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Pesquisa : A11.284.149.707 [Categoria DeCS]
Referências encontradas : 5433 [refinar]
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[PMID]:29179175
[Au] Autor:Tu RH; Li QJ; Huang Z; He Y; Meng JJ; Zheng HL; Zeng ZY; Zhong GQ
[Ad] Endereço:Department of Geriatric Cardiology, Nanning, China.
[Ti] Título:Novel Functional Role of Heat Shock Protein 90 in Mitochondrial Connexin 43-Mediated Hypoxic Postconditioning.
[So] Source:Cell Physiol Biochem;44(3):982-997, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Previous studies have shown that heat shock protein 90 (HSP90)-mediated mitochondrial import of connexin 43 (Cx43) is critical in preconditioning cardioprotection. The present study was designed to test whether postconditioning has the same effect as preconditioning in promoting Cx43 translocation to mitochondria and whether mitochondrial HSP90 modulates this effect. METHODS: Cellular models of hypoxic postconditioning (HPC) from rat heart-derived H9c2 cells and neonatal rat cardiomyocytes were employed. The effects of HPC on cardiomyocytes apoptosis were examined by flow cytometry and Hoechst 33342 fluorescent staining. Reactive oxidative species (ROS) production was assessed with the peroxide-sensitive fluorescent probe 2',7'-dichlorofluorescin in diacetate (DCFH-DA). The anti- and pro-apoptotic markers Bcl-2 and Bax, HSP90 and Cx43 protein levels were studied by Western blot analysis in total cell homogenate and sarcolemmal and mitochondrial fractions. The effects on HPC of the HSP90 inhibitor geldanamycin (GA), ROS scavengers superoxide dismutase (SOD) and catalase (CAT), and small interfering RNA (siRNA) targeting Cx43 and HSP90 were also investigated. RESULTS: HPC significantly reduced hypoxia/reoxygenation (H/R)-induced cardiomyocyte apoptosis. These beneficial effects were accompanied by an increase in Bcl-2 levels and a decrease in Bax levels in both sarcolemmal and mitochondrial fractions. HPC with siRNA targeting Cx43 or the ROS scavengers SOD plus CAT significantly prevented ROS generation and HPC cardioprotection, but HPC with either SOD or CAT did not. These data strongly supported the involvement of Cx43 in HPC cardioprotection, likely via modulation of the ROS balance which plays a central role in HPC protection. Furthermore, HPC increased total and mitochondrial levels of HSP90 and the mitochondria-to-sarcolemma ratio of Cx43; blocking the function of HSP90 with the HSP90 inhibitor geldanamycin (GA) or siRNA targeting HSP90 prevented the protection of HPC and the HPC-induced association of Cx43, indicating that mitochondrial HSP90 was important for mitochondrial translocation of Cx43 during HPC. CONCLUSION: Mitochondrial HSP90 played a central role in HPC cardioprotection, and its activity was linked to the mitochondrial targeting of Cx43, the activation of which triggered ROS signaling and the subsequent reduction of redox stress. Consequently, its target gene, Bcl-2, was upregulated, and proapoptotic Bax was inhibited in the sarcolemma and mitochondria, ultimately attenuating H/R-induced cardiomyocyte apoptosis. These data reveal a novel mechanism of HPC protection.
[Mh] Termos MeSH primário: Conexina 43/metabolismo
Proteínas de Choque Térmico HSP90/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Benzoquinonas/farmacologia
Catalase/farmacologia
Hipóxia Celular
Linhagem Celular
Conexina 43/antagonistas & inibidores
Conexina 43/genética
Proteínas de Choque Térmico HSP90/antagonistas & inibidores
Proteínas de Choque Térmico HSP90/genética
Lactamas Macrocíclicas/farmacologia
Microscopia de Fluorescência
Mitocôndrias/metabolismo
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Ratos
Ratos Sprague-Dawley
Espécies Reativas de Oxigênio/química
Espécies Reativas de Oxigênio/metabolismo
Sarcolema/metabolismo
Superóxido Dismutase/farmacologia
Proteína X Associada a bcl-2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzoquinones); 0 (Connexin 43); 0 (HSP90 Heat-Shock Proteins); 0 (Lactams, Macrocyclic); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (RNA, Small Interfering); 0 (Reactive Oxygen Species); 0 (bcl-2-Associated X Protein); EC 1.11.1.6 (Catalase); EC 1.15.1.1 (Superoxide Dismutase); Z3K3VJ16KU (geldanamycin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1159/000485399


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[PMID]:29183798
[Au] Autor:McElhanon KE; Bhattacharya S
[Ad] Endereço:Department of Physiology and Cell Biology, Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, 473 W. 12th Ave, Columbus, OH 43210-1252, United States.
