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Pesquisa : C05.651.534 [Categoria DeCS]
Referências encontradas : 356 [refinar]
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[PMID]:29278025
[Au] Autor:Kataoka H; Nakano J; Kondo Y; Honda Y; Sakamoto J; Origuchi T; Okita M
[Ad] Endereço:1 Department of Locomotive Rehabilitation Science, Unit of Rehabilitation Sciences, Nagasaki University Graduate School of Biomedical Sciences , Nagasaki, Japan.
[Ti] Título:The influence of aging on the effectiveness of heat stress in preventing disuse muscle atrophy.
[So] Source:Physiol Int;104(4):316-328, 2017 Dec 01.
[Is] ISSN:2498-602X
[Cp] País de publicação:Hungary
[La] Idioma:eng
[Ab] Resumo:This study examined the aging effect on disuse muscle atrophy prevention using heat stress. Wistar rats aged 7 and 60 weeks were divided into three groups as follows: control, immobilized (Im), and immobilized and heat stressed (ImH). Heat stress was given by immersing the hindlimbs in hot water (42 °C) for 60 min, once in every 3 days and the gastrocnemius (GAS) and soleus (SOL) muscles were extracted after 14 days. Muscle-fiber types were classified using ATPase staining. Heat shock protein 70 (HSP70) was assessed through Western blotting. In GAS muscle of both groups and SOL muscle of 7-week-old rats, the fiber diameter of each muscle type in the ImH group significantly increased compared with that in the Im group. However, this could not be observed in the SOL muscle of the 60-week-old rats. The increased percentage of type-I fibers and variability of types I and II muscle-fiber diameter were evident in the SOL muscle of the 60-week rats. HSP70 was significantly elevated in the ImH group compared with in the Im group in both muscle types of both age groups. Thus, effectiveness of heat stress in the prevention of disuse muscle atrophy appears unsatisfactory in aging muscle fibers.
[Mh] Termos MeSH primário: Envelhecimento
Proteínas de Choque Térmico HSP70/metabolismo
Hipertermia Induzida/métodos
Músculo Esquelético/fisiopatologia
Transtornos Musculares Atróficos/prevenção & controle
Transtornos Musculares Atróficos/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Resposta ao Choque Térmico
Masculino
Fibras Musculares Esqueléticas/patologia
Músculo Esquelético/patologia
Transtornos Musculares Atróficos/diagnóstico
Ratos
Ratos Wistar
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HSP70 Heat-Shock Proteins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171227
[St] Status:MEDLINE
[do] DOI:10.1556/2060.104.2017.4.1


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[PMID]:28511915
[Au] Autor:Jiménez Garduño AM; Juárez-Hernández LJ; Polanco MJ; Tosatto L; Michelatti D; Arosio D; Basso M; Pennuto M; Musio C
[Ad] Endereço:Institute of Biophysics (IBF), Trento Unit, National Research Council (CNR), Via alla Cascata 56/C, 38123 Trento, Italy & Bruno Kessler Foundation (FBK), LabSSAH, Via alla Cascata 56/C, 38123 Trento, Italy.
[Ti] Título:Altered ionic currents and amelioration by IGF-1 and PACAP in motoneuron-derived cells modelling SBMA.
[So] Source:Biophys Chem;229:68-76, 2017 Oct.
[Is] ISSN:1873-4200
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Spinal and bulbar muscular atrophy (SBMA), also known as Kennedy's disease, is a motor neuron disease caused by the expansion of a polymorphic CAG tandem repeat encoding a polyglutamine (polyQ) tract in the androgen receptor (AR) gene. SBMA is triggered by the binding of mutant AR to its natural ligands, testosterone and dihydrotestosterone (DHT). To investigate the neuronal alterations of motor neuron cell models of SBMA, we applied patch-clamp methods to verify how polyQ expansions in the AR alter cell ionic currents. We used mouse motoneuron-derived MN-1 cells expressing normal AR (MN24Q) and mutant AR (MN100Q treated cells with vehicle EtOH and DHT). We observed a reduction of the current flux mainly at depolarizing potentials in the DHT-treated cells, while the dissection of macroscopic currents showed single different cationic currents belonging to voltage-gated channels. Also, we treated the cells with IGF-1 and PACAP, which have previously been shown to protect MN-1 cells from the toxicity of mutant AR, and we found an amelioration of the altered currents. Our results suggest that the electrophysiological correlate of SBMA is a suitable reference point for the identification of disease symptoms and for future therapeutic targets.
