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1
Mitchell, Patrick O., and Grace K. Pavlath. "Skeletal muscle atrophy leads to loss and dysfunction of muscle precursor cells." American Journal of Physiology-Cell Physiology 287, no. 6 (December 2004): C1753—C1762. http://dx.doi.org/10.1152/ajpcell.00292.2004.
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Atrophy of skeletal muscle leads to decreases in myofiber size and nuclear number; however, the effects of atrophic conditions on muscle precursor cells (MPC) are largely unknown. MPC lie outside myofibers and represent the main source of additional myonuclei necessary for muscle growth and repair. In the present study, we examined the properties of MPC after hindlimb suspension (HS)-induced atrophy and subsequent recovery of the mouse hindlimb muscles. We demonstrated that the number of MPC in atrophied muscles was decreased. RT-PCR analysis of cells isolated from atrophied muscles indicated that several mRNA characteristic of the myogenic program in MPC were absent. Cells isolated from atrophied muscles failed to properly proliferate and undergo differentiation into multinucleated myotubes. Thus atrophy led to a decrease in MPC and caused dysfunction in those MPC that remained. Upon regrowth of the atrophied muscles, these deleterious effects were reversed. Our data suggest that preventing loss or dysfunction of MPC may be a new pharmacological target during muscle atrophy.
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Kim, Young In, Hyunjung Lee, Farida S. Nirmala, Hyo-Deok Seo, Tae Youl Ha, Chang Hwa Jung, and Jiyun Ahn. "Antioxidant Activity of Valeriana fauriei Protects against Dexamethasone-Induced Muscle Atrophy." Oxidative Medicine and Cellular Longevity 2022 (January 12, 2022): 1–16. http://dx.doi.org/10.1155/2022/3645431.
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Skeletal muscle atrophy is defined as wasting or loss of muscle. Although glucocorticoids (GCs) are well-known anti-inflammatory drugs, their long-term or high-dose use induces skeletal muscle atrophy. Valeriana fauriei (VF) is used to treat restlessness, anxiety, and sleep disorders; however, its effects on skeletal muscle health have not been investigated. This study investigated whether Valeriana fauriei could ameliorate muscle atrophy. We induced muscle atrophy in vitro and in vivo, by treatment with dexamethasone (DEX), a synthetic GC. In DEX-induced myotube atrophy, Valeriana fauriei treatment increased the fusion index and decreased the expression of muscle atrophic genes such as muscle atrophy F-box (MAFbx/Atrogin-1) and muscle RING-finger protein 1 (MuRF1). In DEX-treated mice with muscle atrophy, Valeriana fauriei supplementation increased the ability to exercise, muscle weight, and cross-sectional area, whereas it inhibited myosin heavy chain isoform transition and the expression of muscle atrophy biomarkers. Valeriana fauriei treatment led to via the downregulation of muscle atrophic genes via inhibition of GC receptor translocation. Valeriana fauriei was also found to act as a reactive oxygen species (ROS) scavenger. Didrovaltrate (DI), an iridoid compound from Valeriana fauriei, was found to downregulate atrophic genes and decrease ROS in the DEX-induced myotube atrophy. Consolidated, our results indicate that Valeriana fauriei prevents DEX-induced muscle atrophy by inhibiting GC receptor translocation. Further, Valeriana fauriei acts as a ROS scavenger, and its functional compound is didrovaltrate. We suggest that Valeriana fauriei and its functional compound didrovaltrate possess therapeutic potentials against muscle atrophy.
3
Buckingham, Richard A. "Fascia and Perichondrium Atrophy in Tympanoplasty and Recurrent Middle Ear Atelectasis." Annals of Otology, Rhinology & Laryngology 101, no. 9 (September 1992): 755–58. http://dx.doi.org/10.1177/000348949210100907.
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Fascia and perichondrium grafts to replace and reinforce thin, atrophic tympanic membranes (TMs) are recommended by several authors to correct middle ear atelectasis by forming a fibrous, collapse-resistant TM. This study reviewed the status of connective tissue grafts performed over the 10-year period from 1979 to 1988 to determine if these grafts would maintain sufficient strength and fibrous character to resist recurrent atelectasis. The author used fascia or perichondrium to repair 89 TM defects, and 63 ears were available for follow-up: 54 had cholesteatomas and 9 had perforations. Graft atrophy was judged by microscopic otoscopy and Kodachrome otophotography. Fascia TM grafts atrophied in 35 of 43 ears (80%), and perichondrium atrophied in 8 of 20 ears (40%). Grafts maintained their relatively thick and fibrous character in only 20 of 63 ears (32%). If fascia and perichondrium used to correct atelectasis were to atrophy at the same rate as the grafts in this series, atelectasis would recur after attempts to reinforce atrophic TMs. Atelectasis-prone middle ears require intubation despite surgery.
4
Nakao, Reiko, Katsuya Hirasaka, Jumpei Goto, Kazumi Ishidoh, Chiharu Yamada, Ayako Ohno, Yuushi Okumura, et al. "Ubiquitin Ligase Cbl-b Is a Negative Regulator for Insulin-Like Growth Factor 1 Signaling during Muscle Atrophy Caused by Unloading." Molecular and Cellular Biology 29, no. 17 (June 22, 2009): 4798–811. http://dx.doi.org/10.1128/mcb.01347-08.
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ABSTRACT Skeletal muscle atrophy caused by unloading is characterized by both decreased responsiveness to myogenic growth factors (e.g., insulin-like growth factor 1 [IGF-1] and insulin) and increased proteolysis. Here, we show that unloading stress resulted in skeletal muscle atrophy through the induction and activation of the ubiquitin ligase Cbl-b. Upon induction, Cbl-b interacted with and degraded the IGF-1 signaling intermediate IRS-1. In turn, the loss of IRS-1 activated the FOXO3-dependent induction of atrogin-1/MAFbx, a dominant mediator of proteolysis in atrophic muscle. Cbl-b-deficient mice were resistant to unloading-induced atrophy and the loss of muscle function. Furthermore, a pentapeptide mimetic of tyrosine608-phosphorylated IRS-1 inhibited Cbl-b-mediated IRS-1 ubiquitination and strongly decreased the Cbl-b-mediated induction of atrogin-1/MAFbx. Our results indicate that the Cbl-b-dependent destruction of IRS-1 is a critical dual mediator of both increased protein degradation and reduced protein synthesis observed in unloading-induced muscle atrophy. The inhibition of Cbl-b-mediated ubiquitination may be a new therapeutic strategy for unloading-mediated muscle atrophy.
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MATTAR, Rejane, Sergio Barbosa MARQUES, Igor Braga RIBEIRO, Thiago Arantes de Carvalho VISCONTI, Mateus FUNARI, and Eduardo Guimarães Hourneaux DE MOURA. "DIAGNOSTIC ACCURACY OF GASTROPANEL® FOR ATROPHIC GASTRITIS IN BRAZILIAN SUBJECTS AND THE EFFECT OF PROTON PUMP INHIBITORS." Arquivos de Gastroenterologia 57, no. 2 (June 2020): 154–60. http://dx.doi.org/10.1590/s0004-2803.202000000-29.
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ABSTRACT BACKGROUND: It has been proposed that the combination of gastrin-17 (G-17), pepsinogens I and II (PGI and PGII), and anti-Helicobacter pylori (H. pylori) antibodies (GastroPanel®, BIOHIT HealthCare, Helsinki, Finland) could serve as biomarkers of atrophic gastritis. OBJECTIVE: This study aimed to ensure the diagnostic accuracy of GastroPanel® and evaluate the effect of proton pump inhibitors (PPIs) on these biomarkers. METHODS: Dyspeptic patients who underwent gastrointestinal endoscopy were enrolled in the present study. Histological findings, which were the gold standard to stratify groups, were as follows: no atrophy (controls); antrum atrophy; corpus atrophy; multifocal atrophy; and neoplasia. G-17, PGI, PGII, and anti-H. pylori immunoglobulin (Ig)G antibodies were assayed using commercially available kits. The ratio of PGI/PGII was calculated. RESULTS: Among 308 patients, 159 (51.6%) were PPI users. The overall prevalence of atrophy was 43.8% (n=135). Ninety-two (29.9%) patients were H. pylori positive according to anti-H. pylori IgG levels. G-17 levels were not low in those with antrum atrophy but were high in those with corpus and multifocal atrophies. PGI levels were significantly lower in those with corpus and multifocal atrophies. The sensitivity of PGI <30 µg/L to detect corpus atrophy was 50% (95% CI 27.8-72.1%), with a specificity of 93.2% (95% CI 84.3-97.5%), a positive likelihood ratio of 7.4 (95% CI 2.9-19.2), and a negative likelihood ratio of 0.5 (95% CI 0.3-0.8). A small number of subjects (n=6) exhibited moderate to intense atrophy (4%), among whom 66.7% exhibited decreased PGI levels. PPI significantly increased the levels of G-17 and PGI, except in those with corpus and multifocal atrophies, in whom PGI levels were not increased by PPIs. CONCLUSION: GastroPanel® (Gastrin-17, PGI, and PGI/PGII ratio) did not demonstrate high sensitivity for detecting gastric atrophy.
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Le, Ngoc Hoan, Chu-Sook Kim, Taesun Park, Jung Han Yoon Park, Mi-Kyung Sung, Dong Gun Lee, Sun-Myung Hong, et al. "Quercetin Protects against Obesity-Induced Skeletal Muscle Inflammation and Atrophy." Mediators of Inflammation 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/834294.
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Skeletal muscle inflammation and atrophy are closely associated with metabolic impairment such as insulin resistance. Quercetin, a natural polyphenol flavonoid, is known to elicit anti-inflammatory and antioxidant activities. In this study, we investigated its effect on obesity-induced skeletal muscle inflammation and atrophy in mice. Male C57BL/6 mice were fed a regular diet, a high-fat diet (HFD), and an HFD supplemented with quercetin for nine weeks. Quercetin reduced levels of inflammatory cytokines and macrophage accumulation in the skeletal muscle of the HFD-fed obese mice. It also reduced transcript and protein levels of the specific atrophic factors, Atrogin-1 and MuRF1, in the skeletal muscle of the HFD-fed obese mice, and protected against the reduction of muscle mass and muscle fiber size. In vitro, quercetin markedly diminished transcript levels of inflammatory receptors and activation of their signaling molecules (ERK, p38 MAPK, and NF-κB) in cocultured myotubes/macrophages, and this was accompanied by reduced expression of the atrophic factors. Together, these findings suggest that quercetin reduces obesity-induced skeletal muscle atrophy by inhibiting inflammatory receptors and their signaling pathway. Quercetin may be useful for preventing obesity-induced muscle inflammation and sarcopenia.