[Ti] Título:Altered membrane integrity in the progression of muscle diseases.
[So] Source:Life Sci;192:166-172, 2018 Jan 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Sarcolemmal integrity is orchestrated through the interplay of preserving membrane strength and fast tracking the membrane repair process during an event of compromised membrane fragility. Several molecular players have been identified that act in a concerted fashion to maintain the barrier function of the muscle membrane. Substantial research findings in the field of muscle biology point out the importance of maintaining membrane integrity as a key contributory factor to cellular homeostasis. Innumerable data on the progression of membrane pathology associated with compromised muscle membrane integrity support targeting sarcolemmal integrity in skeletal and cardiac muscle as a model therapeutic strategy to alleviate some of the pathologic conditions. This review will discuss strategies that researchers have undertaken to compensate for an imbalance in sarcolemma membrane fragility and membrane repair to maintain muscle membrane integrity.
[Mh] Termos MeSH primário: Membranas/patologia
Doenças Musculares/patologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Músculo Esquelético/patologia
Miocárdio/patologia
Miócitos Cardíacos/patologia
Sarcolema/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE


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[PMID]:29065150
[Au] Autor:Quattrocelli M; Capote J; Ohiri JC; Warner JL; Vo AH; Earley JU; Hadhazy M; Demonbreun AR; Spencer MJ; McNally EM
[Ad] Endereço:Center for Genetic Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States of America.
[Ti] Título:Genetic modifiers of muscular dystrophy act on sarcolemmal resealing and recovery from injury.
[So] Source:PLoS Genet;13(10):e1007070, 2017 Oct.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Genetic disruption of the dystrophin complex produces muscular dystrophy characterized by a fragile muscle plasma membrane leading to excessive muscle degeneration. Two genetic modifiers of Duchenne Muscular Dystrophy implicate the transforming growth factor ß (TGFß) pathway, osteopontin encoded by the SPP1 gene and latent TGFß binding protein 4 (LTBP4). We now evaluated the functional effect of these modifiers in the context of muscle injury and repair to elucidate their mechanisms of action. We found that excess osteopontin exacerbated sarcolemmal injury, and correspondingly, that loss of osteopontin reduced injury extent both in isolated myofibers and in muscle in vivo. We found that ablation of osteopontin was associated with reduced expression of TGFß and TGFß-associated pathways. We identified that increased TGFß resulted in reduced expression of Anxa1 and Anxa6, genes encoding key components of the muscle sarcolemma resealing process. Genetic manipulation of Ltbp4 in dystrophic muscle also directly modulated sarcolemmal resealing, and Ltbp4 alleles acted in concert with Anxa6, a distinct modifier of muscular dystrophy. These data provide a model in which a feed forward loop of TGFß and osteopontin directly impacts the capacity of muscle to recover from injury, and identifies an intersection of genetic modifiers on muscular dystrophy.