[Mh] Termos MeSH primário: Potenciais de Ação/efeitos dos fármacos
Fator de Crescimento Insulin-Like I/farmacologia
Modelos Biológicos
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/farmacologia
[Mh] Termos MeSH secundário: Animais
Cálcio/metabolismo
Linhagem Celular
Seres Humanos
Camundongos
Neurônios Motores/citologia
Neurônios Motores/efeitos dos fármacos
Neurônios Motores/metabolismo
Transtornos Musculares Atróficos/metabolismo
Transtornos Musculares Atróficos/patologia
Técnicas de Patch-Clamp
Peptídeos/metabolismo
Potássio/metabolismo
Receptores Androgênicos/genética
Receptores Androgênicos/metabolismo
Sequências de Repetição em Tandem/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Peptides); 0 (Pituitary Adenylate Cyclase-Activating Polypeptide); 0 (Receptors, Androgen); 26700-71-0 (polyglutamine); 67763-96-6 (Insulin-Like Growth Factor I); RWP5GA015D (Potassium); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170518
[St] Status:MEDLINE


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[PMID]:28331320
[Au] Autor:Márquez-Miranda V; Abrigo J; Rivera JC; Araya-Durán I; Aravena J; Simon F; Pacheco N; González-Nilo FD; Cabello-Verrugio C
[Ad] Endereço:Center for Bioinformatics and Integrative Biology (CBIB), Facultad de Ciencias Biologicas, Universidad Andres Bello, Santiago; Fundación Fraunhofer Chile Research, Las Condes.
[Ti] Título:The complex of PAMAM-OH dendrimer with Angiotensin (1-7) prevented the disuse-induced skeletal muscle atrophy in mice.
[So] Source:Int J Nanomedicine;12:1985-1999, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:Angiotensin (1-7) (Ang-(1-7)) is a bioactive heptapeptide with a short half-life and has beneficial effects in several tissues - among them, skeletal muscle - by preventing muscle atrophy. Dendrimers are promising vehicles for the protection and transport of numerous bioactive molecules. This work explored the use of a neutral, non-cytotoxic hydroxyl-terminated poly(amidoamine) (PAMAM-OH) dendrimer as an Ang-(1-7) carrier. Bioinformatics analysis showed that the Ang-(1-7)-binding capacity of the dendrimer presented a 2:1 molar ratio. Molecular dynamics simulation analysis revealed the capacity of neutral PAMAM-OH to protect Ang-(1-7) and form stable complexes. The peptide coverage ability of the dendrimer was between ~50% and 65%. Furthermore, an electrophoretic mobility shift assay demonstrated that neutral PAMAM-OH effectively bonded peptides. Experimental results showed that the Ang-(1-7)/PAMAM-OH complex, but not Ang-(1-7) alone, had an anti-atrophic effect when administered intraperitoneally, as evaluated by muscle strength, fiber diameter, myofibrillar protein levels, and atrogin-1 and MuRF-1 expressions. The results of the Ang-(1-7)/PAMAM-OH complex being intraperitoneally injected were similar to the results obtained when Ang-(1-7) was systemically administered through mini-osmotic pumps. Together, the results suggest that Ang-(1-7) can be protected for PAMAM-OH when this complex is intraperitoneally injected. Therefore, the Ang-(1-7)/PAMAM-OH complex is an efficient delivery method for Ang-(1-7), since it improves the anti-atrophic activity of this peptide in skeletal muscle.