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Lee, Jun Ho, Jung Yoon Jang, Young Hoon Kwon, Seung Ho Lee, Cheol Park, Yung Hyun Choi, and Nam Deuk Kim. "Effects of Rosemary Extract on C2C12 Myoblast Differentiation and 5-Aminoimidazole-4-carboxamide Ribonucleoside (AICAR)-Induced Muscle Cell Atrophy." Applied Sciences 13, no. 2 (January 11, 2023): 986. http://dx.doi.org/10.3390/app13020986.
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Sarcopenia is an aging-related disease that involves the gradual loss of muscle mass and function. However, no suitable therapeutic drugs are currently available. Accordingly, the purpose of the present study was to evaluate the effectiveness of rosemary extract (RE) in inducing myotube differentiation and inhibiting 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR)-induced muscle atrophy in mouse C2C12 cells. Morphological changes associated with the onset of RE-induced differentiation were evaluated by measuring myotube diameter, and the expression of proteins related to muscle differentiation and atrophy was measured using western blot analysis. Treatment with RE increased myotube thickness and the expression of the myogenic differentiation 1 (MyoD) and myogenin proteins. The effect of RE treatment on 5′-adenosine monophosphate-activated protein kinase (AMPK), acetyl-CoA carboxylase (ACC), MyoD, myogenin, muscle atrophy factors forkhead box O3a (FoxO3a), MAFbx/atrogin-1, and muscle RING finger-1 (MuRF-1) protein expression in AICAR-induced muscle-atrophied C2C12 cells was evaluated using western blot analysis. Treatment with RE reduced FoxO3a, MAFbx/atrogin-1, and MuRF-1 expression and significantly increased MyoD and myogenin expression. These findings suggest that RE has the potential to be used as an active ingredient in sarcopenia treatments.
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Madahi, Mehdi, Reza Gharakhanlou, Abdolreza Kazemi, and Mohammad Ali Azarbayjani. "Effect of Reduced Physical Activity on Murf-1 and Atrogin-1 Gene Expression in Soleus Muscle of Wistar Rats Following Endurance, Resistance and Combined Training." Scientific Journal of Rehabilitation Medicine 11, no. 2 (May 22, 2022): 250–63. http://dx.doi.org/10.32598/sjrm.11.2.9.
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Background and Aims Understanding the involved mechanisms in muscle atrophy can help develop new treatment methods for atrophic conditions. Skeletal muscle atrophy via biochemical and transcriptional pathways can increase the expression of some muscle atrophy related genes. The present study aims to assess the effect of reduced physical activity by the spinal nerve ligation (SNL) after a period of resistance, endurance and combined exercises on the expression of MuRF-1 and Atrogin-1 genes in male rats. Methods In this experimental study, 30 male Wistar rats were randomly divided into four groups: Control+SNL, combined exercise+SNL, endurance exercise+SNL, and resistance training+SNL. The exercises were performed for six weeks. After this period, the protocol of reduced physical activity by the SNL was implemented for four weeks. At the end, soleus muscle was isolated and the expression levels of MuRF-1 and Atrogin-1 genes were measured by real-time polymerase chain reaction technique. To examine the gene expression differences between the groups, analysis of variance and Tukey’s post hoc test were used. The significant level was set at 0.05. Results The results showed that the expression of MuRF-1 gene in the combined exercise+SNL and resistance training+SNL groups was significantly lower than in the control group (P<0.05). The Atrogin-1 gene expression was significantly reduced only in the combined exercise+SNL group compared to the control group (P<0.05). Conclusion It seems that the rats with resistance training are more resistant to SNL-induced atrophy than the group with endurance exercise.
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Aravena, Javier, Johanna Abrigo, Francisco Gonzalez, Francisco Aguirre, Andrea Gonzalez, Felipe Simon, and Claudio Cabello-Verrugio. "Angiotensin (1-7) Decreases Myostatin-Induced NF-κB Signaling and Skeletal Muscle Atrophy." International Journal of Molecular Sciences 21, no. 3 (February 10, 2020): 1167. http://dx.doi.org/10.3390/ijms21031167.
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Myostatin is a myokine that regulates muscle function and mass, producing muscle atrophy. Myostatin induces the degradation of myofibrillar proteins, such as myosin heavy chain or troponin. The main pathway that mediates protein degradation during muscle atrophy is the ubiquitin proteasome system, by increasing the expression of atrogin-1 and MuRF-1. In addition, myostatin activates the NF-κB signaling pathway. Renin–angiotensin system (RAS) also regulates muscle mass. Angiotensin (1-7) (Ang-(1-7)) has anti-atrophic properties in skeletal muscle. In this paper, we evaluated the effect of Ang-(1-7) on muscle atrophy and signaling induced by myostatin. The results show that Ang-(1-7) prevented the decrease of the myotube diameter and myofibrillar protein levels induced by myostatin. Ang-(1-7) also abolished the increase of myostatin-induced reactive oxygen species production, atrogin-1, MuRF-1, and TNF-α gene expressions and NF-κB signaling activation. Ang-(1-7) inhibited the activity mediated by myostatin through Mas receptor, as is demonstrated by the loss of all Ang-(1-7)-induced effects when the Mas receptor antagonist A779 was used. Our results show that the effects of Ang-(1-7) on the myostatin-dependent muscle atrophy and signaling are blocked by MK-2206, an inhibitor of Akt/PKB. Together, these data indicate that Ang-(1-7) inhibited muscle atrophy and signaling induced by myostatin through a mechanism dependent on Mas receptor and Akt/PKB.
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Zou, Yun-Yi, Zhang-Lin Chen, Chen-Chen Sun, Dong Yang, Zuo-Qiong Zhou, Qin Xiao, Xi-Yang Peng, and Chang-Fa Tang. "A High-Fat Diet Induces Muscle Mitochondrial Dysfunction and Impairs Swimming Capacity in Zebrafish: A New Model of Sarcopenic Obesity." Nutrients 14, no. 9 (May 9, 2022): 1975. http://dx.doi.org/10.3390/nu14091975.
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Obesity is a highly prevalent disease that can induce metabolic syndrome and is associated with a greater risk of muscular atrophy. Mitochondria play central roles in regulating the physiological metabolism of skeletal muscle; however, whether a decreased mitochondrial function is associated with impaired muscle function is unclear. In this study, we evaluated the effects of a high-fat diet on muscle mitochondrial function in a zebrafish model of sarcopenic obesity (SOB). In SOB zebrafish, a significant decrease in exercise capacity and skeletal muscle fiber cross-sectional area was detected, accompanied by high expression of the atrophy-related markers Atrogin-1 and muscle RING-finger protein-1. Zebrafish with SOB exhibited inhibition of mitochondrial biogenesis and fatty acid oxidation as well as disruption of mitochondrial fusion and fission in atrophic muscle. Thus, our findings showed that muscle atrophy was associated with SOB-induced mitochondrial dysfunction. Overall, these results showed that the SOB zebrafish model established in this study may provide new insights into the development of therapeutic strategies to manage mitochondria-related muscular atrophy.
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Gardiner, Phillip F., Michèle Favron, and Pierre Corriveau. "Histochemical and contractile responses of rat medial gastrocnemius to 2 weeks of complete disuse." Canadian Journal of Physiology and Pharmacology 70, no. 8 (August 1, 1992): 1075–81. http://dx.doi.org/10.1139/y92-149.
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We studied the histochemical and in situ contractile changes in a rat ankle extensor, medial gastrocnemius, in which activation of muscle fibres by motoneurones was blocked for 14 days, using the sodium channel blocker tetrodotoxin applied to the sciatic nerve. Muscles were atrophied and showed slower twitch responses, greater fusion at subtetanic frequencies of stimulation, and higher twitch/tetanic ratios. Tetanic force/mm2 of fibre area and fatiguability were unchanged. Type II fibres were more atrophied and showed greater decreases in mitochondrial succinate dehydrogenase activity than type I fibres. The contractile changes resulting from complete disuse do not occur in models in which weight-bearing alone has been removed (space flight, hindlimb suspension), suggesting that the residual motoneurone activity reported in models of weightlessness is sufficient to prevent these responses. Similarly, the finding of a greater type II fibre susceptibility to complete disuse, which differs from the pattern seen in models of weightlessness, suggests that this residual motoneurone activity in the latter influences atrophic responses in a manner that is variable among motor unit types, to produce the reported preferential type I atrophy characteristic of removal of weight-bearing.Key words: disuse, atrophy, fibre types, succinate dehydrogenase, contractile properties.
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Vilchinskaya, Natalia A., Sergey V. Rozhkov, Olga V. Turtikova, Timur M. Mirzoev, and Boris S. Shenkman. "AMPK Phosphorylation Impacts Apoptosis in Differentiating Myoblasts Isolated from Atrophied Rat Soleus Muscle." Cells 12, no. 6 (March 16, 2023): 920. http://dx.doi.org/10.3390/cells12060920.
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Regrowth of atrophied myofibers depends on muscle satellite cells (SCs) that exist outside the plasma membrane. Muscle atrophy appears to result in reduced number of SCs due to apoptosis. Given reduced AMP-activated protein kinase (AMPK) activity during differentiation of primary myoblasts derived from atrophic muscle, we hypothesized that there may be a potential link between AMPK and susceptibility of differentiating myoblasts to apoptosis. The aim of this study was to estimate the effect of AMPK activation (via AICAR treatment) on apoptosis in differentiating myoblasts derived from atrophied rat soleus muscle. Thirty rats were randomly assigned to the following two groups: control (C, n = 10) and 7-day hindlimb suspension (HS, n = 20). Myoblasts derived from the soleus muscles of HS rats were divided into two parts: AICAR-treated cells and non-treated cells. Apoptotic processes were evaluated by using TUNEL assay, RT-PCR and WB. In differentiating myoblasts derived from the atrophied soleus, there was a significant decrease (p < 0.05) in AMPK and ACC phosphorylation in parallel with increased number of apoptotic nuclei and a significant upregulation of pro-apoptotic markers (caspase-3, -9, BAX, p53) compared to the cells derived from control muscles. AICAR treatment of atrophic muscle-derived myoblasts during differentiation prevented reductions in AMPK and ACC phosphorylation as well as maintained the number of apoptotic nuclei and the expression of pro-apoptotic markers at the control levels. Thus, the maintenance of AMPK activity can suppress enhanced apoptosis in differentiating myoblasts derived from atrophied rat soleus muscle.
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Choi, Ra-Yeong, Bong Sun Kim, Eu-Jin Ban, Minchul Seo, Joon Ha Lee, and In-Woo Kim. "Mealworm Ethanol Extract Enhances Myogenic Differentiation and Alleviates Dexamethasone-Induced Muscle Atrophy in C2C12 Cells." Life 13, no. 1 (December 24, 2022): 58. http://dx.doi.org/10.3390/life13010058.