[Mh] Termos MeSH primário: Genes Modificadores
Proteínas de Ligação a TGF-beta Latente/fisiologia
Músculo Esquelético/fisiologia
Distrofia Muscular Animal/genética
Osteopontina/metabolismo
[Mh] Termos MeSH secundário: Animais
Anexina A1/genética
Anexina A1/metabolismo
Anexina A6/genética
Anexina A6/metabolismo
Feminino
Regulação da Expressão Gênica
Masculino
Camundongos
Camundongos Endogâmicos DBA
Camundongos Knockout
Músculo Esquelético/lesões
Distrofia Muscular Animal/metabolismo
Distrofia Muscular Animal/patologia
Osteopontina/genética
Receptores de Fatores de Crescimento Transformadores beta/genética
Receptores de Fatores de Crescimento Transformadores beta/metabolismo
Recuperação de Função Fisiológica
Sarcolema/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A1); 0 (Annexin A6); 0 (LTBP-4 protein, mouse); 0 (Latent TGF-beta Binding Proteins); 0 (Receptors, Transforming Growth Factor beta); 0 (Spp1 protein, mouse); 0 (annexin A1, mouse); 106441-73-0 (Osteopontin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171119
[Lr] Data última revisão:
171119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171025
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007070


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[PMID]:28945810
[Au] Autor:Sirenko SG; Yang D; Maltseva LA; Kim MS; Lakatta EG; Maltsev VA
[Ad] Endereço:Laboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America.
[Ti] Título:Spontaneous, local diastolic subsarcolemmal calcium releases in single, isolated guinea-pig sinoatrial nodal cells.
[So] Source:PLoS One;12(9):e0185222, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Uptake and release calcium from the sarcoplasmic reticulum (SR) (dubbed "calcium clock"), in the form of spontaneous, rhythmic, local diastolic calcium releases (LCRs), together with voltage-sensitive ion channels (membrane clock) form a coupled system that regulates the action potential (AP) firing rate. LCRs activate Sodium/Calcium exchanger (NCX) that accelerates diastolic depolarization and thus participating in regulation of the time at which the next AP will occur. Previous studies in rabbit SA node cells (SANC) demonstrated that the basal AP cycle length (APCL) is tightly coupled to the basal LCR period (time from the prior AP-induced Ca2+ transient to the diastolic LCR occurrence), and that this coupling is further modulated by autonomic receptor stimulation. Although spontaneous LCRs during diastolic depolarization have been reported in SANC of various species (rabbit, cat, mouse, toad), prior studies have failed to detect LCRs in spontaneously beating SANC of guinea-pig, a species that has been traditionally used in studies of cardiac pacemaker cell function. We performed a detailed investigation of whether guinea-pig SANC generate LCRs and whether they play a similar key role in regulation of the AP firing rate. We used two different approaches, 2D high-speed camera and classical line-scan confocal imaging. Positioning the scan-line beneath sarcolemma, parallel to the long axis of the cell, we found that rhythmically beating guinea-pig SANC do, indeed, generate spontaneous, diastolic LCRs beneath the surface membrane. The average key LCR characteristics measured in confocal images in guinea-pig SANC were comparable to rabbit SANC, both in the basal state and in the presence of ß-adrenergic receptor stimulation. Moreover, the relationship between the LCR period and APCL was subtended by the same linear function. Thus, LCRs in guinea-pig SANC contribute to the diastolic depolarization and APCL regulation. Our findings indicate that coupled-clock system regulation of APCL is a general, species-independent, mechanism of pacemaker cell normal automaticity. Lack of LCRs in prior studies is likely explained by technical issues, as individual LCRs are small stochastic events occurring mainly near the cell border.
[Mh] Termos MeSH primário: Sinalização do Cálcio
Nó Sinoatrial/metabolismo
[Mh] Termos MeSH secundário: Potenciais de Ação
Animais
Relógios Biológicos
Gatos
Diástole
Cobaias
Técnicas In Vitro
Camundongos
Microscopia Confocal
Microscopia de Vídeo
Coelhos
Receptores Adrenérgicos beta/metabolismo
Sarcolema/metabolismo
Análise de Célula Única
Nó Sinoatrial/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Adrenergic, beta)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170926
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185222


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[PMID]:28850625
[Au] Autor:Lai N; Kummitha C; Hoppel C
[Ad] Endereço:Department of Electrical and Computer Engineering, Old Dominion University, Norfolk, Virginia, United States of America.
[Ti] Título:Defects in skeletal muscle subsarcolemmal mitochondria in a non-obese model of type 2 diabetes mellitus.