[Mh] Termos MeSH primário: Angiotensina I/uso terapêutico
Dendrímeros/química
Músculo Esquelético/patologia
Atrofia Muscular/tratamento farmacológico
Atrofia Muscular/prevenção & controle
Transtornos Musculares Atróficos/tratamento farmacológico
Transtornos Musculares Atróficos/prevenção & controle
Fragmentos de Peptídeos/uso terapêutico
[Mh] Termos MeSH secundário: Angiotensina I/farmacologia
Animais
Ensaio de Desvio de Mobilidade Eletroforética
Imobilização
Injeções Intraperitoneais
Masculino
Camundongos Endogâmicos C57BL
Simulação de Dinâmica Molecular
Proteínas Musculares/metabolismo
Músculo Esquelético/efeitos dos fármacos
Transtornos Musculares Atróficos/patologia
Cadeias Pesadas de Miosina/metabolismo
Fragmentos de Peptídeos/farmacologia
Peptídeos/uso terapêutico
Proteínas Ligases SKP Culina F-Box/metabolismo
Eletricidade Estática
Proteínas com Motivo Tripartido/metabolismo
Ubiquitina-Proteína Ligases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dendrimers); 0 (Muscle Proteins); 0 (PAMAM Starburst); 0 (Peptide Fragments); 0 (Peptides); 0 (Tripartite Motif Proteins); 9041-90-1 (Angiotensin I); EC 2.3.2.27 (Fbxo32 protein, mouse); EC 2.3.2.27 (SKP Cullin F-Box Protein Ligases); EC 2.3.2.27 (Trim63 protein, mouse); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 3.6.4.1 (Myosin Heavy Chains); IJ3FUK8MOF (angiotensin I (1-7))
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170522
[Lr] Data última revisão:
170522
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170324
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S125521


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[PMID]:28274922
[Au] Autor:Petrov AM; Kravtsova VV; Matchkov VV; Vasiliev AN; Zefirov AL; Chibalin AV; Heiny JA; Krivoi II
[Ad] Endereço:Department of Normal Physiology, Kazan State Medical University, Kazan, Russia.
[Ti] Título:Membrane lipid rafts are disturbed in the response of rat skeletal muscle to short-term disuse.
[So] Source:Am J Physiol Cell Physiol;312(5):C627-C637, 2017 May 01.
[Is] ISSN:1522-1563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Marked loss of skeletal muscle mass occurs under various conditions of disuse, but the molecular and cellular mechanisms leading to atrophy are not completely understood. We investigate early molecular events that might play a role in skeletal muscle remodeling during mechanical unloading (disuse). The effects of acute (6-12 h) hindlimb suspension on the soleus muscles from adult rats were examined. The integrity of plasma membrane lipid rafts was tested utilizing cholera toxin B subunit or fluorescent sterols. In addition, resting intracellular Ca level was analyzed. Acute disuse disturbed the plasma membrane lipid-ordered phase throughout the sarcolemma and was more pronounced in junctional membrane regions. Ouabain (1 µM), which specifically inhibits the Na-K-ATPase α2 isozyme in rodent skeletal muscles, produced similar lipid raft changes in control muscles but was ineffective in suspended muscles, which showed an initial loss of α2 Na-K-ATPase activity. Lipid rafts were able to recover with cholesterol supplementation, suggesting that disturbance results from cholesterol loss. Repetitive nerve stimulation also restores lipid rafts, specifically in the junctional sarcolemma region. Disuse locally lowered the resting intracellular Ca concentration only near the neuromuscular junction of muscle fibers. Our results provide evidence to suggest that the ordering of lipid rafts strongly depends on motor nerve input and may involve interactions with the α2 Na-K-ATPase. Lipid raft disturbance, accompanied by intracellular Ca dysregulation, is among the earliest remodeling events induced by skeletal muscle disuse.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Colesterol/metabolismo
Microdomínios da Membrana/metabolismo
Microdomínios da Membrana/patologia
Músculo Esquelético/fisiopatologia
Transtornos Musculares Atróficos/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Sinalização do Cálcio
Elevação dos Membros Posteriores
Masculino
Músculo Esquelético/patologia
Transtornos Musculares Atróficos/patologia
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
97C5T2UQ7J (Cholesterol); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE
[do] DOI:10.1152/ajpcell.00365.2016


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[PMID]:28270443
[Au] Autor:Lee S; Leone TC; Rogosa L; Rumsey J; Ayala J; Coen PM; Fitts RH; Vega RB; Kelly DP
[Ad] Endereço:Center for Metabolic Origins of Disease, Sanford Burnham Prebys Medical Discovery Institute, Orlando, Florida.
[Ti] Título:Skeletal muscle PGC-1ß signaling is sufficient to drive an endurance exercise phenotype and to counteract components of detraining in mice.
[So] Source:Am J Physiol Endocrinol Metab;312(5):E394-E406, 2017 May 01.
