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Satoshi Okumura - One of the best experts on this subject based on the ideXlab platform.
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protective effects of clenbuterol against dexamethasone induced Masseter Muscle atrophy and myosin heavy chain transition
PLOS ONE, 2015Co-Authors: Daisuke Umeki, Yoshiki Ohnuki, Yasumasa Mototani, Kouichi Shiozawa, Takayuki Fujita, Yoshiki Nakamura, Yasutake Saeki, Kenji Suita, Satoshi OkumuraAbstract:Background Glucocorticoid has a direct catabolic effect on skeletal Muscle, leading to Muscle atrophy, but no effective pharmacotherapy is available. We reported that clenbuterol (CB) induced Masseter Muscle hypertrophy and slow-to-fast myosin heavy chain (MHC) isoform transition through direct Muscle β2-adrenergic receptor stimulation. Thus, we hypothesized that CB would antagonize glucocorticoid (dexamethasone; DEX)-induced Muscle atrophy and fast-to-slow MHC isoform transition. Methodology We examined the effect of CB on DEX-induced Masseter Muscle atrophy by measuring Masseter Muscle weight, fiber diameter, cross-sectional area, and myosin heavy chain (MHC) composition. To elucidate the mechanisms involved, we used immunoblotting to study the effects of CB on Muscle hypertrophic signaling (insulin growth factor 1 (IGF1) expression, Akt/mammalian target of rapamycin (mTOR) pathway, and calcineurin pathway) and atrophic signaling (Akt/Forkhead box-O (FOXO) pathway and myostatin expression) in Masseter Muscle of rats treated with DEX and/or CB. Results and Conclusion Masseter Muscle weight in the DEX-treated group was significantly lower than that in the Control group, as expected, but co-treatment with CB suppressed the DEX-induced Masseter Muscle atrophy, concomitantly with inhibition of fast-to-slow MHC isoforms transition. Activation of the Akt/mTOR pathway in Masseter Muscle of the DEX-treated group was significantly inhibited compared to that of the Control group, and CB suppressed this inhibition. DEX also suppressed expression of IGF1 (positive regulator of Muscle growth), and CB attenuated this inhibition. Myostatin protein expression was unchanged. CB had no effect on activation of the Akt/FOXO pathway. These results indicate that CB antagonizes DEX-induced Muscle atrophy and fast-to-slow MHC isoform transition via modulation of Akt/mTOR activity and IGF1 expression. CB might be a useful pharmacological agent for treatment of glucocorticoid-induced Muscle atrophy.
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effects of chronic akt mtor inhibition by rapamycin on mechanical overload induced hypertrophy and myosin heavy chain transition in Masseter Muscle
Journal of Pharmacological Sciences, 2013Co-Authors: Daisuke Umeki, Yoshiki Ohnuki, Yasumasa Mototani, Kouichi Shiozawa, Takayuki Fujita, Yoshiki Nakamura, Yasutake Saeki, Satoshi OkumuraAbstract:To examine the effects of the Akt/mammalian target of rapamycin (mTOR) pathway on Masseter Muscle hypertrophy and myosin heavy chain (MHC) transition in response to mechanical overload, we analyzed the effects of bite-opening (BO) on the hypertrophy and MHC composition of Masseter Muscle of BO-rats treated or not treated with rapamycin (RAPA), a selective mTOR inhibitor. The Masseter Muscle weight in BO-rats was significantly greater than that in controls, and this increase was attenuated by RAPA treatment. Expression of slow-twitch MHC isoforms was significantly increased in BO-rats with/without RAPA treatment, compared with controls, but the magnitude of the increase was much smaller in RAPA-treated BO-rats. Phosphorylation of p44/42 MAPK (ERK1/2), which preserves fast-twitch MHC isoforms in skeletal Muscle, was significantly decreased in BO-rats, but the decrease was abrogated by RAPA treatment. Calcineurin signaling is known to be important for Masseter Muscle hypertrophy and fast-to-slow MHC isoform transition, but expression of known calcineurin activity modulators was unaffected by RAPA treatment. Taken together, these results indicate that the Akt/mTOR pathway is involved in both development of Masseter Muscle hypertrophy and fast-to-slow MHC isoform transition in response to mechanical overload with inhibition of the ERK1/2 pathway and operates independently of the calcineurin pathway.
