.3% in soleus and 2.6% in gastrocnemius Muscle weight to bodyweight ratio after only HLS compared to wild-type mice incurring a loss of 27.1% in soleus and 21.5% in gastrocnemius Muscle after HLS. Our data indicates TFAM may play a critical role in protecting Skeletal Muscle from disuse Atrophy and is correlated with increased expression of antioxidants (SOD-2) and potential redox balance. TFAM may be an attractive molecule of interest for potential, future therapeutic development. New and noteworthy To the best of our knowledge, this is the first time a TFAM overexpression transgenic mouse model is being used in the analysis of disuse-induced Skeletal Muscle Atrophy. Here we provide evidence of a potential role for TFAM in diminishing Skeletal Muscle Atrophy.
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Exercise preconditioning diminishes Skeletal Muscle Atrophy after hindlimb suspension in mice
Journal of applied physiology (Bethesda Md. : 1985), 2018Co-Authors: Nicholas T. Theilen, Nevena Jeremic, Gregory J. Weber, Suresh C. TyagiAbstract:Mitochondrial dysfunction is associated with disuse-induced Skeletal Muscle Atrophy, whereas exercise is known to increase mitochondrial biogenesis and function. Here we provide evidence of short-t...
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The Role of Exercise and TFAM in Preventing Skeletal Muscle Atrophy
Journal of Cellular Physiology, 2017Co-Authors: Nicholas T. Theilen, George H. Kunkel, Suresh C. TyagiAbstract:Skeletal Muscle Atrophy is the consequence of protein degradation exceeding protein synthesis. This arises for a multitude of reasons including the unloading of Muscle during microgravity, post-surgery bedrest, immobilization of a limb after injury, and overall disuse of the musculature. The development of therapies prior to Skeletal Muscle Atrophy settings to diminish protein degradation is scarce. Mitochondrial dysfunction is associated with Skeletal Muscle Atrophy and contributes to the induction of protein degradation and cell apoptosis through increased levels of ROS observed with the loss of organelle function. ROS binds mtDNA, leading to its degradation and decreasing functionality. Mitochondrial transcription factor A (TFAM) will bind and coat mtDNA, protecting it from ROS and degradation while increasing mitochondrial function. Exercise stimulates cell signaling pathways that converge on and increase PGC-1α, a well-known activator of the transcription of TFAM and mitochondrial biogenesis. Therefore, in the present review we are proposing, separately, exercise and TFAM treatments prior to atrophic settings (Muscle unloading or disuse) alleviate Skeletal Muscle Atrophy through enhanced mitochondrial adaptations and function. Additionally, we hypothesize the combination of exercise and TFAM leads to a synergistic effect in targeting mitochondrial function to prevent Skeletal Muscle Atrophy. J. Cell. Physiol. 232: 2348–2358, 2017. © 2016 Wiley Periodicals, Inc.
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The Role of Exercise and TFAM in Preventing Skeletal Muscle Atrophy.
Journal of cellular physiology, 2017Co-Authors: Nicholas T. Theilen, George H. Kunkel, Suresh C. TyagiAbstract:Skeletal Muscle Atrophy is the consequence of protein degradation exceeding protein synthesis. This arises for a multitude of reasons including the unloading of Muscle during microgravity, post-surgery bedrest, immobilization of a limb after injury, and overall disuse of the musculature. The development of therapies prior to Skeletal Muscle Atrophy settings to diminish protein degradation is scarce. Mitochondrial dysfunction is associated with Skeletal Muscle Atrophy and contributes to the induction of protein degradation and cell apoptosis through increased levels of ROS observed with the loss of organelle function. ROS binds mtDNA, leading to its degradation and decreasing functionality. Mitochondrial transcription factor A (TFAM) will bind and coat mtDNA, protecting it from ROS and degradation while increasing mitochondrial function. Exercise stimulates cell signaling pathways that converge on and increase PGC-1α, a well-known activator of the transcription of TFAM and mitochondrial biogenesis. Therefore, in the present review we are proposing, separately, exercise and TFAM treatments prior to atrophic settings (Muscle unloading or disuse) alleviate Skeletal Muscle Atrophy through enhanced mitochondrial adaptations and function. Additionally, we hypothesize the combination of exercise and TFAM leads to a synergistic effect in targeting mitochondrial function to prevent Skeletal Muscle Atrophy. J. Cell. Physiol. 232: 2348-2358, 2017. © 2016 The Authors. Journal of Cellular Physiology Published by © 2016 Wiley Periodicals, Inc.