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Aging, and other disease-related muscle disorders are serious health problems. Dexamethasone (DEX), a synthetic glucocorticoid, can trigger skeletal muscle atrophy. This study examined the effects of mealworm (Tenebrio molitor larva) ethanol extract (TME) on C2C12 myoblast differentiation and DEX-induced myotube atrophy. TME induced myotube formation compared to the differentiation medium (DM) group. TME also significantly increased the mRNA expression of muscle creatine kinase (CKm) and myogenic regulatory factors (MRFs), such as myogenin (MyoG), myogenic factor (Myf)5, and MRF4 (Myf6). TME dramatically increased the muscle-specific protein, MyoG, compared to the control, whereas the expression of myogenic differentiation 1 (MyoD) remained unchanged. It also activated the mammalian target of rapamycin (mTOR) signaling pathway. In the DEX-induced muscle atrophy C2C12 model, TME reduced the gene expression of atrogin-1, muscle RING finger protein-1 (MuRF-1), and myostatin, which are involved in protein degradation in skeletal muscles. Furthermore, TME elevated the phosphorylation of forkhead box O3 (FoxO3α) and protein kinase B (Akt). These findings suggest that TME can enhance myotube hypertrophy by regulating the mTOR signaling pathway, and can rescue DEX-induced muscle atrophy by alleviating atrophic muscle markers mediated by Akt activation. Thus, TME can be a potential therapeutic agent for treating muscle weakness and atrophy.
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Ku, Sae-Kwang, Jong-Min Lim, Hyung-Rae Cho, Khawaja Muhammad Imran Bashir, Young Suk Kim, and Jae-Suk Choi. "Tart Cherry (Fruit of Prunus cerasus) Concentrated Powder (TCcp) Ameliorates Glucocorticoid-Induced Muscular Atrophy in Mice." Medicina 57, no. 5 (May 12, 2021): 485. http://dx.doi.org/10.3390/medicina57050485.
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Background and Objectives: The present study investigated the beneficial effects of tart cherry (fruit of Prunus cerasus) concentrated powder (TCcp) on glucocorticoid (GLU)-induced catabolic muscular atrophy in the skeletal muscle of mice. Furthermore, its potential mechanism was also studied. Materials and Methods: Changes in calf thickness, calf muscle weight, calf muscle strength, body weight, gastrocnemius muscle histology, immunohistochemistry, serum creatinine, creatine kinase, lactate dehydrogenase, and antioxidant defense systems were measured. Malondialdehyde, reactive oxygen species, glutathione content, catalase, and superoxide dismutase activities in the gastrocnemius muscle, and muscle-specific mRNA expressions were evaluated. Results: After 24 days, GLU control mice showed muscular atrophy at all criteria of indexes. The muscular atrophy symptoms were significantly inhibited by oral treatment with 250 mg/kg and 500 mg/kg of TCcp through antioxidative and anti-inflammatory modulated expression of genes involved in muscle protein degradation (myostatin, atrogin-1, SIRT1, and MuRF1) and synthesis (A1R, Akt1, TRPV4, and PI3K). Conclusions: This study shows that the TCcp (500 mg/kg and 250 mg/kg) could improve muscular atrophies caused by various etiologies.
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LeBlanc, A., C. Marsh, H. Evans, P. Johnson, V. Schneider, and S. Jhingran. "Bone and muscle atrophy with suspension of the rat." Journal of Applied Physiology 58, no. 5 (May 1, 1985): 1669–75. http://dx.doi.org/10.1152/jappl.1985.58.5.1669.
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A modification of the Morey tail suspension model was used to determine atrophic responses of rat bone and muscle with 14–90 days unloading of the hindlimbs. Bone uptake of methylene diphosphonate followed a phasic pattern similar to changes in bone formation rate in immobilized dogs and rats. Increased uptake at 60 days (P = 0.01, femur) indicated an increased bone metabolism. Regional densitometry demonstrated a preferential loss of bone mineral in the trabecular mass (P = 0.02) at 30 days and in the cortical shaft by 90 days (P = 0.03). Maximal muscle atrophy occurred within 14–30 days. The gastrocnemius was less severely affected by suspension than by immobilization techniques, whereas the soleus atrophied (by weight) similarly, suggesting that muscle atrophy in the suspension model is distinctly different from immobilization atrophy. One significant response of skeletal muscle to suspension was an altered blood distribution. Muscle blood distribution changes reflect the hypodynamic state of muscle that continues to contract but probably at an altered rate in response to altered functional demands.
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Jeong, Yu-Jin, Jong-Hoon Kim, Ye-Jin Jung, Mi-Sun Kwak, Moon-Hee Sung, and Jee-Young Imm. "KL-Biome (Postbiotic Formulation of Lactiplantibacillus plantarum KM2) Improves Dexamethasone-Induced Muscle Atrophy in Mice." International Journal of Molecular Sciences 25, no. 13 (July 8, 2024): 7499. http://dx.doi.org/10.3390/ijms25137499.
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Sarcopenia refers to an age-related decrease in muscle mass and strength. The gut–muscle axis has been proposed as a promising target to alleviate muscle atrophy. The effect of KL-Biome—a postbiotic preparation comprising heat-killed Lactiplantibacillus plantarum KM-2, its metabolites, and an excipient (soybean powder)—on muscle atrophy was evaluated using dexamethasone (DEX)-induced atrophic C2C12 myoblasts and C57BL/6J mice. KL-Biome significantly downregulated the expression of genes (Atrogin-1 and MuRF1) associated with skeletal muscle degradation but increased the anabolic phosphorylation of FoxO3a, Akt, and mTOR in C2C12 cells. Oral administration of KL-Biome (900 mg/kg) for 8 weeks significantly improved muscle mass, muscle function, and serum lactate dehydrogenase levels in DEX-treated mice. KL-Biome administration increased gut microbiome diversity and reversed DEX-mediated gut microbiota alterations. Furthermore, it significantly increased the relative abundances of the genera Subdologranulum, Alistipes, and Faecalibacterium prausnitzii, which are substantially involved in short-chain fatty acid production. These findings suggest that KL-Biome exerts beneficial effects on muscle atrophy by regulating gut microbiota.
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Frost, Robert A., Gerald J. Nystrom, Leonard S. Jefferson, and Charles H. Lang. "Hormone, cytokine, and nutritional regulation of sepsis-induced increases in atrogin-1 and MuRF1 in skeletal muscle." American Journal of Physiology-Endocrinology and Metabolism 292, no. 2 (February 2007): E501—E512. http://dx.doi.org/10.1152/ajpendo.00359.2006.
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Various atrophic stimuli increase two muscle-specific E3 ligases, muscle RING finger 1 (MuRF1) and atrogin-1, and knockout mice for these “atrogenes” display resistance to denervation-induced atrophy. The present study determined whether increased atrogin-1 and MuRF1 mRNA are mediated by overproduction of endogenous glucocorticoids or inflammatory cytokines in adult rats and whether atrogene expression can be downregulated by anabolic agents such as insulin-like growth factor (IGF)-I and the nutrient-signaling amino acid leucine. Both atrogin-1 and MuRF1 mRNA in gastrocnemius was upregulated dose and time dependently by endotoxin. Additionally, peritonitis produced by cecal ligation and puncture increased atrogin-1 and MuRF1 mRNA in gastrocnemius (but not soleus or heart) by 8 h, which was sustained for 72 and 24 h, respectively. Whereas the sepsis-induced increase in atrogin-1 expression was completely prevented by IGF-I, the increased MuRF1 was not altered. In contrast to the IGF-I effect, the sepsis-induced increased mRNA of both atrogenes was unresponsive to either acute or repetitive administration of leucine. Whereas exogenous infusion of TNF-α increased atrogin-1 and MuRF1 in gastrocnemius, pretreatment of septic rats with the TNF antagonist TNF-binding protein did not prevent increased expression of either atrogene. Similarly, whereas dexamethasone increased atrogene expression, pretreatment with the glucocorticoid receptor antagonist RU-486 failed to ameliorate the sepsis-induced increase in atrogin-1 and MuRF1. Thus, under in vivo conditions in mature adult rats, the sepsis-induced increase in muscle atrogin-1 and MuRF1 mRNA appears both glucocorticoid and TNF independent and is unresponsive to leucine.
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Lee, Myung-Hun, Jin-Ho Lee, Wan-Joong Kim, Seo Ho Kim, Sun-Young Kim, Han Sung Kim, and Tack-Joong Kim. "Linoleic Acid Attenuates Denervation-Induced Skeletal Muscle Atrophy in Mice through Regulation of Reactive Oxygen Species-Dependent Signaling." International Journal of Molecular Sciences 23, no. 9 (April 26, 2022): 4778. http://dx.doi.org/10.3390/ijms23094778.
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Muscle atrophy is a major muscle disease, the symptoms of which include decreased muscle volume leading to insufficient muscular support during exercise. One cause of muscle atrophy is the induction of oxidative stress by reactive oxygen species (ROS). This study aimed to identify the antioxidant mechanism of linoleic acid (LA) in muscle atrophy caused by oxidative stress. H2O2 has been used to induce oxidative stress in myoblasts in vitro. C2C12 myoblasts treated with H2O2 exhibited decreased viability and increased ROS synthesis. However, with LA treatment, the cells tended to recover from oxidative effects similar to those of the control groups. At the molecular level, the expression of superoxide dismutase 1 (SOD1), Bax, heat shock protein 70 (HSP70), and phosphorylated forkhead box protein O1 was increased by oxidative stress, causing apoptosis. LA treatment suppressed these changes. In addition, the expression of MuRF1 and Atrogin-1/MAFbx mRNA increased under oxidative stress but not in the LA-treated group. Sciatic denervation of C57BL/6 mice manifested as atrophy of the skeletal muscle in micro-computed tomography (micro-CT). The protein expression levels of SOD1, HSP70, and MuRF1 did not differ between the atrophied muscle tissues and C2C12 myoblasts under oxidative stress. With LA treatment, muscle atrophy recovered and protein expression was restored to levels similar to those in the control. Therefore, this study suggests that LA may be a candidate substance for preventing muscle atrophy.
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Lee, Myung-Hun, Jin-Ho Lee, Wan-Joong Kim, Seo Ho Kim, Sun-Young Kim, Han Sung Kim, and Tack-Joong Kim. "Linoleic Acid Attenuates Denervation-Induced Skeletal Muscle Atrophy in Mice through Regulation of Reactive Oxygen Species-Dependent Signaling." International Journal of Molecular Sciences 23, no. 9 (April 26, 2022): 4778. http://dx.doi.org/10.3390/ijms23094778.