Peter Svensson - One of the best experts on this subject based on the ideXlab platform.
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functional change in experimental allodynia after glutamate induced pain in the human Masseter Muscle
Frontiers in Oral Health, 2020Co-Authors: Akiko Shimada, Peter Svensson, Malin Ernberg, Abdelrahman M Alhilou, Nikolaos ChristidisAbstract:Background: Glutamate, as well as nerve growth factor (NGF), is involved in nociception from peripheral tissues, such as Muscles. However, the potential interaction between glutamate and NGF still remains unclear. This study investigated the interaction between glutamate-induced Masseter Muscle pain and NGF-induced allodynia on pain perception and jaw function in healthy individuals, and any possible sex differences in the response. Materials and methods: Thirty pain-free adult participants (15 men and 15 women, mean age ± SD: 24 ± 4 years) participated in this study consisting of three sessions (Day 0, Day 3 and Day 4). NGF (5 μg/mL, 1.0 mL) was injected into the Masseter Muscle on Day 0 to induce Muscle allodynia. On Day 3, glutamate (1M, 0.2 mL) was injected into the same Masseter Muscle. Before and after injections on Day 0 and 3, and post-injection (Day 4), spontaneous pain, temporal summation pain, as well as functional pain and fatigue in response to chewing were assessed with validated scales, and the pressure pain threshold (PPT) was recorded. Results: Spontaneous pain intensity was significantly higher after glutamate than NGF (P 0.189). Chewing pain (P = 0.022) and fatigue increased after glutamate injection to a higher degree in the women than men (P = 0.037). Conclusion: Taken together, while glutamate injected into the NGF-sensitized Muscle was painful, it did not alter Muscle tenderness in women versus men. However, pain and fatigue evoked by jaw function were higher in women after glutamate injection. This suggest that sex differences reported for Masseter myalgia, mimicked by glutamate and NGF mediated pain in this study, may be greater for measures of perceived jaw function, which should be considered in a clinical evaluation.
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referred pain and sensations evoked by standardized palpation of the Masseter Muscle in healthy participants
Journal of oral and facial pain and headache, 2018Co-Authors: Manabu Masuda, Takashi Iida, Fernando G Exposto, Lene Baadhansen, Misao Kawara, Osamu Komiyama, Peter SvenssonAbstract:Aims: To determine if standardized palpation of the Masseter Muscle can evoke referred pain and/or sensations in healthy individuals and to compare the mechanical sensitivities in response to three different levels of palpation force. Methods: A total of 32 pain-free individuals participated. The right Masseter Muscle was divided into 15 test sites. Mechanical sensitivity of the Masseter was assessed with three mechanical stimuli (0.5 kg, 1.0 kg, or 2.0 kg) applied by palpometers to the 15 test sites for 5 seconds each site. Participants scored the perceived intensity of pain and unpleasantness of each of the three mechanical stimuli on 0-100 numeric rating scales (NRS). After each stimulus, the duration of aftersensation was measured, and the participants were also asked to indicate areas within the orofacial region with referred pain/sensations. Data were tested using analysis of variance, Tukey post hoc, and McNemar's tests with a 5% level of significance. Results: Referred pain/sensations were most commonly evoked with the 2.0-kg stimulus (34.4% of participants; P < .05) compared to the 1.0-kg (12.5%) and 0.5-kg stimuli (3.1%). There were significant effects of stimulus intensity on NRS scores for pain and unpleasantness, as well as for aftersensation (P < .05). There were significant effects on NRS scores for pain and unpleasantness for the 1.0- and 2.0-kg stimuli (P < .05) and on aftersensation for the 2.0-kg stimulus (P < .05). Conclusion: These results indicate that referred pain/sensations in the orofacial region are frequent phenomena among healthy individuals during standardized palpation of the Masseter Muscle.