[Is] ISSN:1522-1555
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α and -1ß serve as master transcriptional regulators of muscle mitochondrial functional capacity and are capable of enhancing muscle endurance when overexpressed in mice. We sought to determine whether muscle-specific transgenic overexpression of PGC-1ß affects the detraining response following endurance training. First, we established and validated a mouse exercise-training-detraining protocol. Second, using multiple physiological and gene expression end points, we found that PGC-1ß overexpression in skeletal muscle of sedentary mice fully recapitulated the training response. Lastly, PGC-1ß overexpression during the detraining period resulted in partial prevention of the detraining response. Specifically, an increase in the plateau at which O uptake (V̇o ) did not change from baseline with increasing treadmill speed [peak V̇o (ΔV̇o )] was maintained in trained mice with PGC-1ß overexpression in muscle 6 wk after cessation of training. However, other detraining responses, including changes in running performance and in situ half relaxation time (a measure of contractility), were not affected by PGC-1ß overexpression. We conclude that while activation of muscle PGC-1ß is sufficient to drive the complete endurance phenotype in sedentary mice, it only partially prevents the detraining response following exercise training, suggesting that the process of endurance detraining involves mechanisms beyond the reversal of muscle autonomous mechanisms involved in endurance fitness. In addition, the protocol described here should be useful for assessing early-stage proof-of-concept interventions in preclinical models of muscle disuse atrophy.
[Mh] Termos MeSH primário: Músculo Esquelético/fisiologia
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/metabolismo
Condicionamento Físico Animal/métodos
Resistência Física/fisiologia
Aptidão Física/fisiologia
Corrida/fisiologia
[Mh] Termos MeSH secundário: Animais
Masculino
Camundongos
Camundongos Transgênicos
Transtornos Musculares Atróficos/fisiopatologia
Transtornos Musculares Atróficos/prevenção & controle
Fenótipo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha); 0 (Ppargc1a protein, mouse)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170309
[St] Status:MEDLINE
[do] DOI:10.1152/ajpendo.00380.2016


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[PMID]:28148932
[Au] Autor:Crunkhorn S
[Ti] Título:Neurodegenerative disease: Pituitary adenylate cyclase activator ameliorates SBMA.
[So] Source:Nat Rev Drug Discov;16(2):88, 2017 Feb 02.
[Is] ISSN:1474-1784
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Adenilil Ciclases/metabolismo
Transtornos Musculares Atróficos/metabolismo
Doenças Neurodegenerativas/metabolismo
Hipófise/metabolismo
[Mh] Termos MeSH secundário: Animais
Quinase 2 Dependente de Ciclina/metabolismo
Camundongos
Peptídeos/metabolismo
Receptores Androgênicos/metabolismo
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Peptides); 0 (Receptors, Androgen); 26700-71-0 (polyglutamine); EC 2.7.11.22 (Cyclin-Dependent Kinase 2); EC 4.6.1.1 (Adenylyl Cyclases)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170203
[St] Status:MEDLINE
[do] DOI:10.1038/nrd.2017.11


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[PMID]:28087734
[Au] Autor:Borgia D; Malena A; Spinazzi M; Desbats MA; Salviati L; Russell AP; Miotto G; Tosatto L; Pegoraro E; Sorarù G; Pennuto M; Vergani L
[Ad] Endereço:Department of Neurosciences, University of Padova, Padova, Italy.
[Ti] Título:Increased mitophagy in the skeletal muscle of spinal and bulbar muscular atrophy patients.
[So] Source:Hum Mol Genet;26(6):1087-1103, 2017 Mar 15.
[Is] ISSN:1460-2083
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Spinal and bulbar muscular atrophy (SBMA) is a neuromuscular disorder caused by polyglutamine expansion in the androgen receptor (AR) and characterized by the loss of lower motor neurons. Here we investigated pathological processes occurring in muscle biopsy specimens derived from SBMA patients and, as controls, age-matched healthy subjects and patients suffering from amyotrophic lateral sclerosis (ALS) and neurogenic atrophy. We detected atrophic fibers in the muscle of SBMA, ALS and neurogenic atrophy patients. In addition, SBMA muscle was characterized by the presence of a large number of hypertrophic fibers, with oxidative fibers having a larger size compared with glycolytic fibers. Polyglutamine-expanded AR expression was decreased in whole muscle, yet enriched in the nucleus, and localized to mitochondria. Ultrastructural analysis revealed myofibrillar disorganization and streaming in zones lacking mitochondria and degenerating mitochondria. Using molecular (mtDNA copy number), biochemical (citrate synthase and respiratory chain enzymes) and morphological (dark blue area in nicotinamide adenine dinucleotide-stained muscle cross-sections) analyses, we found a depletion of the mitochondria associated with enhanced mitophagy. Mass spectrometry analysis revealed an increase of phosphatidylethanolamines and phosphatidylserines in mitochondria isolated from SBMA muscles, as well as a 50% depletion of cardiolipin associated with decreased expression of the cardiolipin synthase gene. These observations suggest a causative link between nuclear polyglutamine-expanded AR accumulation, depletion of mitochondrial mass, increased mitophagy and altered mitochondrial membrane composition in SBMA muscle patients. Given the central role of mitochondria in cell bioenergetics, therapeutic approaches toward improving the mitochondrial network are worth considering to support SBMA patients.
[Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/genética
Transtornos Musculares Atróficos/genética
Peptídeos/genética
Receptores Androgênicos/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Esclerose Amiotrófica Lateral/fisiopatologia
Androgênios/metabolismo
Animais
Biópsia
DNA Mitocondrial/genética
Feminino
Seres Humanos
Masculino
Meia-Idade
Degradação Mitocondrial/genética
Neurônios Motores/metabolismo
Neurônios Motores/patologia
Músculo Esquelético/irrigação sanguínea
Músculo Esquelético/metabolismo
Músculo Esquelético/patologia
Transtornos Musculares Atróficos/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Androgens); 0 (DNA, Mitochondrial); 0 (Peptides); 0 (Receptors, Androgen); 26700-71-0 (polyglutamine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170115
[St] Status:MEDLINE
[do] DOI:10.1093/hmg/ddx019


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[PMID]:28056188
[Au] Autor:Hu NF; Chang H; Du B; Zhang QW; Arfat Y; Dang K; Gao YF
[Ad] Endereço:a Key Laboratory of Resource Biology and Biotechnology in Western China, College of Life Sciences, Northwest University, Ministry of Education, Xi'an 710069, China.
[Ti] Título:Tetramethylpyrazine ameliorated disuse-induced gastrocnemius muscle atrophy in hindlimb unloading rats through suppression of Ca /ROS-mediated apoptosis.
[So] Source:Appl Physiol Nutr Metab;42(2):117-127, 2017 Feb.
[Is] ISSN:1715-5320
[Cp] País de publicação:Canada
[La] Idioma:eng
[Ab] Resumo:The purpose of this study was to examine the possible mechanism underlying the protective effect of tetramethylpyrazine (TMP) against disuse-induced muscle atrophy. Sprague-Dawley rats were randomly assigned to receive 14 days of hindlimb unloading (HLU, a model of disuse atrophy) or cage controls. The rats were given TMP (60 mg/kg body mass) or vehicle (water) by gavage. Compared with vehicle treatment, TMP significantly attenuated the loss of gastrocnemius muscle mass (-33.56%, P < 0.01), the decrease of cross-sectional area of slow fiber (-10.99%, P < 0.05) and fast fiber (-15.78%, P < 0.01) during HLU. Although TMP failed to further improve recovery of muscle function or fatigability compared with vehicle treatment, it can suppress the higher level of lactate (-22.71%, P < 0.01) induced by HLU. Besides, TMP could effectually reduce the increased protein expression of muscle RING-finger protein 1 induced by HLU (-14.52%, P < 0.01). Furthermore, TMP can ameliorate the calcium overload (-54.39%, P < 0.05), the increase of malondialdehyde content (-19.82%, P < 0.05), the decrease of superoxide dismutase activity (21.34%, P < 0.05), and myonuclear apoptosis (-78.22%, P < 0.01) induced by HLU. Moreover, TMP significantly reduced HLU-induced increase of Bax to B-cell lymphoma 2 (-36.36%, P < 0.01) and cytochrome c release (-36.16%, P < 0.05). In conclusion, TMP attenuated HLU-induced gastrocnemius muscle atrophy through suppression of Ca /reactive oxygen species increase and consequent proteolysis and apoptosis. Therefore, TMP might exhibit therapeutic effect against oxidative stress, cytosolic calcium overload, and mitochondrial damage in disuse-induced muscle atrophy.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Músculo Esquelético/efeitos dos fármacos
Transtornos Musculares Atróficos/prevenção & controle
Estresse Oxidativo/efeitos dos fármacos
Inibidores da Agregação de Plaquetas/uso terapêutico
Pirazinas/uso terapêutico
Vasodilatadores/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Sinalização do Cálcio/efeitos dos fármacos
Repressão Enzimática/efeitos dos fármacos