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Muscle atrophy is a major muscle disease, the symptoms of which include decreased muscle volume leading to insufficient muscular support during exercise. One cause of muscle atrophy is the induction of oxidative stress by reactive oxygen species (ROS). This study aimed to identify the antioxidant mechanism of linoleic acid (LA) in muscle atrophy caused by oxidative stress. H2O2 has been used to induce oxidative stress in myoblasts in vitro. C2C12 myoblasts treated with H2O2 exhibited decreased viability and increased ROS synthesis. However, with LA treatment, the cells tended to recover from oxidative effects similar to those of the control groups. At the molecular level, the expression of superoxide dismutase 1 (SOD1), Bax, heat shock protein 70 (HSP70), and phosphorylated forkhead box protein O1 was increased by oxidative stress, causing apoptosis. LA treatment suppressed these changes. In addition, the expression of MuRF1 and Atrogin-1/MAFbx mRNA increased under oxidative stress but not in the LA-treated group. Sciatic denervation of C57BL/6 mice manifested as atrophy of the skeletal muscle in micro-computed tomography (micro-CT). The protein expression levels of SOD1, HSP70, and MuRF1 did not differ between the atrophied muscle tissues and C2C12 myoblasts under oxidative stress. With LA treatment, muscle atrophy recovered and protein expression was restored to levels similar to those in the control. Therefore, this study suggests that LA may be a candidate substance for preventing muscle atrophy.
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Bortoloso, Elena, Aram Megighian, Sandra Furlan, Luisa Gorza, and Pompeo Volpe. "Homer 2 antagonizes protein degradation in slow-twitch skeletal muscles." American Journal of Physiology-Cell Physiology 304, no. 1 (January 1, 2013): C68—C77. http://dx.doi.org/10.1152/ajpcell.00108.2012.
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Homer represents a new and diversified family of proteins made up of several isoforms. The presence of Homer isoforms, referable to 1b/c and 2a/b, was investigated in fast- and slow-twitch skeletal muscles from both rat and mouse. Homer 1b/c was identical irrespective of the muscle, and Homer 2a/b was instead characteristic of the slow-twitch phenotype. Transition in Homer isoform composition was studied in two established experimental models of atrophy, i.e., denervation and disuse of slow-twitch skeletal muscles of the rat. No change of Homer 1b/c was observed up to 14 days after denervation, whereas Homer 2a/b was found to be significantly decreased at 7 and 14 days after denervation by 70 and 90%, respectively, and in parallel to reduction of muscle mass; 3 days after denervation, relative mRNA was reduced by 90% and remained low thereafter. Seven-day hindlimb suspension decreased Homer 2a/b protein by 70%. Reconstitution of Homer 2 complement by in vivo transfection of denervated soleus allowed partial rescue of the atrophic phenotype, as far as muscle mass, muscle fiber size, and ubiquitinazion are concerned. The counteracting effects of exogenous Homer 2 were mediated by downregulation of MuRF1, Atrogin, and Myogenin, i.e., all genes known to be upregulated at the onset of atrophy. On the other hand, slow-to-fast transition of denervated soleus, another landmark of denervation atrophy, was not rescued by Homer 2 replacement. The present data show that 1) downregulation of Homer 2 is an early event of atrophy, and 2) Homer 2 participates in the control of ubiquitinization and ensuing proteolysis via transcriptional downregulation of MuRF1, Atrogin, and Myogenin. Homers are key players of skeletal muscle plasticity, and Homer 2 is required for trophic homeostasis of slow-twitch skeletal muscles.
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Chen, Renyu, Yingfang Zheng, Chenchen Zhou, Hongkai Dai, Yurou Wang, Yun Chu, and Jinlong Luo. "N-Acetylcysteine Attenuates Sepsis-Induced Muscle Atrophy by Downregulating Endoplasmic Reticulum Stress." Biomedicines 12, no. 4 (April 18, 2024): 902. http://dx.doi.org/10.3390/biomedicines12040902.
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(1) Background: Sepsis-induced muscle atrophy is characterized by a loss of muscle mass and function which leads to decreased quality of life and worsens the long-term prognosis of patients. N-acetylcysteine (NAC) has powerful antioxidant and anti-inflammatory properties, and it relieves muscle wasting caused by several diseases, whereas its effect on sepsis-induced muscle atrophy has not been reported. The present study investigated the effect of NAC on sepsis-induced muscle atrophy and its possible mechanisms. (2) Methods: The effect of NAC on sepsis-induced muscle atrophy was assessed in vivo and in vitro using cecal ligation and puncture-operated (CLP) C57BL/6 mice and LPS-treated C2C12 myotubes. We used immunofluorescence staining to analyze changes in the cross-sectional area (CSA) of myofibers in mice and the myotube diameter of C2C12. Protein expressions were analyzed by Western blotting. (3) Results: In the septic mice, the atrophic response manifested as a reduction in skeletal muscle weight and myofiber cross-sectional area, which is mediated by muscle-specific ubiquitin ligases—muscle atrophy F-box (MAFbx)/Atrogin-1 and muscle ring finger 1 (MuRF1). NAC alleviated sepsis-induced skeletal muscle wasting and LPS-induced C2C12 myotube atrophy. Meanwhile, NAC inhibited the sepsis-induced activation of the endoplasmic reticulum (ER) stress signaling pathway. Furthermore, using 4-Phenylbutyric acid (4-PBA) to inhibit ER stress in LPS-treated C2C12 myotubes could partly abrogate the anti-muscle-atrophy effect of NAC. Finally, NAC alleviated myotube atrophy induced by the ER stress agonist Thapsigargin (Thap). (4) Conclusions: NAC can attenuate sepsis-induced muscle atrophy, which may be related to downregulating ER stress.
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Makino, Naoki, Paul Ganguly, Vijayan Elimban, and Naranjan Dhalla. "Sarcolemmal Alterations in Unloaded Rat Heart after Heterotopic Transplantation." International Journal of Angiology 27, no. 04 (October 18, 2018): 196–201. http://dx.doi.org/10.1055/s-0038-1673646.
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AbstractFollowing heterotopic transplantation, the rat heart undergoes atrophy and exhibits delayed cardiac relaxation without any changes in contraction and systolic Ca2+ transients. Furthermore, the sarcoplasmic reticular Ca2+ uptake and release activities were reduced and Ca2+ influx through L-type Ca2+ channels was increased in the atrophied heart. Since Ca2+ movements at sarcolemma are intimately involved in the regulation of intracellular Ca2+ concentration, the present study was undertaken to test if sarcolemma plays any role to maintain cardiac function in the atrophied heart.The characteristics of sarcolemmal Ca2+ pump and Na+–Ca2+ exchange activities were examined in 8 weeks heterotopically isotransplanted rat hearts which did not support hemodynamic load and underwent atrophy. Sarcolemmal ATP (adenosine triphosphate)-dependent Ca2+ uptake and Ca2+-stimulated ATPase (adenosine triphosphatase) activities were increased without any changes in Na+–K+ ATPase activities in the transplanted hearts. Although no alterations in the Na+-dependent Ca2+ uptake were evident, Na+-induced Ca2+ release was increased in the transplanted heart sarcolemmal vesicles. The increase in Na+-induced Ca2+ release was observed at different times of incubation as well as at 5, 20, and 40 mM Na+. The sarcolemma from transplanted hearts also showed higher contents of phosphatidic acid, sphingomyelin, and cholesterol.These results indicate that increases in the sarcolemmal, Ca2+ transport activities in unloaded heart may provide an insight into adaptive mechanism to maintain normal contractile behavior of the atrophic heart.
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Kim, Jinjoo, Youngmo Yang, Eunwon Choi, Sumin Lee, and Jiyoung Choi. "Effects of C-Peptide on Dexamethasone-Induced In Vitro and In Vivo Models as a Potential Therapeutic Agent for Muscle Atrophy." International Journal of Molecular Sciences 24, no. 20 (October 21, 2023): 15433. http://dx.doi.org/10.3390/ijms242015433.
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This study aimed to investigate the effects of C-peptide on C2C12 myotubes and a mouse model. Both in vitro and in vivo experiments were conducted to elucidate the role of C-peptide in muscle atrophy. Various concentrations (0, 0.01, 0.1, 1, 10, and 100 nM) of C-peptide were used on the differentiated C2C12 myotubes with or without dexamethasone (DEX). C57BL/6J mice were administered with C-peptide and DEX for 8 days, followed by C-peptide treatment for 12 days. Compared to the DEX group, C-peptide increased the fusion and differentiation indices and suppressed atrophic factor expression in C2C12 myotubes. However, 100 nM C-peptide decreased the fusion and differentiation indices and increased atrophic factor expression regardless of DEX treatment. In C57BL/6J mice, DEX + C-peptide co-treatment significantly attenuated the body and muscle weight loss and improved the grip strength and cross-sectional area of the gastrocnemius (Gas) and quadriceps (Quad) muscles. C-peptide downregulated the mRNA and protein levels of muscle degradation-related markers, particularly Atrogin-1, in Gas and Quad muscles. This study underscores the potential of C-peptides in mitigating muscle weight reduction and preserving muscle function during muscle atrophy via molecular regulation. In addition, the work presents basic data for future studies on the effect of C-peptide on diabetic muscular dystrophy.
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Kotelevets, Sergey M., Sergey A. Chekh, and Sergey Z. Chukov. "Effectiveness of serological markers of gastric mucosal atrophy in the gastric precancer screening and in cancer prevention." World Journal of Gastrointestinal Endoscopy 16, no. 8 (August 16, 2024): 462–71. http://dx.doi.org/10.4253/wjge.v16.i8.462.
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BACKGROUND New markers are needed to improve the effectiveness of serological screening for atrophic gastritis. AIM To develop a cost-effective method for serological screening of atrophic gastritis with a high level of sensitivity. METHODS Of the 169 patients with atrophic gastritis, selected by the visual endoscopic Kimura-Takemoto method, 165 showed histological mucosal atrophy using the updated Kimura-Takemoto method. All 169 patients were examined for postprandial levels of gastrin-17 (G17) and pepsinogen-1 (PG1) using GastroPanel® (Biohit Plc, Helsinki, Finland). RESULTS We used the histological standard of five biopsies of the gastric mucosa, in accordance with the Kimura-Takemoto classification system to assess the sensitivity of G17 in detecting gastric mucosal atrophy. We also compared the morpho-functional relationships between the detected histological degree of gastric mucosal atrophy and the serological levels of G17 and PG1, as the markers of atrophic gastritis. The sensitivity of postprandial G17 was 62.2% for serological levels of G17 (range: 0-4 pmol/L) and 100% for serological G17 (range: 0-10 pmol/L) for the detection of monofocal severe atrophic gastritis. No strong correlation was found between the levels of PG1 and degree of histological atrophy determined by the Kimura-Takemoto classification system to identify the severity of mucosal atrophy of the gastric corpus. In the presented clinical case of a 63-year-old man with multifocal atrophic gastritis, there is a pronounced positive long-term dynamics of the serological marker of atrophy - postprandial G17, after five months of rennet replacement therapy. CONCLUSION Serological screening of multifocal atrophic gastritis by assessment of postprandial G17 is a cost-effective method with high sensitivity. Postprandial G17 is an earlier marker of regression of atrophic gastritis than a morphological examination of a gastric biopsy in accordance with the Sydney system. Therefore, postprandial G17 is recommended for dynamic monitoring of atrophic gastritis after treatment.