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experimental stressors alter hypertonic saline evoked Masseter Muscle pain and autonomic response
Journal of Orofacial Pain, 2012Co-Authors: Karina H Bendixen, Brian E Cairns, Lene Baadhansen, Astrid Juhl Terkelsen, Peter SvenssonAbstract:Aims: To test in a randomized controlled trial, if hypertonic saline (HS)–evoked pain and autonomic function are modulated by either a cold pressor test (CPT) or mental arithmetic stress induced by a paced auditory serial addition task (PASAT). Methods: Fourteen healthy women participated in three sessions. Pain was induced by two 5% HS infusions (5 minutes each, 30 minutes apart) infused into the Masseter Muscle. During the second HS infusion, pain was modulated by PASAT, CPT, or control (HS alone). HS-evoked pain intensity was scored on a 0 to 10 numeric rating scale (NRS). Heart rate variability (HRV) and hemodynamic measures were recorded noninvasively (Task Force Monitor). Data were analyzed using repeated measurements ANOVAs and Spearman correlation analysis. Results: HS-evoked pain was significantly and similarly reduced by both PASAT (30.8 ± 27.6%; P .05). PASAT and CPT increased the heart rate compared with control (P .05). Conclusion: CPT and PASAT reduced HS-evoked Masseter Muscle pain and altered the autonomic response. The increase in heart rate following CPT and PASAT may be caused by different mechanisms. CPT reduced measures of efferent cardiac vagal (parasympathetic) activity, while the PASAT-induced increase in heart rate, but unchanged HRV, may suggest neurohumoral activation. J OROFAC PAIN 2012;26:191–205
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human nerve growth factor sensitizes Masseter Muscle nociceptors in female rats
Pain, 2010Co-Authors: Mian Wei Wang, Peter Svensson, Xudong Dong, Ujendra Kumar, Brian E CairnsAbstract:Abstract Injection of nerve growth factor (NGF) into the Masseter Muscle is not painful but does induce a localized, quick onset (∼1 h) and long-lasting mechanical sensitization in healthy human subjects. We tested the hypothesis that human NGF mechanically sensitizes Masseter Muscle nociceptors by increasing the sensitivity of peripheral N-methyl- d -aspartate (NMDA) receptors. Co-expression of the NR2B subunit of the NMDA receptor with P75 and TrkA NGF receptors by trigeminal ganglion neurons that innervate the Masseter Muscle was investigated immunohistochemically. Nociceptor activity was recorded extracellularly from the trigeminal ganglion of anaesthetized female rats. Nociceptor mechanical threshold was assessed before and every 30 min for 3 h after injection of human NGF (25 μg/ml, 10 μl, n = 12), and in subsequent experiments NGF with TrkA ( n = 12) or P75 ( n = 11) receptor antibodies. Glutamate (1 M, 10 μl) was injected at the end of each experiment. Approximately 85% of NR2B positive Masseter ganglion neurons co-expressed P75 or TrkA receptors, suggesting the potential for interaction. When compared with the vehicle control, it was found that injection of NGF into the Masseter Muscle did not evoke significant nociceptor discharge but did significantly reduce nociceptor mechanical threshold (∼30%). There was no effect of NGF on glutamate-evoked nociceptor discharge or glutamate-induced mechanical sensitization. Additional experiments indicated that NGF-induced mechanical sensitization could be partially attenuated with TrkA receptor antibodies, but not P75 receptor antibodies. These findings indicate that human NGF-induced sensitization of Masseter nociceptors results, in part, from the activation of TrkA receptors, but does not appear to be mediated through enhanced peripheral NMDA receptor activity.