Feminino
Elevação dos Membros Posteriores/efeitos adversos
Fibras Musculares de Contração Rápida/efeitos dos fármacos
Fibras Musculares de Contração Rápida/metabolismo
Fibras Musculares de Contração Rápida/patologia
Fibras Musculares de Contração Lenta/efeitos dos fármacos
Fibras Musculares de Contração Lenta/metabolismo
Fibras Musculares de Contração Lenta/patologia
Músculo Esquelético/metabolismo
Músculo Esquelético/patologia
Transtornos Musculares Atróficos/etiologia
Transtornos Musculares Atróficos/metabolismo
Transtornos Musculares Atróficos/patologia
Complexo Repressor Polycomb 1/antagonistas & inibidores
Complexo Repressor Polycomb 1/metabolismo
Proteólise/efeitos dos fármacos
Distribuição Aleatória
Ratos Sprague-Dawley
Espécies Reativas de Oxigênio/antagonistas & inibidores
Espécies Reativas de Oxigênio/metabolismo
Ubiquitina-Proteína Ligases/antagonistas & inibidores
Ubiquitina-Proteína Ligases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Platelet Aggregation Inhibitors); 0 (Pyrazines); 0 (Reactive Oxygen Species); 0 (Vasodilator Agents); EC 2.3.2.27 (Polycomb Repressive Complex 1); EC 2.3.2.27 (Ring1 protein, rat); EC 2.3.2.27 (Ubiquitin-Protein Ligases); V80F4IA5XG (tetramethylpyrazine)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170203
[Lr] Data última revisão:
170203
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170106
[St] Status:MEDLINE
[do] DOI:10.1139/apnm-2016-0363


  9 / 356 MEDLINE  
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[PMID]:28005993
[Au] Autor:Yamada S; Hashizume A; Hijikata Y; Inagaki T; Suzuki K; Kondo N; Kawai K; Noda S; Nakanishi H; Banno H; Hirakawa A; Koike H; Halievski K; Jordan CL; Katsuno M; Sobue G
[Ad] Endereço:Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
[Ti] Título:Decreased Peak Expiratory Flow Associated with Muscle Fiber-Type Switching in Spinal and Bulbar Muscular Atrophy.
[So] Source:PLoS One;11(12):e0168846, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to characterize the respiratory function profile of subjects with spinal and bulbar muscular atrophy (SBMA), and to explore the underlying pathological mechanism by comparing the clinical and biochemical indices of this disease with those of amyotrophic lateral sclerosis (ALS). We enrolled male subjects with SBMA (n = 40) and ALS (n = 25) along with 15 healthy control subjects, and assessed their respiratory function, motor function, and muscle strength. Predicted values of peak expiratory flow (%PEF) and forced vital capacity were decreased in subjects with SBMA compared with controls. In SBMA, both values were strongly correlated with the trunk subscores of the motor function tests and showed deterioration relative to disease duration. Compared with activities of daily living (ADL)-matched ALS subjects, %PEF, tongue pressure, and grip power were substantially decreased in subjects with SBMA. Both immunofluorescence and RT-PCR demonstrated a selective decrease in the expression levels of the genes encoding the myosin heavy chains specific to fast-twitch fibers in SBMA subjects. The mRNA levels of peroxisome proliferator-activated receptor gamma coactivator 1-alpha and peroxisome proliferator-activated receptor delta were up-regulated in SBMA compared with ALS and controls. In conclusion, %PEF is a disease-specific respiratory marker for the severity and progression of SBMA. Explosive muscle strength, including %PEF, was selectively affected in subjects with SBMA and was associated with activation of the mitochondrial biogenesis-related molecular pathway in skeletal muscles.