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Lee, Sang-Jin, Minju Im, Sun Kyu Park, Jeom-Yong Kim, Eui-Young So, Olin D. Liang, Jong-Sun Kang, and Gyu-Un Bae. "BST204, a Rg3 and Rh2 Enriched Ginseng Extract, Upregulates Myotube Formation and Mitochondrial Function in TNF-α-Induced Atrophic Myotubes." American Journal of Chinese Medicine 48, no. 03 (January 2020): 631–50. http://dx.doi.org/10.1142/s0192415x20500329.
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The loss of skeletal muscle mass and function is a serious consequence of chronic diseases and aging. BST204 is a purified ginseng (the root of Panax ginseng) extract that has been processed using ginsenoside-[Formula: see text]-glucosidase and acid hydrolysis to enrich ginsenosides Rg3 and Rh2 from the crude ginseng. BST204 has a broad range of health benefits, but its effects and mechanism on muscle atrophy are currently unknown. In this study, we have examined the effects and underlying mechanisms of BST204 on myotube formation and myotube atrophy induced by tumor necrosis factor-[Formula: see text] (TNF-[Formula: see text]). BST204 promotes myogenic differentiation and multinucleated myotube formation through Akt activation. BST204 prevents myotube atrophy induced by TNF-[Formula: see text] through the activation of Akt/mTOR signaling and down-regulation of muscle-specific ubiquitin ligases, MuRF1, and Atrogin-1. Furthermore, BST204 treatment in atrophic myotubes suppresses mitochondrial reactive oxygen species (ROS) production and regulates mitochondrial transcription factors such as NRF1 and Tfam, through enhancing the activity and expression of peroxisome proliferator-activated receptor-[Formula: see text] coactivator1[Formula: see text] (PGC1[Formula: see text]). Collectively, our findings indicate that BST204 improves myotube formation and PGC1[Formula: see text]-mediated mitochondrial function, suggesting that BST204 is a potential therapeutic or neutraceutical remedy to intervene muscle weakness and atrophy.
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Park, Eunji, Hojung Choi, Cao-Sang Truong, and Hee-Sook Jun. "The Inhibition of Autophagy and Pyroptosis by an Ethanol Extract of Nelumbo nucifera Leaf Contributes to the Amelioration of Dexamethasone-Induced Muscle Atrophy." Nutrients 15, no. 4 (February 4, 2023): 804. http://dx.doi.org/10.3390/nu15040804.
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Muscle atrophy is characterized by a decline in muscle mass and function. Excessive glucocorticoids in the body due to aging or drug treatment can promote muscle wasting. In this study, we investigated the preventive effect of Nelumbo nucifera leaf (NNL) ethanolic extract on muscle atrophy induced by dexamethasone (DEX), a synthetic glucocorticoid, in mice and its underlying mechanisms. The administration of NNL extract increased weight, cross-sectional area, and grip strength of quadriceps (QD) and gastrocnemius (GA) muscles in DEX-induced muscle atrophy in mice. The NNL extract administration decreased the expression of muscle atrophic factors, such as muscle RING-finger protein-1 and atrogin-1, and autophagy factors, such as Beclin-1, microtubule-associated protein 1A/1B-light chain 3 (LC3-I/II), and sequestosome 1 (p62/SQSTM1) in DEX-injected mice. DEX injection increased the protein expression levels of NOD-like receptor pyrin domain-containing protein 3 (NLRP3), cleaved-caspase-1, interleukin-1beta (IL-1β), and cleaved-gasdermin D (GSDMD), which were significantly reduced by NNL extract administration (500 mg/kg/day). In vitro studies using C2C12 myotubes also revealed that NNL extract treatment inhibited the DEX-induced increase in autophagy factors, pyroptosis-related factors, and NF-κB. Overall, the NNL extract prevented DEX-induced muscle atrophy by downregulating the ubiquitin–proteasome system, autophagy pathway, and GSDMD-mediated pyroptosis pathway, which are involved in muscle degradation.
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Yeon, Myeong-Hoon, Eunhui Seo, Jong-Han Lee, and Hee-Sook Jun. "Bavachin and Corylifol A Improve Muscle Atrophy by Enhancing Mitochondria Quality Control in Type 2 Diabetic Mice." Antioxidants 12, no. 1 (January 6, 2023): 137. http://dx.doi.org/10.3390/antiox12010137.
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Type 2 diabetes reduces muscle mass and function. Chronic inflammation and mitochondrial dysfunction play critical roles in muscle atrophy pathogenesis. Here, we investigated the effects of bavachin and corylifol A from Psoralea corylifolia L. seeds on muscle atrophy in dexamethasone-treated mice and in db/db mice. Bavachin and corylifol A enhanced muscle strength and muscle mass in dexamethasone-treated mice. In diabetic mice, they enhanced muscle strength and cross-sectional areas. Bavachin and corylifol A suppressed inflammatory cytokine (interleukin-6 and tumor necrosis factor-α) expression levels by downregulating nuclear factor-κB phosphorylation. They decreased the muscle atrophic factor (myostatin, atrogin-1, and muscle RING finger-1) expression levels. They activated the AKT synthetic signaling pathway and induced a switch from fast-type glycolytic fibers (type 2B) to slow-type oxidative fibers (types I and 2A). They increased mitochondrial biogenesis and dynamic factor (optic atrophy-1, mitofusin-1/2, fission, mitochondrial 1, and dynamin 1-like) expression levels via the AMP-activated protein kinase–peroxisome proliferator-activated receptor gamma coactivator 1-alpha signaling pathway. They also improved mitochondrial quality by upregulating the mitophagy factor (p62, parkin, PTEN-induced kinase-1, and BCL2-interacting protein-3) expression levels. Therefore, bavachin and corylifol A exert potential therapeutic effects on muscle atrophy by suppressing inflammation and improving mitochondrial function.
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Vazeille, Emilie, Audrey Codran, Agnès Claustre, Julien Averous, Anne Listrat, Daniel Béchet, Daniel Taillandier, Dominique Dardevet, Didier Attaix, and Lydie Combaret. "The ubiquitin-proteasome and the mitochondria-associated apoptotic pathways are sequentially downregulated during recovery after immobilization-induced muscle atrophy." American Journal of Physiology-Endocrinology and Metabolism 295, no. 5 (November 2008): E1181—E1190. http://dx.doi.org/10.1152/ajpendo.90532.2008.
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Immobilization produces morphological, physiological, and biochemical alterations in skeletal muscle leading to muscle atrophy and long periods of recovery. Muscle atrophy during disuse results from an imbalance between protein synthesis and proteolysis but also between apoptosis and regeneration processes. This work aimed to characterize the mechanisms underlying muscle atrophy and recovery following immobilization by studying the regulation of the mitochondria-associated apoptotic and the ubiquitin-proteasome-dependent proteolytic pathways. Animals were subjected to hindlimb immobilization for 4–8 days (I4 to I8) and allowed to recover after cast removal for 10–40 days (R10 to R40). Soleus and gastrocnemius muscles atrophied from I4 to I8 to a greater extent than extensor digitorum longus and tibialis anterior muscles. Gastrocnemius muscle atrophy was first stabilized at R10 before being progressively reduced until R40. Polyubiquitinated proteins accumulated from I4, whereas the increased ubiquitination rates and chymotrypsin-like activity of the proteasome were detectable from I6 to I8. Apoptosome and caspase-3 or -9 activities increased at I6 and I8, respectively. The ubiquitin-proteasome-dependent pathway was normalized early when muscle stops to atrophy (R10). By contrast, the mitochondria-associated apoptotic pathway was first downregulated below basal levels when muscle started to recover at R15 and completely normalized at R20. Myf 5 protein levels decreased from I4 to I8 and were normalized at R10. Altogether, our results suggest a two-stage process in which the ubiquitin-proteasome pathway is rapidly up- and downregulated when muscle atrophies and recovers, respectively, whereas apoptotic processes may be involved in the late stages of atrophy and recovery.
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M, Komínek. "Myopia Control in European Children – Study Protocol and Methodology." Neonatology and Clinical Pediatrics 9, no. 1 (October 17, 2022): 1–9. http://dx.doi.org/10.24966/ncp-878x/100096.
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To report study protocol and methodology of multicentre, randomized, double-blind, placebo-controlled study of the efficacy and safety of low dose atropine eye drops (0.02%, 0.04%) in slowing the progression of short-sightedness (myopia) in children. M.A.R.S. (Myopia and Atropin ReStriction)
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Verhees, Koen J. P., Annemie M. W. J. Schols, Marco C. J. M. Kelders, Céline M. H. Op den Kamp, Jos L. J. van der Velden, and Ramon C. J. Langen. "Glycogen synthase kinase-3β is required for the induction of skeletal muscle atrophy." American Journal of Physiology-Cell Physiology 301, no. 5 (November 2011): C995—C1007. http://dx.doi.org/10.1152/ajpcell.00520.2010.
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Skeletal muscle atrophy commonly occurs in acute and chronic disease. The expression of the muscle-specific E3 ligases atrogin-1 (MAFbx) and muscle RING finger 1 (MuRF1) is induced by atrophy stimuli such as glucocorticoids or absence of IGF-I/insulin and subsequent Akt signaling. We investigated whether glycogen synthase kinase-3β (GSK-3β), a downstream molecule in IGF-I/Akt signaling, is required for basal and atrophy stimulus-induced expression of atrogin-1 and MuRF1, and myofibrillar protein loss in C2C12 skeletal myotubes. Abrogation of basal IGF-I signaling, using LY294002, resulted in a prominent induction of atrogin-1 and MuRF1 mRNA and was accompanied by a loss of myosin heavy chain fast (MyHC-f) and myosin light chains 1 (MyLC-1) and -3 (MyLC-3). The synthetic glucocorticoid dexamethasone (Dex) also induced the expression of both atrogenes and likewise resulted in the loss of myosin protein abundance. Genetic ablation of GSK-3β using small interfering RNA resulted in specific sparing of MyHC-f, MyLC-1, and MyLC-3 protein levels after Dex treatment or impaired IGF-I/Akt signaling. Interestingly, loss of endogenous GSK-3β suppressed both basal and atrophy stimulus-induced atrogin-1 and MuRF1 expression, whereas pharmacological GSK-3β inhibition, using CHIR99021 or LiCl, only reduced atrogin-1 mRNA levels in response to LY294002 or Dex. In conclusion, our data reveal that myotube atrophy and myofibrillar protein loss are GSK-3β dependent, and demonstrate for the first time that basal and atrophy stimulus-induced atrogin-1 mRNA expression requires GSK-3β enzymatic activity, whereas MuRF1 expression depends solely on the physical presence of GSK-3β.
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Alakoski, Anna, Teea T. Salmi, Kaisa Hervonen, Hannu Kautiainen, Maarit Salo, Katri Kaukinen, Timo Reunala, and Pekka Collin. "Chronic Gastritis in Dermatitis Herpetiformis: A Controlled Study." Clinical and Developmental Immunology 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/640630.