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interstitial glutamate concentration is elevated in the Masseter Muscle of myofascial temporomandibular disorder patients
Journal of Orofacial Pain, 2010Co-Authors: Eduardo Castrillon, Brian E Cairns, Lars Arendtnielsen, Malin Ernberg, Kelun Wang, Barry J Sessle, Peter SvenssonAbstract:Aim: To determine if myofascial temporomandibular disorder (TMD) pain patients have elevated interstitial concentrations of glutamate in the Masseter Muscle. Methods: Thirteen patients (3 men, 10 women) diagnosed with myofascial TMD pain and 10 (2 men, 8 women) age-matched healthy controls participated in a single microdialysis session. Microdialysis was performed in the patients in the most painful point of the Masseter Muscle, while in the healthy subjects a standardized point in the Muscle was chosen. Two microdialysis samples were collected over 40-minute epochs. A blood sample was also taken for analysis of plasma glutamate concentration. Numeric rating scale (NRS) scores of pain intensity and unpleasantness, McGill Pain Questionnaire data, pain drawing areas, pressure pain thresholds, pressure pain tolerances, maximum voluntary bite force, and maximum voluntary mouth opening were collected as secondary measurements. Results: The median concentration of glutamate in the Masseter Muscle of the myofascial TMD pain patients (7.5 ± 2.6 µM) was significantly higher (P < .023, Mann-Whitney test) than the concentration in healthy controls (0.5 ± 0.4 µM). There were, however, no significant correlations between glutamate concentrations in the Masseter Muscle and NRS pain scores. Plasma concentrations of glutamate were similar in patients and healthy controls. Conclusions: The present study demonstrates a marked increase in interstitial glutamate concentration in the Masseter Muscle of myofascial TMD pain patients. These novel findings suggest that peripheral glutamate could be involved in the pathophysiology of myofascial TMD pain.
Brian E Cairns - One of the best experts on this subject based on the ideXlab platform.
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experimental stressors alter hypertonic saline evoked Masseter Muscle pain and autonomic response
Journal of Orofacial Pain, 2012Co-Authors: Karina H Bendixen, Brian E Cairns, Lene Baadhansen, Astrid Juhl Terkelsen, Peter SvenssonAbstract:Aims: To test in a randomized controlled trial, if hypertonic saline (HS)–evoked pain and autonomic function are modulated by either a cold pressor test (CPT) or mental arithmetic stress induced by a paced auditory serial addition task (PASAT). Methods: Fourteen healthy women participated in three sessions. Pain was induced by two 5% HS infusions (5 minutes each, 30 minutes apart) infused into the Masseter Muscle. During the second HS infusion, pain was modulated by PASAT, CPT, or control (HS alone). HS-evoked pain intensity was scored on a 0 to 10 numeric rating scale (NRS). Heart rate variability (HRV) and hemodynamic measures were recorded noninvasively (Task Force Monitor). Data were analyzed using repeated measurements ANOVAs and Spearman correlation analysis. Results: HS-evoked pain was significantly and similarly reduced by both PASAT (30.8 ± 27.6%; P .05). PASAT and CPT increased the heart rate compared with control (P .05). Conclusion: CPT and PASAT reduced HS-evoked Masseter Muscle pain and altered the autonomic response. The increase in heart rate following CPT and PASAT may be caused by different mechanisms. CPT reduced measures of efferent cardiac vagal (parasympathetic) activity, while the PASAT-induced increase in heart rate, but unchanged HRV, may suggest neurohumoral activation. J OROFAC PAIN 2012;26:191–205
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human nerve growth factor sensitizes Masseter Muscle nociceptors in female rats
Pain, 2010Co-Authors: Mian Wei Wang, Peter Svensson, Xudong Dong, Ujendra Kumar, Brian E CairnsAbstract:Abstract Injection of nerve growth factor (NGF) into the Masseter Muscle is not painful but does induce a localized, quick onset (∼1 h) and long-lasting mechanical sensitization in healthy human subjects. We tested the hypothesis that human NGF mechanically sensitizes Masseter Muscle nociceptors by increasing the sensitivity of peripheral N-methyl- d -aspartate (NMDA) receptors. Co-expression of the NR2B subunit of the NMDA receptor with P75 and TrkA NGF receptors by trigeminal ganglion neurons that innervate the Masseter Muscle was investigated immunohistochemically. Nociceptor activity was recorded extracellularly from the trigeminal ganglion of anaesthetized female rats. Nociceptor mechanical threshold was assessed before and every 30 min for 3 h after injection of human NGF (25 μg/ml, 10 μl, n = 12), and in subsequent experiments NGF with TrkA ( n = 12) or P75 ( n = 11) receptor antibodies. Glutamate (1 M, 10 μl) was injected at the end of each experiment. Approximately 85% of NR2B positive Masseter ganglion neurons co-expressed P75 or TrkA receptors, suggesting the potential for interaction. When compared with the vehicle control, it was found that injection of NGF into the Masseter Muscle did not evoke significant nociceptor discharge but did significantly reduce nociceptor mechanical threshold (∼30%). There was no effect of NGF on glutamate-evoked nociceptor discharge or glutamate-induced mechanical sensitization. Additional experiments indicated that NGF-induced mechanical sensitization could be partially attenuated with TrkA receptor antibodies, but not P75 receptor antibodies. These findings indicate that human NGF-induced sensitization of Masseter nociceptors results, in part, from the activation of TrkA receptors, but does not appear to be mediated through enhanced peripheral NMDA receptor activity.