[So] Source:PLoS One;12(8):e0183978, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Skeletal muscle resistance to insulin is related to accumulation of lipid-derived products, but it is not clear whether this accumulation is caused by skeletal muscle mitochondrial dysfunction. Diabetes and obesity are reported to have a selective effect on the function of subsarcolemmal and interfibrillar mitochondria in insulin-resistant skeletal muscle. The current study investigated the role of the subpopulations of mitochondria in the pathogenesis of insulin resistance in the absence of obesity. A non-obese spontaneous rat model of type 2 diabetes mellitus, (Goto-Kakizaki), was used to evaluate function and biochemical properties in both populations of skeletal muscle mitochondria. In subsarcolemmal mitochondria, minor defects are observed whereas in interfibrillar mitochondria function is preserved. Subsarcolemmal mitochondria defects characterized by a mild decline of oxidative phosphorylation efficiency are related to ATP synthase and structural alterations of inner mitochondria membrane but are considered unimportant because of the absence of defects upstream as shown with polarographic and spectrophometric assays. Fatty acid transport and oxidation is preserved in both population of mitochondria, whereas palmitoyl-CoA increased 25% in interfibrillar mitochondria of diabetic rats. Contrary to popular belief, these data provide compelling evidence that mitochondrial function is unaffected in insulin-resistant skeletal muscle from T2DM non-obese rats.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/metabolismo
Mitocôndrias Musculares/metabolismo
Músculo Esquelético/metabolismo
Sarcolema/metabolismo
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Masculino
ATPases Mitocondriais Próton-Translocadoras/metabolismo
Fosforilação Oxidativa
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.6.3.- (Mitochondrial Proton-Translocating ATPases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170830
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183978


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[PMID]:28808062
[Au] Autor:Whitfield J; Paglialunga S; Smith BK; Miotto PM; Simnett G; Robson HL; Jain SS; Herbst EAF; Desjardins EM; Dyck DJ; Spriet LL; Steinberg GR; Holloway GP
[Ad] Endereço:From the Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario N1G 2W1, Canada and.
[Ti] Título:Ablating the protein TBC1D1 impairs contraction-induced sarcolemmal glucose transporter 4 redistribution but not insulin-mediated responses in rats.
[So] Source:J Biol Chem;292(40):16653-16664, 2017 Oct 06.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TBC1 domain family member 1 (TBC1D1), a Rab GTPase-activating protein and paralogue of Akt substrate of 160 kDa (AS160), has been implicated in both insulin- and 5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase-mediated glucose transporter type 4 (GLUT4) translocation. However, the role of TBC1D1 in contracting muscle remains ambiguous. We therefore explored the metabolic consequence of ablating TBC1D1 in both resting and contracting skeletal muscles, utilizing a rat TBC1D1 KO model. Although insulin administration rapidly increased ( < 0.05) plasma membrane GLUT4 content in both red and white gastrocnemius muscles, the TBC1D1 ablation did not alter this response nor did it affect whole-body insulin tolerance, suggesting that TBC1D1 is not required for insulin-induced GLUT4 trafficking events. Consistent with findings in other models of altered TBC1D1 protein levels, whole-animal and skeletal muscle fat oxidation was increased in the TBC1D1 KO rats. Although there was no change in mitochondrial content in the KO rats, maximal ADP-stimulated respiration was higher in permeabilized muscle fibers, which may contribute to the increased reliance on fatty acids in resting KO animals. Despite this increase in mitochondrial oxidative capacity, run time to exhaustion at various intensities was impaired in the KO rats. Moreover, contraction-induced increases in sarcolemmal GLUT4 content and glucose uptake were lower in the white gastrocnemius of the KO animals. Altogether, our results highlight a critical role for TBC1D1 in exercise tolerance and contraction-mediated translocation of GLUT4 to the plasma membrane in skeletal muscle.