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Background and Objective. Previous small studies suggest that chronic atrophic gastritis is common in dermatitis herpetiformis (DH). We here examined the frequency and topography of chronic gastritis in 93 untreated DH subjects and in 186 controls with dyspepsia.Methods. Specimens were drawn from the gastric corpus and antrum and examined for atrophy, intestinal metaplasia, andHelicobacter pylori. Duodenal biopsies were taken.Results. Atrophic corpus gastritis was more frequent in DH than in controls (16.0% and 2.7%, resp.,P<0.001); atrophy in the antrum was rare in both groups (3.2% and 1.1%,P=0.34). Intestinal metaplasia was present in 13 (14.0%) DH and 12 (6.5%) control patients (P=0.038) andH. pyloriin 17 (18.3%) and 17 (9.3%) (P=0.028), respectively. Small-bowel villous atrophy was seen in 76% of the DH patients, equally in patients with and without chronic gastritis. One DH patient with atrophic gastritis developed gastric cancer.Conclusion. In DH, chronic atrophic gastritis was common in the corpus, but not in the antrum.H. pyloriwill partly explain this, but corpus atrophy is suggestive of an autoimmune etiology. Atrophic gastritis may increase the risk of gastric cancer. We advocate performing upper endoscopy with sufficient histologic samples in DH.
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Park, Do Youn. "Histopathologic Diagnosis of Atrophic Gastritis and Intestinal Metaplasia." Korean Journal of Helicobacter and Upper Gastrointestinal Research 20, no. 2 (June 10, 2020): 96–100. http://dx.doi.org/10.7704/kjhugr.2020.0011.
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Atrophic gastritis and intestinal metaplasia are well-known to be reliable indicators of gastric cancer risk. They are clinically important in deciding whether to recommend endoscopic surveillance. Herein I review the histopathologic diagnosis of atrophic gastritis and IM. Gastric atrophy is divided into metaplastic atrophy and non-metaplastic atrophy. IM is categorized as complete (type I) and incomplete (type II, III). Systematic interpretation of gastric atrophy and IM using the updated Sydney system or operative link on gastritis assessment is recommended. Furthermore, I suggest using the consensus definition of gastric atrophy and incomplete IM in the gastric biopsy pathology report to support the surveillance of high-risk gastric cancer group.
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Uda, Munehiro, Toshinori Yoshihara, Noriko Ichinoseki-Sekine, Takeshi Baba, and Toshitada Yoshioka. "Potential roles of neuronal nitric oxide synthase and the PTEN-induced kinase 1 (PINK1)/Parkin pathway for mitochondrial protein degradation in disuse-induced soleus muscle atrophy in adult rats." PLOS ONE 15, no. 12 (December 9, 2020): e0243660. http://dx.doi.org/10.1371/journal.pone.0243660.
Full textAbstract:
Excessive nitric oxide (NO) production and mitochondrial dysfunction can activate protein degradation in disuse-induced skeletal muscle atrophy. However, the increase in NO production in atrophied muscles remains controversial. In addition, although several studies have investigated the PTEN-induced kinase 1 (PINK1)/Parkin pathway, a mitophagy pathway, in atrophied muscle, the involvement of this pathway in soleus muscle atrophy is unclear. In this study, we investigated the involvement of neuronal nitric oxide synthase (nNOS) and the PINK1/Parkin pathway in soleus muscle atrophy induced by 14 days of hindlimb unloading (HU) in adult rats. HU lowered the weight of the soleus muscles. nNOS expression showed an increase in atrophied soleus muscles. Although HU increased malondialdehyde as oxidative modification of the protein, it decreased 6-nitrotryptophan, a marker of protein nitration. Additionally, the nitrosocysteine content and S-nitrosylated Parkin were not altered, suggesting the absence of excessive nitrosative stress after HU. The expression of PINK1 and Parkin was also unchanged, whereas the expression of heat shock protein 70 (HSP70), which is required for Parkin activity, was reduced in atrophied soleus muscles. Moreover, we observed accumulation and reduced ubiquitination of high molecular weight mitofusin 2, which is a target of Parkin, in atrophied soleus muscles. These results indicate that excessive NO is not produced in atrophied soleus muscles despite nNOS accumulation, suggesting that excessive NO dose not mediate in soleus muscle atrophy at least after 14 days of HU. Furthermore, the PINK1/Parkin pathway may not play a role in mitophagy at this time point. In contrast, the activity of Parkin may be downregulated because of reduced HSP70 expression, which may contribute to attenuated degradation of target proteins in the atrophied soleus muscles after 14 days of HU. The present study provides new insights into the roles of nNOS and a protein degradation pathway in soleus muscle atrophy.
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Pavlovich, I. M., G. A. Al’per, A. V. Gordienko, D. I. Proskunov, and V. V. Yakovlev. "Сhronic gastritis: impaired motor-evacuation function of the stomach." Bulletin of the Russian Military Medical Academy 22, no. 4 (December 15, 2020): 37–42. http://dx.doi.org/10.17816/brmma62802.
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The effect of morphological changes in the gastric mucosa on the motor-evacuation function of the stomach was evaluated in 90 patients with chronic atrophic gastritis and 93 patients with chronic non-atrophic gastritis aged 18 to 82 years. Motor function disturbances were discovered of 90% of patients with chronic atrophic gastritis and 80,6% with chronic non-atrophic gastritis. It was established that the pyloric insufficiency compared with its spasm was significantly more (p0,01) often in chronic atrophic gastritis. Insufficiency of the lower esophageal sphincter in patients with atrophic gastritis was significantly (p0,01). Insufficiency of the lower esophageal sphincter in combination with duodenogastric reflux in patients with chronic atrophic gastritis was significantly more (p0,01) often observed during diffuse atrophy, i. e. when mucous membrane of stomach corpus and antrum is involved in the process. With the localization of atrophy in the antrum alone, pyloric insufficiency was observed significantly more (p 0,01) often than spasm. Thus, an interrelation between the insufficiency of the lower esophageal and pyloric sphincters with the diffuse atrophic process has been established. There are no significant differences of disorders of gastric motor function in patients with different types of chronic gastritis. Accelerated evacuation from the stomach with localization of atrophy in the mucous membrane of the stomach corpus is more (p 0,01) often observed in patients with chronic atrophic gastritis.
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Sultan, Karim R., Birgit Henkel, Maarten Terlou, and Henk P. Haagsman. "Quantification of hormone-induced atrophy of large myotubes from C2C12 and L6 cells: atrophy-inducible and atrophy-resistant C2C12 myotubes." American Journal of Physiology-Cell Physiology 290, no. 2 (February 2006): C650—C659. http://dx.doi.org/10.1152/ajpcell.00163.2005.
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Myofiber atrophy is the final outcome of muscle wasting induced by catabolic factors such as glucocorticoids and thyroid hormones. We set up an in vitro system to define the catabolic reaction based on myotube atrophy. Both mouse C2C12 and rat L6 cells were used. C2C12 myotube formation was improved by replacing horse serum with the serum substitute Ultroser G. A new method was developed to quantify size changes of large (0.5–1 mm) myotubes only, excluding remaining myoblasts and small myotubes. Dexamethasone reduced myotube size by 30% in L6 but not in C2C12 myotubes. Expression of the glucocorticoid receptor was twofold higher in L6 myotubes than in C2C12 myotubes. In both cell lines, 3,3′,5-triiodo-l-thyronine (T3) did not induce a significant size reduction. Expression of the major T3 receptor (T3Rβ1) was higher in L6 myotubes. We investigated whether the changes in myotube size are related to changes in atrogin-1 expression, as this enzyme is thought to be a key factor in the initiation of muscle atrophy. Dexamethasone induced a twofold increase of atrogin-1 mRNA; again, only L6 myotubes were susceptible. Interestingly, atrogin-1 expression in Ultroser G-fused C2C12 myotubes was lower than that in horse serum-fused myotubes. Furthermore, dexamethasone treatment increased atrogin-1 expression only in horse serum-fused myotubes but not in Ultroser G-fused myotubes. Ultroser G-induced fusion may result in atrophy-resistant C2C12 myotubes. Therefore, C2C12 myotubes offer an ideal system in which to study skeletal muscle atrophy because, depending on differentiation conditions, C2C12 cells produce atrophy-inducible and atrophy-resistant myotubes.
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Gonçalves, Ana Carolina Rodrigues, Carla Resende Vaz Oliveira, Laíssa de Oliveira Fernandes Barbosa, and Bruno Cezario Costa Reis. "Triagem neonatal e terapia gênica na atrofia muscular espinhal: uma revisão integrativa." Revista Eletrônica Acervo Médico 4 (March 17, 2022): e9873. http://dx.doi.org/10.25248/reamed.e9873.2022.
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Objetivo: Analisar o impacto da triagem neonatal e terapia gênica no prognóstico da atrofia muscular espinhal. Métodos: A abordagem metodológica se propõe a um compilado de pesquisa bibliográfica de abordagem qualitativa e caráter descritivo através de uma revisão integrativa de literatura nas bases de dados National Libary of Medicine, Biblioteca Virtual em Saúde e Cochrane Database of Systematic Reviews. Os descritores utilizados foram “muscular atrophy spinal”, “spinal muscular atrofies of childhood” e “genetic therapy”. Os critérios de inclusão foram artigos de jornal article, clinical trial, ensaios clínicos randomizados ou não randomizados, estudos de caso-controle, estudo de coorte, livre acesso, publicados em inglês, português e espanhol, no intervalo de 2017 a 2022 e faixa etária infantil. Resultados: Os materiais de estudo são triagem neonatal e terapias gênicas, utilizadas para o diagnóstico e tratamento da atrofia muscular espinhal, respectivamente, dentre suas principais aplicações, constituindo impactos no prognóstico e qualidade de vida dos pacientes, frente a uma melhor função motora e obtenção de novos marcos do desenvolvimento infantil. Considerações finais: A triagem neonatal e a terapia gênica oferecem impactos positivos, juntamente com as perspectivas futuras para o tratamento dessa enfermidade, visando um diagnóstico e suporte terapêuticos precoces e mais efetivos.
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Sacheck, Jennifer M., Akira Ohtsuka, S. Christine McLary, and Alfred L. Goldberg. "IGF-I stimulates muscle growth by suppressing protein breakdown and expression of atrophy-related ubiquitin ligases, atrogin-1 and MuRF1." American Journal of Physiology-Endocrinology and Metabolism 287, no. 4 (October 2004): E591—E601. http://dx.doi.org/10.1152/ajpendo.00073.2004.