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interstitial glutamate concentration is elevated in the Masseter Muscle of myofascial temporomandibular disorder patients
Journal of Orofacial Pain, 2010Co-Authors: Eduardo Castrillon, Brian E Cairns, Lars Arendtnielsen, Malin Ernberg, Kelun Wang, Barry J Sessle, Peter SvenssonAbstract:Aim: To determine if myofascial temporomandibular disorder (TMD) pain patients have elevated interstitial concentrations of glutamate in the Masseter Muscle. Methods: Thirteen patients (3 men, 10 women) diagnosed with myofascial TMD pain and 10 (2 men, 8 women) age-matched healthy controls participated in a single microdialysis session. Microdialysis was performed in the patients in the most painful point of the Masseter Muscle, while in the healthy subjects a standardized point in the Muscle was chosen. Two microdialysis samples were collected over 40-minute epochs. A blood sample was also taken for analysis of plasma glutamate concentration. Numeric rating scale (NRS) scores of pain intensity and unpleasantness, McGill Pain Questionnaire data, pain drawing areas, pressure pain thresholds, pressure pain tolerances, maximum voluntary bite force, and maximum voluntary mouth opening were collected as secondary measurements. Results: The median concentration of glutamate in the Masseter Muscle of the myofascial TMD pain patients (7.5 ± 2.6 µM) was significantly higher (P < .023, Mann-Whitney test) than the concentration in healthy controls (0.5 ± 0.4 µM). There were, however, no significant correlations between glutamate concentrations in the Masseter Muscle and NRS pain scores. Plasma concentrations of glutamate were similar in patients and healthy controls. Conclusions: The present study demonstrates a marked increase in interstitial glutamate concentration in the Masseter Muscle of myofascial TMD pain patients. These novel findings suggest that peripheral glutamate could be involved in the pathophysiology of myofascial TMD pain.
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ketamine attenuates glutamate induced mechanical sensitization of the Masseter Muscle in human males
Experimental Brain Research, 2006Co-Authors: Brian E Cairns, Peter Svensson, Eduardo Castrillon, Kelun Wang, Barry J Sessle, Steen Hupfeld, Lars ArendtnielsenAbstract:The purpose of the present study was to determine whether glutamate-induced mechanical sensitization of the Masseter Muscle in human volunteers involves activation of peripheral N-methyl-d-aspartate (NMDA) receptors. Healthy male volunteers (n=18) participated in this randomized, two-session study. During each session, the volunteers received two injections into the right Masseter Muscle. An initial injection of glutamate (1 M, 0.2 ml) alone was followed 30 min later by a second injection of glutamate alone or glutamate combined with ketamine (10 mM). Pressure pain threshold (PPT) was assessed over the right Masseter Muscle at and 2 cm above the injection site, as well as over the right temporalis Muscle and left Masseter Muscle prior to the first injection. The PPT was reassessed at all four sites every 5 min from 10 to 30 min after the second injection and once again 60 min after the second injection. Glutamate-evoked Muscle pain, pain area and the sensory pain response index of the McGill pain questionnaire were all significantly reduced by co-injection of ketamine. The mean PPT values were significantly decreased by ~10%, 10, 15 and 25 min after injection of glutamate, but only over the site of injection. Co-injection of ketamine with glutamate also completely blocked the glutamate-induced mechanical sensitization 15 min post-injection as compared with glutamate alone. The lack of spread of mechanical sensitization outside the area of glutamate injection is consistent with the view that glutamate-induced mechanical sensitization results from a peripheral mechanism. The attenuation of glutamate-induced mechanical sensitization by ketamine suggests that this effect is mediated, in part, through activation of peripheral NMDA receptors.