[Mh] Termos MeSH primário: Tolerância ao Exercício/fisiologia
Transportador de Glucose Tipo 4/metabolismo
Contração Muscular/fisiologia
Músculo Esquelético/metabolismo
Proteínas/metabolismo
Sarcolema/metabolismo
[Mh] Termos MeSH secundário: Animais
Transportador de Glucose Tipo 4/genética
Insulina/genética
Insulina/metabolismo
Oxirredução
Consumo de Oxigênio/fisiologia
Transporte Proteico/fisiologia
Proteínas/genética
Ratos
Ratos Sprague-Dawley
Ratos Transgênicos
Sarcolema/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucose Transporter Type 4); 0 (Insulin); 0 (Proteins); 0 (Slc2a4 protein, rat); 0 (TBC1D1 protein, rat)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.806786


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[PMID]:28638919
[Au] Autor:Xu YM; Cao JM; Li JP; Huang QT; Wang P
[Ad] Endereço:Sports and Health College of Hangzhou Normal University, Hangzhou 310036, China. xuyuming110@126.com.
[Ti] Título:[Analyses of exercise-induced muscle damage-specific microRNA expression and molecular target of sarcolemmal damage in rats].
[So] Source:Sheng Li Xue Bao;69(3):276-284, 2017 Jun 25.
[Is] ISSN:0371-0874
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:In the present study, we were to screen the specific microRNA (miRNA) of exercise-induced muscle damage (EIMD) and assess the EIMD-specific miRNAs-regulated target of sarcolemmal damage in rats. Twenty-four male Sprague-Dawley (SD) rats were randomly divided into 3 groups, which included sedentary (C), 24 h post-exercise (E24) and 48 h post-exercise (E48) groups. Rat EIMD model was established by an acute eccentric exercise, i.e., a downhill running treatment at -16º gradient. EIMD characteristics were verified by Evans blue dye staining, differentially expressed miRNAs were detected by microarray assay, EIMD-specific miRNAs expressions were further validated by real-time quantitative RT-PCR (RT-qPCR), and targets of the miRNAs were predicted based on mRNA expressions of associated proteins and related pathway core molecules of sarcolemmal damage. Two EIMD-specific expressed miRNAs, including miR-206-3p and miR-139-3p, were found in the study. There was a significantly negative correlation (P < 0.05) between miR-206-3p expression and dystrophin (r = -0.68), utrophin (r = -0.64), JNK (r = -0.62) or ERK1 (r = -0.68) respectively, but no correlation was found between miR-139-3p and these biomolecules. The results suggest that: i) the expression profile of miRNAs in rat is significantly affected by EIMD, ii) miR-206-3p and miR-139-3p are the EIMD-specific miRNAs, and iii) miR-206-3p may control sarcolemmal damage by regulating dystrophin, utrophin, JNK and ERK1.
[Mh] Termos MeSH primário: MicroRNAs/genética
Condicionamento Físico Animal/efeitos adversos
Corrida
Sarcolema/patologia
[Mh] Termos MeSH secundário: Animais
Distrofina/genética
MAP Quinase Quinase 4/genética
Sistema de Sinalização das MAP Quinases
Masculino
Distribuição Aleatória
Ratos
Ratos Sprague-Dawley
Reação em Cadeia da Polimerase em Tempo Real
Utrofina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dystrophin); 0 (MicroRNAs); 0 (Utrophin); EC 2.7.12.2 (MAP Kinase Kinase 4)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE


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[PMID]:28634272
[Au] Autor:Schultz J; Lee SJ; Cole T; Hoang HD; Vibbert J; Cottee PA; Miller MA; Han SM
[Ad] Endereço:Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
[Ti] Título:The secreted MSP domain of VAPB homolog VPR-1 patterns the adult striated muscle mitochondrial reticulum via SMN-1.
[So] Source:Development;144(12):2175-2186, 2017 06 15.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The major sperm protein domain (MSPd) has an extracellular signaling function implicated in amyotrophic lateral sclerosis. Secreted MSPds derived from the VAPB homolog VPR-1 promote mitochondrial localization to actin-rich I-bands in body wall muscle. Here we show that the nervous system and germ line are key MSPd secretion tissues. MSPd signals are transduced through the CLR-1 Lar-like tyrosine phosphatase receptor. We show that CLR-1 is expressed throughout the muscle plasma membrane, where it is accessible to MSPd within the pseudocoelomic fluid. MSPd signaling is sufficient to remodel the muscle mitochondrial reticulum during adulthood. An RNAi suppressor screen identified survival of motor neuron 1 (SMN-1) as a downstream effector. SMN-1 acts in muscle, where it colocalizes at myofilaments with ARX-2, a component of the Arp2/3 actin-nucleation complex. Genetic studies suggest that SMN-1 promotes Arp2/3 activity important for localizing mitochondria to I-bands. Our results support the model that VAPB homologs are circulating hormones that pattern the striated muscle mitochondrial reticulum. This function is crucial in adults and requires SMN-1 in muscle, likely independent of its role in pre-mRNA splicing.