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Muscle atrophy results primarily from accelerated protein degradation and is associated with increased expression of two muscle-specific ubiquitin ligases (E3s): atrogin-1 and muscle ring finger 1 (MuRF1). Glucocorticoids are essential for many types of muscle atrophy, and their effects are opposite to those of insulin-like growth factor I (IGF-I) and insulin, which promote growth. In myotubes, dexamethasone (Dex) inhibited growth and enhanced breakdown of long-lived cell proteins, especially myofibrillar proteins (as measured by 3-methylhistidine release), while also increasing atrogin-1 and MuRF1 mRNA. Conversely, IGF-I suppressed protein degradation and prevented the Dex-induced increase in proteolysis. IGF-I rapidly reduced atrogin-1 expression within 1 h by blocking mRNA synthesis without affecting mRNA degradation, whereas IGF-I decreased MuRF1 mRNA slowly. IGF-I and insulin also blocked Dex induction of these E3s and several other atrophy-related genes (“atrogenes”). Changes in overall proteolysis with Dex and IGF-I correlated tightly with changes in atrogin-1 mRNA content, but not with changes in MuRF1 mRNA. IGF-I activates the phosphatidylinositol 3-kinase (PI3K)-Akt pathway, and inhibition of this pathway [but not the calcineurin-nuclear factor of activated T cell (NFAT) or the MEK-ERK pathway] increased proteolysis and atrogin-1 mRNA expression. Thus an important component of growth stimulation by IGF-I, through the PI3K-Akt pathway, is its ability to rapidly suppress transcription of the atrophy-related E3 atrogin-1 and other atrogenes and degradation of myofibrillar proteins.
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Pandit, Lotika, and Joseph G. Ouslander. "Postmenopausal Vaginal Atrophy and Atrophic Vaginitis." American Journal of the Medical Sciences 314, no. 4 (October 1997): 228–31. http://dx.doi.org/10.1016/s0002-9629(15)40205-8.
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PANDIT, LOTIKA, and JOSEPH G. OUSLANDER. "Postmenopausal Vaginal Atrophy and Atrophic Vaginitis." American Journal of the Medical Sciences 314, no. 4 (October 1997): 228–31. http://dx.doi.org/10.1097/00000441-199710000-00004.
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Song, Ji Hyun, Sang Gyun Kim, Eun Hyo Jin, Joo Hyun Lim, and Sun Young Yang. "Risk factors of gastric carcinogenesis in underlying gastric mucosal atrophy." Journal of Clinical Oncology 34, no. 4_suppl (February 1, 2016): 28. http://dx.doi.org/10.1200/jco.2016.34.4_suppl.28.
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28 Background: Atrophic gastritis and intestinal metaplasia were considered as premalignant lesions. The prevalence of chronic atrophic gastritis is very high in Korea. The aims of this study were to evaluate the risk factors of gastric carcinogenesis in underlying gastric mucosal atrophy. Methods: A total of 10187 subjects underwent upper gastrointestinal endoscopy for health checkup between 2003 and 2004 were enrolled in this retrospective cohort study. Follow-up endoscopy was performed between 2005 and 2014. Atrophic gastritis and intestinal metaplasia were assessed according to the Kimura-Takemoto classification by endoscopy. Helicobacter pylori (Hp) was evaluated by serum IgG antibody. Results: The number of atrophic gastritis was 3716 (36.5%) in baseline endoscopy, and 2146 were undergone follow-up endoscopy (82.8±38.3month); 1139 showed aggravation of atrophy and 1007 showed no change. A total of 71 subjects were diagnosed as gastric neoplasms (34 adenoma, 37 carcinoma). Age (HR = 1.019, 95%CI 1.010-1.028), alcohol intake (HR = 1.002, 95%CI 1.001-1.002), Salt intake (HR = 1.295, 95%CI 1.038-1.617) and Hp infection (HR = 1.584, 95%CI 1.220-2.057) were associated with aggravation of mucosal atrophy. The risk factors for gastric neoplasm in underlying mucosal atrophy were age (HR = 1.041, 95%CI 1.004-1.079), alcohol intake (HR = 1.003, 95% CI 1.001-1.005), Salt intake (HR = 2.553, 95% CI 1.141-5.712), Extent of mucosal atrophy (HR = 2.375, 95% CI 1.201-4.695 in C3-O1; HR = 4.255, 95% CI 1.612-11.229 in O2-O3), and intestinal metaplasia (HR = 2.599, 95% CI 1.286-5.251). Conclusions: Hp was a risk factor for aggravation of atrophy, but not for gastric neoplasm. Salt intake, extent of mucosal atrophy, and intestinal metaplasia were important risk factors for gastric neoplasm.
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Schakman, O., S. Kalista, L. Bertrand, P. Lause, J. Verniers, J. M. Ketelslegers, and J. P. Thissen. "Role of Akt/GSK-3β/β-Catenin Transduction Pathway in the Muscle Anti-Atrophy Action of Insulin-Like Growth Factor-I in Glucocorticoid-Treated Rats." Endocrinology 149, no. 8 (May 8, 2008): 3900–3908. http://dx.doi.org/10.1210/en.2008-0439.
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Decrease of muscle IGF-I plays a critical role in muscle atrophy caused by glucocorticoids (GCs) because IGF-I gene electrotransfer prevents muscle atrophy caused by GCs. The goal of the present study was to identify the intracellular mediators responsible for the IGF-I anti-atrophic action in GC-induced muscle atrophy. We first assessed the IGF-I transduction pathway alterations caused by GC administration and their reversibility by local IGF-I overexpression performed by electrotransfer. Muscle atrophy induced by dexamethasone (dexa) administration occurred with a decrease in Akt (−53%; P <0.01) phosphorylation together with a decrease in β-catenin protein levels (−40%; P <0.001). Prevention of atrophy by IGF-I was associated with restoration of Akt phosphorylation and β-catenin levels. We then investigated whether muscle overexpression of these intracellular mediators could mimic the IGF-I anti-atrophic effects. Overexpression of a constitutively active form of Akt induced a marked fiber hypertrophy in dexa-treated animals (+175% of cross-sectional area; P <0.001) and prevented dexa-induced atrophy. This hypertrophy was associated with an increase in phosphorylated GSK-3β (+17%; P <0.05) and in β-catenin content (+35%; P <0.05). Furthermore, overexpression of a dominant-negative GSK-3β or a stable form of β-catenin increased fiber cross-sectional area by, respectively, 23% (P <0.001) and 29% (P <0.001) in dexa-treated rats, preventing completely the atrophic effect of GC. In conclusion, this work indicates that Akt, GSK-3β, and β-catenin probably contribute together to the IGF-I anti-atrophic effect in GC-induced muscle atrophy.
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Allen, David L., Gary E. McCall, Amanda S. Loh, Molly C. Madden, and Ryan S. Mehan. "Acute daily psychological stress causes increased atrophic gene expression and myostatin-dependent muscle atrophy." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 299, no. 3 (September 2010): R889—R898. http://dx.doi.org/10.1152/ajpregu.00296.2010.
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Psychological stress is known to attenuate body size and lean body mass. We tested the effects of 1, 3, or 7 days of two different models of psychological stress, 1 h of daily restraint stress (RS) or daily cage-switching stress (CS), on skeletal muscle size and atrophy-associated gene expression in mice. Thymus weights decreased in both RS and CS mice compared with unstressed controls, suggesting that both models activated the hypothalamic-pituitary-adrenal axis. Body mass was significantly decreased at all time points for both models of stress but was greater for RS than CS. Mass of the tibialis anterior (TA) and soleus (SOL) muscles was significantly decreased after 3 and 7 days of RS, but CS only significantly decreased SOL mass after 7 days. TA mRNA levels of the atrophy-associated genes myostatin (MSTN), atrogin-1, and the phosphatidylinositol 3-kinase inhibitory subunit p85α were all significantly increased relative to unstressed mice after 1 and 3 days of RS, and expression of MSTN and p85α mRNA remained elevated after 7 days of RS. Expression of muscle ring finger 1 was increased after 1 day of RS but returned to baseline at 3 and 7 days of RS. MSTN, atrogin-1, and p85α mRNA levels also significantly increased after 1 and 3 days of CS but atrogen-1 mRNA levels had resolved back to normal levels by 3 days and p85α with 7 days of CS. p21CIP mRNA levels were significantly decreased by 3 days of CS or RS. Finally, body mass was minimally affected, and muscle mass was completely unaffected by 3 days of RS in mice null for the MSTN gene, and MSTN inactivation attenuated the increase in atrogin-1 mRNA levels with 4 days of RS compared with wild-type mice. Together these data suggest that acute daily psychological stress induces atrophic gene expression and loss of muscle mass that appears to be MSTN dependent.
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Chen, Shaohua, Lixiong Ying, Mei Kong, Yu Zhang, and Youming Li. "The Prevalence ofHelicobacter pyloriInfection Decreases with Older Age in Atrophic Gastritis." Gastroenterology Research and Practice 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/494783.
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The clinical pathological characteristics of 3969 adult patients with chronic atrophic gastritis were retrospectively studied. The positivity of intestinal metaplasia and dysplasia in atrophic gastric specimens increased with age; however,H. pyloripositivity and inflammatory activity decreased significantly with increased age.H. pyloriinfection was present in 21.01% of chronic atrophic gastritis patients, and 92.33% of the subjects withH. pyloriinfection were found to have simultaneous inflammatory activity. The intestinal metaplasia and dysplasia positivity markedly increased as the degree of gastric atrophy increased. In conclusion, the incidence ofH. pyloriinfection decreased with age and correlated significantly with inflammatory activity in atrophic gastritis patients. The intestinal metaplasia and dysplasia positivity notably increased as the degree of gastric atrophy increased. Large population-based prospective studies are needed to better understand the progression of CAG.
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Sawano, Shoko, Misaki Fukushima, Taiki Akasaka, Mako Nakamura, Ryuichi Tatsumi, Yoshihide Ikeuchi, and Wataru Mizunoya. "Up- and Downregulated Genes after Long-Term Muscle Atrophy Induced by Denervation in Mice Detected Using RNA-Seq." Life 13, no. 5 (April 29, 2023): 1111. http://dx.doi.org/10.3390/life13051111.
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Skeletal muscle atrophy occurs rapidly as a result of inactivity. Although there are many reports on changes in gene expression during the early phase of muscle atrophy, the patterns of up-and downregulated gene expression after long-term and equilibrated muscle atrophy are poorly understood. In this study, we comprehensively examined the changes in gene expression in long-term denervated mouse muscles using RNA-Seq. The murine right sciatic nerve was denervated, and the mice were housed for five weeks. The cross-sectional areas of the hind limb muscles were measured using an X-ray CT system 35 days after denervation. After 28 d of denervation, the cross-sectional area of the muscle decreased to approximately 65% of that of the intact left muscle and reached a plateau. Gene expression in the soleus and extensor digitorum longus (EDL) muscles on the 36th day was analyzed using RNA-Seq and validated using RT-qPCR. RNA-Seq analysis revealed that three genes—Adora1, E230016M11Rik, and Gm10718—were upregulated and one gene—Gm20515—was downregulated in the soleus muscle; additionally, four genes—Adora1, E230016M11Rik, Pigh, and Gm15557—were upregulated and one gene—Fzd7—was downregulated in the EDL muscle (FDR < 0.05). Among these genes, E230016M11Rik, one of the long non-coding RNAs, was significantly upregulated in both the muscles. These findings indicate that E230016M11Rik could be a candidate gene for the maintenance of atrophied skeletal muscle size and an atrophic state.