[Mh] Termos MeSH primário: Fibras Musculares Esqueléticas/fisiologia
Atrofia Muscular Espinal/fisiopatologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Esclerose Amiotrófica Lateral/metabolismo
Esclerose Amiotrófica Lateral/fisiopatologia
Progressão da Doença
Seres Humanos
Masculino
Meia-Idade
Fibras Musculares Esqueléticas/metabolismo
Força Muscular
Atrofia Muscular Espinal/metabolismo
Transtornos Musculares Atróficos/metabolismo
Transtornos Musculares Atróficos/fisiopatologia
PPAR delta/metabolismo
Pico do Fluxo Expiratório
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/metabolismo
RNA Mensageiro/metabolismo
Testes de Função Respiratória
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (PPAR delta); 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha); 0 (RNA, Messenger)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170724
[Lr] Data última revisão:
170724
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161223
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0168846


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[PMID]:27841025
[Au] Autor:Jang J; Park J; Chang H; Lim K
[Ad] Endereço:a Laboratory of Exercise Nutrition, Department of Physical Education, Konkuk University, 120, Neungdong-ro, Gwangjin-gu, Seoul 143-701, Korea.
[Ti] Título:l-Carnitine supplement reduces skeletal muscle atrophy induced by prolonged hindlimb suspension in rats.
[So] Source:Appl Physiol Nutr Metab;41(12):1240-1247, 2016 Dec.
[Is] ISSN:1715-5320
[Cp] País de publicação:Canada
[La] Idioma:eng
[Ab] Resumo:l-Carnitine was recently found to downregulate the ubiquitin proteasome pathway (UPP) and increase insulin-like growth factor 1 concentrations in animal models. However, the effect of l-carnitine administration on disuse muscle atrophy induced by hindlimb suspension has not yet been studied. Thus, we hypothesized that l-carnitine may have a protective effect on muscle atrophy induced by hindlimb suspension via the Akt1/mTOR and/or UPP. Male Wistar rats were assigned to 3 groups: hindlimb suspension group, hindlimb suspension with l-carnitine administration (1250 mg·kg ·day ) group, and pair-fed group adjusted hindlimb suspension. l-Carnitine administration for 2 weeks of hindlimb suspension alleviated the decrease in weight and fiber size in the soleus muscle. In addition, l-carnitine suppressed atrogin-1 mRNA expression, which has been reported to play a pivotal role in muscle atrophy. The present study shows that l-carnitine has a protective effect against soleus muscle atrophy caused by hindlimb suspension and decreased E3 ligase messenger RNA expression, suggesting the possibility that l-carnitine protects against muscle atrophy, at least in part, through the inhibition of the UPP. These observations suggest that l-carnitine could serve as an effective supplement in the decrease of muscle atrophy caused by weightlessness in the fields of clinical and rehabilitative research.
[Mh] Termos MeSH primário: Carnitina/uso terapêutico
Suplementos Nutricionais
Repressão Enzimática
Proteínas Musculares/antagonistas & inibidores
Músculo Esquelético/metabolismo
Transtornos Musculares Atróficos/prevenção & controle
Proteínas Ligases SKP Culina F-Box/antagonistas & inibidores
Ubiquitina-Proteína Ligases/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Elevação dos Membros Posteriores/efeitos adversos
Imuno-Histoquímica
Masculino
Proteínas Musculares/genética
Proteínas Musculares/metabolismo
Músculo Esquelético/enzimologia
Músculo Esquelético/patologia
Atrofia Muscular/etiologia
Atrofia Muscular/metabolismo
Atrofia Muscular/patologia
Atrofia Muscular/prevenção & controle
Transtornos Musculares Atróficos/etiologia
Transtornos Musculares Atróficos/metabolismo
Transtornos Musculares Atróficos/patologia
Complexo de Endopeptidases do Proteassoma
Inibidores de Proteassoma/uso terapêutico
Distribuição Aleatória
Ratos
Ratos Wistar
Proteínas Ligases SKP Culina F-Box/genética
Proteínas Ligases SKP Culina F-Box/metabolismo
Proteínas com Motivo Tripartido/genética
Proteínas com Motivo Tripartido/metabolismo
Ubiquitina-Proteína Ligases/genética
Ubiquitina-Proteína Ligases/metabolismo
Ubiquitinação
Ausência de Peso/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Muscle Proteins); 0 (Proteasome Inhibitors); 0 (Tripartite Motif Proteins); EC 2.3.2.27 (Fbxo32 protein, rat); EC 2.3.2.27 (SKP Cullin F-Box Protein Ligases); EC 2.3.2.27 (Trim63 protein, rat); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.3.2.27 (parkin protein); EC 3.4.25.1 (Proteasome Endopeptidase Complex); S7UI8SM58A (Carnitine)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170207
[Lr] Data última revisão:
170207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161115
[St] Status:MEDLINE



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