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glutamate evoked pain and mechanical allodynia in the human Masseter Muscle
Pain, 2003Co-Authors: Peter Svensson, Brian E Cairns, Lars Arendtnielsen, Kelun Wang, James W Hu, Thomas Gravennielsen, Barry J SessleAbstract:Abstract The present study examined the effect of peripheral administration of the excitatory amino acid (EAA) glutamate on the intensity of perceived pain and pressure pain thresholds (PPTs) in healthy young women (n=17) and men (n=18). Two injections separated by 25 min of 0.2 ml, 1.0 M glutamate into the Masseter Muscle produced significantly higher scores of pain on 0–10 cm visual analogue scales (VAS) in women than in men (analysis of variance, ANOVA: P
Daisuke Umeki - One of the best experts on this subject based on the ideXlab platform.
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Role of β-adrenergic signaling in Masseter Muscle
2019Co-Authors: Aiko Ito, Yoshiki Ohnuki, Yasumasa Mototani, Kouichi Shiozawa, Kenji Suita, Misao Ishikawa, Naoya Kawamura, Yuka Yagisawa, Megumi Nariyama, Daisuke UmekiAbstract:In skeletal Muscle, the major isoform of β-adrenergic receptor (β-AR) is β2-AR and the minor isoform is β1-AR, which is opposite to the situation in cardiac Muscle. Despite extensive studies in cardiac Muscle, the physiological roles of the β-AR subtypes in skeletal Muscle are not fully understood. Therefore, in this work, we compared the effects of chronic β1- or β2-AR activation with a specific β1-AR agonist, dobutamine (DOB), or a specific β2-AR agonist, clenbuterol (CB), on Masseter and cardiac Muscles in mice. In cardiac Muscle, chronic β1-AR stimulation induced cardiac hypertrophy, fibrosis and myocyte apoptosis, whereas chronic β2-AR stimulation induced cardiac hypertrophy without histological abnormalities. In Masseter Muscle, however, chronic β1-AR stimulation did not induce Muscle hypertrophy, but did induce fibrosis and apoptosis concomitantly with increased levels of p44/42 MAPK (ERK1/2) (Thr-202/Tyr-204), calmodulin kinase II (Thr-286) and mammalian target of rapamycin (mTOR) (Ser-2481) phosphorylation. On the other hand, chronic β2-AR stimulation in Masseter Muscle induced Muscle hypertrophy without histological abnormalities, as in the case of cardiac Muscle, concomitantly with phosphorylation of Akt (Ser-473) and mTOR (Ser-2448) and increased expression of microtubule-associated protein light chain 3-II, an autophagosome marker. These results suggest that the β1-AR pathway is deleterious and the β2-AR is protective in Masseter Muscle. These data should be helpful in developing pharmacological approaches for the treatment of skeletal Muscle wasting and weakness.