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Bdolah, Yuval, Adam Segal, Preeti Tanksale, S. Ananth Karumanchi, and Stewart H. Lecker. "Atrophy-related ubiquitin ligases atrogin-1 and MuRF-1 are associated with uterine smooth muscle involution in the postpartum period." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 292, no. 2 (February 2007): R971—R976. http://dx.doi.org/10.1152/ajpregu.00617.2006.
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The regulation of cell size depends on a delicate balance between protein synthesis and breakdown. Skeletal and cardiac muscle adapt to hormonal and neuronal stimuli and can rapidly hypertrophy and atrophy; however, the extent to which these processes occur in smooth muscle is less clear. Atrophy in striated muscle results from enhanced protein breakdown and is associated with a common transcriptional profile and activation of the ubiquitin-proteasome pathway, including induction of the muscle-specific ubiquitin protein ligases atrogin-1 and muscle ring-finger protein 1 (MuRF-1). Here we show that atrogin-1 is also expressed in smooth muscle, and that both atrogin-1 and MuRF-1 are upregulated in the uterus following delivery, as rapid involution occurs. While these two genes are similarly induced in all types of muscle during rapid loss of cell mass, other striated muscle atrophy-specific transcriptional changes are not observed during uterine involution, suggesting different underlying molecular mechanisms. These results raise the possibility that activation of atrogin-1 and MuRF-1 may be a common general adaptation in cells undergoing a rapid reduction in size.
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Lu Na, Wang Yijin, Wenxin, and Farra Aidah Jumuddin. "Therapeutic Effect of AAV8-Mediated miR-23a in Immobilization-Induced Muscle Atrophy in Mice." International Journal of Advancement in Life Sciences Research 07, no. 03 (2024): 90–97. http://dx.doi.org/10.31632/ijalsr.2024.v07i03.008.
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bjective: To investigate the therapeutic effect of miR-23a in immobilization-induced muscle atrophy in mice. Methods: (Experiment 1) Twelve C57BL6 wild-type mice were randomly divided into two groups: Sham group (sham surgery) and Immobilization (hind limb immobilization surgery). Fluorescence quantitative PCR was performed to detect the expression changes of miR-23a, MuRF-1, and Atrogin-1 7 days post-surgery. (Experiment 2) Twelve C57BL6 wild-type mice were randomly divided into 4 groups according to surgery type (sham surgery and hind limb immobilization surgery) and injection type (AAV8 or AAV8-OEmiR-23a), fluorescence quantitative PCR to detect changes in MuRF-1 and Atrogin-1 expression in mouse gastrocnemius muscle. (Experiment 3) NFATc3 expression changes were detected by fluorescence quantitative PCR 48 hours post-transfection. (Experiment 4) Twelve C57BL6 wild-type mice underwent hind limb immobilization surgery, divided into 4 groups : Immobilization+AAV8-control, Immobilization+AAV8-OEmiR23a, Immobilization+AAV8-shNFATc3, and Immobilization+AAV8-OEmiR-23a+AAV8-shNFATc3. quantitative PCR to detect changes in MuRF-1 and Atrogin-1 expression in mouse gastrocnemius muscle. Results: Fluorescence quantitative PCR results showed that miR-23a was downregulated in immobilization-induced muscle atrophy, while MuRF-1 and Atrogin-1 expression was upregulated. WGA staining results showed that intramuscular injection of AAV8-OEmiR-23a could significantly alleviate the decrease in muscle fiber cross-sectional area and the increase in expression of muscle atrophy marker genes MuRF-1 and Atrogin-1 caused by hind limb immobilization, Fluorescence quantitative PCR revealed that when miR-23a expression was inhibited, NFATc3 expression was downregulated; when miR-23a was overexpressed, NFATc3 expression was upregulated, Fluorescence quantitative PCR results showed that intramuscular injection of AAV8-OEmiR-23a and AAV8-shNFATc3 could not alleviate the increase in expression of muscle atrophy marker genes MuRF-1 and Atrogin-1 caused by hind limb immobilization. Conclusion: miR-23a can treat hind limb immobilization-induced muscle atrophy in mice.
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Jao, Chi-Wen, Jiann-Horng Yeh, Yu-Te Wu, Li-Ming Lien, Yuh-Feng Tsai, Kuang-En Chu, Chen-Yu Hsiao, Po-Shan Wang, and Chi Ieong Lau. "Alteration of the Intra- and Inter-Lobe Connectivity of the Brain Structural Network in Normal Aging." Entropy 22, no. 8 (July 28, 2020): 826. http://dx.doi.org/10.3390/e22080826.
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The morphological changes in cortical parcellated regions during aging and whether these atrophies may cause brain structural network intra- and inter-lobe connectivity alterations are subjects that have been minimally explored. In this study, a novel fractal dimension-based structural network was proposed to measure atrophy of 68 parcellated cortical regions. Alterations of structural network parameters, including intra- and inter-lobe connectivity, were detected in a middle-aged group (30–45 years old) and an elderly group (50–65 years old). The elderly group exhibited significant lateralized atrophy in the left hemisphere, and most of these fractal dimension atrophied regions were included in the regions of the “last-in, first-out” model. Globally, the elderly group had lower modularity values, smaller component size modules, and fewer bilateral association fibers. They had lower intra-lobe connectivity in the frontal and parietal lobes, but higher intra-lobe connectivity in the temporal and occipital lobes. Both groups exhibited similar inter-lobe connecting pattern. The elderly group revealed separations, sparser long association fibers, commissural fibers, and lateral inter-lobe connectivity lost effect, mainly in the right hemisphere. New wiring and reconfiguring modules may have occurred within the brain structural network to compensate for connectivity, decreasing and preventing functional loss in cerebral intra- and inter-lobe connectivity.
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Pierucci, Federica, Alessia Frati, Chiara Battistini, Fabio Penna, Paola Costelli, and Elisabetta Meacci. "Control of Skeletal Muscle Atrophy Associated to Cancer or Corticosteroids by Ceramide Kinase." Cancers 13, no. 13 (June 30, 2021): 3285. http://dx.doi.org/10.3390/cancers13133285.
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Apart from cytokines and chemokines, sphingolipid mediators, particularly sphingosine-1-phosphate (S1P) and ceramide 1-phosphate (C1P), contribute to cancer and inflammation. Cancer, as well as other inflammatory conditions, are associated with skeletal muscle (SkM) atrophy, which is characterized by the unbalance between protein synthesis and degradation. Although the signaling pathways involved in SkM mass wasting are multiple, the regulatory role of simple sphingolipids is limited. Here, we report the impairment of ceramide kinase (CerK), the enzyme responsible for the phosphorylation of ceramide to C1P, associated with the accomplishment of atrophic phenotype in various experimental models of SkM atrophy: in vivo animal model bearing the C26 adenocarcinoma or Lewis lung carcinoma tumors, in human and murine SkM cells treated with the conditioned medium obtained from cancer cells or with the glucocorticoid dexamethasone. Notably, we demonstrate in all the three experimental approaches a drastic decrease of CerK expression. Gene silencing of CerK promotes the up-regulation of atrogin-1/MAFbx expression, which was also observed after cell treatment with C8-ceramide, a biologically active ceramide analogue. Conversely, C1P treatment significantly reduced the corticosteroid’s effects. Altogether, these findings provide evidence that CerK, acting as a molecular modulator, may be a new possible target for SkM mass regulation associated with cancer or corticosteroids.
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Lee, Chi-Woo, Yeok Boo Chang, Chun Woong Park, Sung Hee Han, Hyung Joo Suh, and Yejin Ahn. "Protein Hydrolysate from Spirulina platensis Prevents Dexamethasone-Induced Muscle Atrophy via Akt/Foxo3 Signaling in C2C12 Myotubes." Marine Drugs 20, no. 6 (May 29, 2022): 365. http://dx.doi.org/10.3390/md20060365.
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Loss of muscle mass is the primary symptom of sarcopenia. Protein intake is recommended to prevent muscle mass loss, and Spirulina platensis, a microalga with high protein content, is a potential protein supplement. Here, we evaluated the differentiation ability of C2C12 cells and the inhibitory effect of Spirulina hydrolysates (SPH) prepared by Collupulin on dexamethasone (DEX)-treated C2C12 cells. SPH contained 578.27 mg/g protein and 92.30 mg/g branched-chain amino acids. SPH increased C2C12 myotube length and diameter, likely owing to increased MyoD1 and Myf5 expression. Inhibition of increased Atrogin-1, MuRF-1, and FoxO3 expression by SPH in DEX-treated C2C12 cells suppressed DEX-induced muscle atrophy. Moreover, SPH inhibited the DEX-induced increase in cytosolic p-Akt protein expression and suppressed the increase in nuclear FoxO3a protein expression, thereby suppressing the increase in the protein expression of the ubiquitin-proteasome-related factors Atrogin-1 and MuRF-1, which are involved in muscle atrophy. SPH suppressed DEX-induced muscle atrophy by activating the Akt/FoxO3a pathway. SPH promoted C2C12 myoblast differentiation into myotubes and inhibited DEX-induced myotube atrophy by suppressing Atrogin-1 and MuRF-1 expression and regulating the FoxO3a transcription factor. Collectively, SPH can be used as a functional food to inhibit muscle atrophy and promote muscle regeneration.
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Martins, Cláudio, Cristina Teixeira, Suzane Ribeiro, Daniel Trabulo, Cláudia Cardoso, João Mangualde, Ricardo Freire, et al. "Seronegative Intestinal Villous Atrophy: A Diagnostic Challenge." Case Reports in Gastrointestinal Medicine 2016 (2016): 1–4. http://dx.doi.org/10.1155/2016/6392028.
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Celiac disease is the most important cause of intestinal villous atrophy. Seronegative intestinal villous atrophy, including those that are nonresponsive to a gluten-free diet, is a diagnostic challenge. In these cases, before establishing the diagnosis of seronegative celiac disease, alternative etiologies of atrophic enteropathy should be considered. Recently, a new clinical entity responsible for seronegative villous atrophy was described—olmesartan-induced sprue-like enteropathy. Herein, we report two uncommon cases of atrophic enteropathy in patients with arterial hypertension under olmesartan, who presented with severe chronic diarrhea and significant involuntary weight loss. Further investigation revealed intestinal villous atrophy and intraepithelial lymphocytosis. Celiac disease and other causes of villous atrophy were ruled out. Drug-induced enteropathy was suspected and clinical improvement and histologic recovery were verified after olmesartan withdrawal. These cases highlight the importance for clinicians to maintain a high index of suspicion for olmesartan as a precipitant of sprue-like enteropathy.