Seung Hyo Jung - One of the best experts on this subject based on the ideXlab platform.
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sabinene prevents Skeletal Muscle Atrophy by inhibiting the mapk murf 1 pathway in rats
International Journal of Molecular Sciences, 2019Co-Authors: Seung Hyo JungAbstract:Chrysanthemum boreale Makino essential oil (CBMEO) has diverse biological activities including a skin regenerating effect. However, its role in Muscle Atrophy remains unknown. This study explored the effects of CBMEO and its active ingredients on Skeletal Muscle Atrophy using in vitro and in vivo models of Muscle Atrophy. CBMEO reversed the size decrease of L6 myoblasts under starvation. Among the eight monoterpene compounds of CBMEO without cytotoxicity for L6 cells, sabinene induced predominant recovery of reductions of myotube diameters under starvation. Sabinene diminished the elevated E3 ubiquitin ligase Muscle ring-finger protein-1 (MuRF-1) expression and p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase1/2 (ERK1/2) phosphorylations in starved myotubes. Moreover, sabinene decreased the increased level of reactive oxygen species (ROS) in myotubes under starvation. The ROS inhibitor antagonized expression of MuRF-1 and phosphorylation of MAPKs, which were elevated in starved myotubes. In addition, levels of Muscle fiber Atrophy and MuRF-1 expression in gastrocnemius from fasted rats were reduced after administration of sabinene. These findings demonstrate that sabinene, a bioactive component from CBMEO, may attenuate Skeletal Muscle Atrophy by regulating the activation mechanism of ROS-mediated MAPK/MuRF-1 pathways in starved myotubes, probably leading to the reverse of reduced Muscle fiber size in fasted rats.
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sabinene prevents Skeletal Muscle Atrophy by inhibiting the mapk murf 1 pathway in rats
International Journal of Molecular Sciences, 2019Co-Authors: Seung Hyo JungAbstract:Chrysanthemum boreale Makino essential oil (CBMEO) has diverse biological activities including a skin regenerating effect. However, its role in Muscle Atrophy remains unknown. This study explored the effects of CBMEO and its active ingredients on Skeletal Muscle Atrophy using in vitro and in vivo models of Muscle Atrophy. CBMEO reversed the size decrease of L6 myoblasts under starvation. Among the eight monoterpene compounds of CBMEO without cytotoxicity for L6 cells, sabinene induced predominant recovery of reductions of myotube diameters under starvation. Sabinene diminished the elevated E3 ubiquitin ligase Muscle ring-finger protein-1 (MuRF-1) expression and p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase1/2 (ERK1/2) phosphorylations in starved myotubes. Moreover, sabinene decreased the increased level of reactive oxygen species (ROS) in myotubes under starvation. The ROS inhibitor antagonized expression of MuRF-1 and phosphorylation of MAPKs, which were elevated in starved myotubes. In addition, levels of Muscle fiber Atrophy and MuRF-1 expression in gastrocnemius from fasted rats were reduced after administration of sabinene. These findings demonstrate that sabinene, a bioactive component from CBMEO, may attenuate Skeletal Muscle Atrophy by regulating the activation mechanism of ROS-mediated MAPK/MuRF-1 pathways in starved myotubes, probably leading to the reverse of reduced Muscle fiber size in fasted rats.