[Mh] Termos MeSH primário: Proteínas de Caenorhabditis elegans/metabolismo
Caenorhabditis elegans/crescimento & desenvolvimento
Caenorhabditis elegans/metabolismo
Proteínas de Membrana/metabolismo
Músculo Estriado/crescimento & desenvolvimento
Músculo Estriado/metabolismo
Proteínas do Complexo SMN/metabolismo
[Mh] Termos MeSH secundário: Proteína 2 Relacionada a Actina/metabolismo
Complexo 2-3 de Proteínas Relacionadas à Actina/metabolismo
Esclerose Amiotrófica Lateral/metabolismo
Animais
Animais Geneticamente Modificados
Caenorhabditis elegans/genética
Proteínas de Caenorhabditis elegans/química
Proteínas de Caenorhabditis elegans/genética
Genes de Helmintos
Células Germinativas/metabolismo
Seres Humanos
Larva/crescimento & desenvolvimento
Larva/metabolismo
Masculino
Proteínas de Membrana/química
Proteínas de Membrana/genética
Mitocôndrias Musculares/metabolismo
Neurônios Motores/metabolismo
Mutação
Domínios Proteicos
Interferência de RNA
Proteínas Tirosina Fosfatases Semelhantes a Receptores/genética
Proteínas Tirosina Fosfatases Semelhantes a Receptores/metabolismo
Proteínas do Complexo SMN/antagonistas & inibidores
Proteínas do Complexo SMN/genética
Sarcolema/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Actin-Related Protein 2); 0 (Actin-Related Protein 2-3 Complex); 0 (Caenorhabditis elegans Proteins); 0 (Membrane Proteins); 0 (SMN Complex Proteins); 0 (VPR-1 protein, C elegans); 0 (arx-2 protein, C elegans); EC 3.1.3.48 (CLR-1 protein, C elegans); EC 3.1.3.48 (Receptor-Like Protein Tyrosine Phosphatases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE
[do] DOI:10.1242/dev.152025


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[PMID]:28483801
[Au] Autor:Chung JO; Koutsari C; Blachnio-Zabielska AU; Hames KC; Jensen MD
[Ad] Endereço:Endocrine Research Unit, Mayo Clinic, Rochester, MN.
[Ti] Título:Intramyocellular Ceramides: Subcellular Concentrations and Fractional De Novo Synthesis in Postabsorptive Humans.
[So] Source:Diabetes;66(8):2082-2091, 2017 Aug.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We investigated the relationship between insulin resistance markers and subsarcolemmal (SS) and intramyofibrillar (IMF) ceramide concentrations, as well as the contribution of plasma palmitate (6.5-h infusion of [U- C]palmitate) to intramyocellular ceramides. Seventy-six postabsorptive men and women had muscle biopsies 1.5, 6.5, and 24 h after starting the tracer infusion. Concentrations and enrichment of muscle ceramides were measured by liquid chromatography-tandem mass spectrometry. We found that HOMA of insulin resistance, plasma insulin, and triglyceride concentrations were positively correlated with SS C16:0 and C18:1 ceramide, but not SS C14:0-Cer, C20:0-Cer, C24:0-Cer, and C24:1-Cer concentrations; IMF ceramide concentrations were not correlated with any metabolic parameters. The fractional contribution of plasma palmitate to 16:0 ceramide was greater in SS than IMF (SS, 18.2% vs. IMF, 8.7%; = 0.0006). Plasma insulin concentrations correlated positively with the fractional contribution of plasma palmitate to SS 16:0 ceramide. The fractional contribution of plasma palmitate to intramyocellular SS 16:0 ceramide was positively correlated with SS C16:0 ceramide concentrations (γ = 0.435; = 0.002). We conclude that skeletal muscle SS ceramides, especially C16 to C18 chain lengths and the de novo synthesis of intramyocellular ceramide from plasma palmitate are associated with markers of insulin resistance.