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protective effects of clenbuterol against dexamethasone induced Masseter Muscle atrophy and myosin heavy chain transition
PLOS ONE, 2015Co-Authors: Daisuke Umeki, Yoshiki Ohnuki, Yasumasa Mototani, Kouichi Shiozawa, Takayuki Fujita, Yoshiki Nakamura, Yasutake Saeki, Kenji Suita, Satoshi OkumuraAbstract:Background Glucocorticoid has a direct catabolic effect on skeletal Muscle, leading to Muscle atrophy, but no effective pharmacotherapy is available. We reported that clenbuterol (CB) induced Masseter Muscle hypertrophy and slow-to-fast myosin heavy chain (MHC) isoform transition through direct Muscle β2-adrenergic receptor stimulation. Thus, we hypothesized that CB would antagonize glucocorticoid (dexamethasone; DEX)-induced Muscle atrophy and fast-to-slow MHC isoform transition. Methodology We examined the effect of CB on DEX-induced Masseter Muscle atrophy by measuring Masseter Muscle weight, fiber diameter, cross-sectional area, and myosin heavy chain (MHC) composition. To elucidate the mechanisms involved, we used immunoblotting to study the effects of CB on Muscle hypertrophic signaling (insulin growth factor 1 (IGF1) expression, Akt/mammalian target of rapamycin (mTOR) pathway, and calcineurin pathway) and atrophic signaling (Akt/Forkhead box-O (FOXO) pathway and myostatin expression) in Masseter Muscle of rats treated with DEX and/or CB. Results and Conclusion Masseter Muscle weight in the DEX-treated group was significantly lower than that in the Control group, as expected, but co-treatment with CB suppressed the DEX-induced Masseter Muscle atrophy, concomitantly with inhibition of fast-to-slow MHC isoforms transition. Activation of the Akt/mTOR pathway in Masseter Muscle of the DEX-treated group was significantly inhibited compared to that of the Control group, and CB suppressed this inhibition. DEX also suppressed expression of IGF1 (positive regulator of Muscle growth), and CB attenuated this inhibition. Myostatin protein expression was unchanged. CB had no effect on activation of the Akt/FOXO pathway. These results indicate that CB antagonizes DEX-induced Muscle atrophy and fast-to-slow MHC isoform transition via modulation of Akt/mTOR activity and IGF1 expression. CB might be a useful pharmacological agent for treatment of glucocorticoid-induced Muscle atrophy.
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effects of chronic akt mtor inhibition by rapamycin on mechanical overload induced hypertrophy and myosin heavy chain transition in Masseter Muscle
Journal of Pharmacological Sciences, 2013Co-Authors: Daisuke Umeki, Yoshiki Ohnuki, Yasumasa Mototani, Kouichi Shiozawa, Takayuki Fujita, Yoshiki Nakamura, Yasutake Saeki, Satoshi OkumuraAbstract:To examine the effects of the Akt/mammalian target of rapamycin (mTOR) pathway on Masseter Muscle hypertrophy and myosin heavy chain (MHC) transition in response to mechanical overload, we analyzed the effects of bite-opening (BO) on the hypertrophy and MHC composition of Masseter Muscle of BO-rats treated or not treated with rapamycin (RAPA), a selective mTOR inhibitor. The Masseter Muscle weight in BO-rats was significantly greater than that in controls, and this increase was attenuated by RAPA treatment. Expression of slow-twitch MHC isoforms was significantly increased in BO-rats with/without RAPA treatment, compared with controls, but the magnitude of the increase was much smaller in RAPA-treated BO-rats. Phosphorylation of p44/42 MAPK (ERK1/2), which preserves fast-twitch MHC isoforms in skeletal Muscle, was significantly decreased in BO-rats, but the decrease was abrogated by RAPA treatment. Calcineurin signaling is known to be important for Masseter Muscle hypertrophy and fast-to-slow MHC isoform transition, but expression of known calcineurin activity modulators was unaffected by RAPA treatment. Taken together, these results indicate that the Akt/mTOR pathway is involved in both development of Masseter Muscle hypertrophy and fast-to-slow MHC isoform transition in response to mechanical overload with inhibition of the ERK1/2 pathway and operates independently of the calcineurin pathway.
Sun Young Kwon - One of the best experts on this subject based on the ideXlab platform.
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intramuscular cavernous hemangioma arising from Masseter Muscle a diagnostic dilemma 2006 12b
European Radiology, 2007Co-Authors: Sang Kwon Lee, Sun Young KwonAbstract:We report here a case of intramuscular cavernous hemangioma of the right Masseter Muscle in a 41-year-old woman—misdiagnosed preoperatively as parotid tumor—along with its imaging and pathologic findings. Preoperative diagnosis of intramuscular cavernous hemangiomas of the Masseter Muscle is problematic, in that they may be confused with parotid tumor or other muscular lesions. In a patient with soft-tissue mass suspected of representing a hemangioma, MR imaging may provide more specific information regarding the characteristics, the origin, and the extent of the lesion than other imaging modalities.