[Mh] Termos MeSH primário: Ceramidas/metabolismo
Resistência à Insulina/fisiologia
Insulina/sangue
Células Musculares/metabolismo
Músculo Esquelético/metabolismo
Sarcolema/metabolismo
[Mh] Termos MeSH secundário: Adulto
Biópsia
Cromatografia Líquida
Jejum/sangue
Ácidos Graxos não Esterificados/sangue
Feminino
Voluntários Saudáveis
Seres Humanos
Masculino
Músculo Esquelético/citologia
Miofibrilas/metabolismo
Palmitatos/sangue
Espectrometria de Massas em Tandem
Fatores de Tempo
Triglicerídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ceramides); 0 (Fatty Acids, Nonesterified); 0 (Insulin); 0 (Palmitates); 0 (Triglycerides)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170510
[St] Status:MEDLINE
[do] DOI:10.2337/db17-0082


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[PMID]:28481224
[Au] Autor:Quattrocelli M; Barefield DY; Warner JL; Vo AH; Hadhazy M; Earley JU; Demonbreun AR; McNally EM
[Ti] Título:Intermittent glucocorticoid steroid dosing enhances muscle repair without eliciting muscle atrophy.
[So] Source:J Clin Invest;127(6):2418-2432, 2017 Jun 01.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glucocorticoid steroids such as prednisone are prescribed for chronic muscle conditions such as Duchenne muscular dystrophy, where their use is associated with prolonged ambulation. The positive effects of chronic steroid treatment in muscular dystrophy are paradoxical because these steroids are also known to trigger muscle atrophy. Chronic steroid use usually involves once-daily dosing, although weekly dosing in children has been suggested for its reduced side effects on behavior. In this work, we tested steroid dosing in mice and found that a single pulse of glucocorticoid steroids improved sarcolemmal repair through increased expression of annexins A1 and A6, which mediate myofiber repair. This increased expression was dependent on glucocorticoid response elements upstream of annexins and was reinforced by the expression of forkhead box O1 (FOXO1). We compared weekly versus daily steroid treatment in mouse models of acute muscle injury and in muscular dystrophy and determined that both regimens provided comparable benefits in terms of annexin gene expression and muscle repair. However, daily dosing activated atrophic pathways, including F-box protein 32 (Fbxo32), which encodes atrogin-1. Conversely, weekly steroid treatment in mdx mice improved muscle function and histopathology and concomitantly induced the ergogenic transcription factor Krüppel-like factor 15 (Klf15) while decreasing Fbxo32. These findings suggest that intermittent, rather than daily, glucocorticoid steroid regimen promotes sarcolemmal repair and muscle recovery from injury while limiting atrophic remodeling.
[Mh] Termos MeSH primário: Glucocorticoides/administração & dosagem
Músculo Esquelético/efeitos dos fármacos
Prednisona/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Anexina A6/genética
Anexina A6/metabolismo
Células Cultivadas
Esquema de Medicação
Avaliação Pré-Clínica de Medicamentos
Expressão Gênica
Glucocorticoides/efeitos adversos
Masculino
Camundongos da Linhagem 129
Camundongos Endogâmicos DBA
Camundongos Endogâmicos mdx
Músculo Esquelético/fisiopatologia
Atrofia Muscular/induzido quimicamente
Distrofia Muscular de Duchenne/tratamento farmacológico
Prednisona/efeitos adversos
Ligação Proteica
Receptores de Glucocorticoides/metabolismo
Regeneração
Sarcolema/efeitos dos fármacos
Sarcolema/fisiologia
Ativação Transcricional/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexin A6); 0 (Glucocorticoids); 0 (Receptors, Glucocorticoid); VB0R961HZT (Prednisone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE



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