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[PMID]:29254922
[Au] Autor:Li XY; Fu LL; Cheng HJ; Zhao SH
[Ad] Endereço:Key Laboratory of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education; Key Laboratory of Swine Genetics and Breeding of Ministry of Agriculture; the Coperative Innovation Center for Sustainable Pig Production; Huazhong Agricultural University, Wuhan 430070, China.
[Ti] Título:Advances on microRNA in regulating mammalian skeletal muscle development.
[So] Source:Yi Chuan;39(11):1046-1053, 2017 Nov 20.
[Is] ISSN:0253-9772
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:MicroRNA (miRNA) is a class of short non-coding RNA, which is about 22 bp in length. In mammals, miRNA exerts its funtion through binding with the 3°-UTR region of target genes and inhibiting their translation. Skeletal muscle development is a complex event, including: proliferation, migration and differentiation of skeletal muscle stem cells; proliferation, differentiation and fusion of myocytes; as well as hypertrophy, energy metabolism and conversion of muscle fiber types. The miRNA plays important roles in all processes of skeletal muscle development through targeting the key factors of different stages. Herein we summarize the miRNA related to muscle development, providing a better understanding of the skeletal muscle development.
[Mh] Termos MeSH primário: MicroRNAs/fisiologia
Desenvolvimento Muscular
Músculo Esquelético/crescimento & desenvolvimento
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Proliferação Celular
Metabolismo Energético
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (MicroRNAs)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE
[do] DOI:10.16288/j.yczz.17-112


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[PMID]:29254923
[Au] Autor:Lu C; Huang YH
[Ad] Endereço:State Key Laboratory of Agrobiotechnology, China Agricultural University, Beijing 100193, China.
[Ti] Título:Progress in long non-coding RNAs in animals.
[So] Source:Yi Chuan;39(11):1054-1065, 2017 Nov 20.
[Is] ISSN:0253-9772
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:Long non-coding RNAs (lncRNAs) are important transcripts that are more than 200 nucleotides in length, and distribute extensively in animal and plant genomes. Accumulated studies demonstrate that lncRNAs play critical roles in biological processes related to embryogenesis, muscle development, lipid deposition and immune responses. They assist protein complexes in translocating to appropriate locations and participate in regulating gene activation and inactivation. Recently, rapid progress of lncRNA research is emerging, largely due to molecular biological technologies and information developed in the human genome project and the Encyclopedia of DNA Elements (ENCODE) project. For example, a dwarf open reading frame (DWORF) encoded by an annotated lncRNA was reported to activate the SERCA pump. Moreover, small regulatory polypeptide of amino acid response (SPAR) encoded by lncRNA LINC00961 was found to regulate muscle regeneration. These new results have revealed a novel model that lncRNA regulates biological processes using its small peptide product. In this review, we summarize the characteristics, databases, biological functions and molecular regulatory models, as well as research interests of lncRNAs in the future.
[Mh] Termos MeSH primário: RNA Longo não Codificante/fisiologia
[Mh] Termos MeSH secundário: Animais
Desenvolvimento Embrionário
Regulação da Expressão Gênica
Metabolismo dos Lipídeos
Desenvolvimento Muscular
Estabilidade de RNA
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (RNA, Long Noncoding)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE
[do] DOI:10.16288/j.yczz.17-120


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[PMID]:29227993
[Au] Autor:McGurk PD; Swartz ME; Chen JW; Galloway JL; Eberhart JK
[Ad] Endereço:Department of Molecular Biosciences, University of Texas at Austin, Austin, TX, United States of America.
[Ti] Título:In vivo zebrafish morphogenesis shows Cyp26b1 promotes tendon condensation and musculoskeletal patterning in the embryonic jaw.
[So] Source:PLoS Genet;13(12):e1007112, 2017 12.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Integrated development of diverse tissues gives rise to a functional, mobile vertebrate musculoskeletal system. However, the genetics and cellular interactions that drive the integration of muscle, tendon, and skeleton are poorly understood. In the vertebrate head, neural crest cells, from which cranial tendons derive, pattern developing muscles just as tendons have been shown to in limb and trunk tissue, yet the mechanisms of this patterning are unknown. From a forward genetic screen, we determined that cyp26b1 is critical for musculoskeletal integration in the ventral pharyngeal arches, particularly in the mandibulohyoid junction where first and second arch muscles interconnect. Using time-lapse confocal analyses, we detail musculoskeletal integration in wild-type and cyp26b1 mutant zebrafish. In wild-type fish, tenoblasts are present in apposition to elongating muscles and condense in discrete muscle attachment sites. In the absence of cyp26b1, tenoblasts are generated in normal numbers but fail to condense into nascent tendons within the ventral arches and, subsequently, muscles project into ectopic locales. These ectopic muscle fibers eventually associate with ectopic tendon marker expression. Genetic mosaic analysis demonstrates that neural crest cells require Cyp26b1 function for proper musculoskeletal development. Using an inhibitor, we find that Cyp26 function is required in a short time window that overlaps the dynamic window of tenoblast condensation. However, cyp26b1 expression is largely restricted to regions between tenoblast condensations during this time. Our results suggest that degradation of RA by this previously undescribed population of neural crest cells is critical to promote condensation of adjacent scxa-expressing tenoblasts and that these condensations are subsequently required for proper musculoskeletal integration.
[Mh] Termos MeSH primário: Desenvolvimento Embrionário/genética
Desenvolvimento Maxilofacial/genética
Morfogênese/genética
Ácido Retinoico 4 Hidroxilase/genética
[Mh] Termos MeSH secundário: Animais
Padronização Corporal/genética
Regulação da Expressão Gênica no Desenvolvimento
Arcada Osseodentária/embriologia
Desenvolvimento Muscular/genética
Músculo Esquelético/embriologia
Músculo Esquelético/metabolismo
Tendões/embriologia
Tendões/crescimento & desenvolvimento
Peixe-Zebra/embriologia
Peixe-Zebra/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
EC 1.14.14.1 (Retinoic Acid 4-Hydroxylase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007112


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[PMID]:29371665
[Au] Autor:Tosic M; Allen A; Willmann D; Lepper C; Kim J; Duteil D; Schüle R
[Ad] Endereço:Urologische Klinik und Zentrale Klinische Forschung, Universitätsklinikum Freiburg, Medizinische Fakultät, Albert-Ludwigs-University Freiburg, Breisacherstrasse 66, 79106, Freiburg, Germany.
[Ti] Título:Lsd1 regulates skeletal muscle regeneration and directs the fate of satellite cells.
[So] Source:Nat Commun;9(1):366, 2018 01 25.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Satellite cells are muscle stem cells required for muscle regeneration upon damage. Of note, satellite cells are bipotent and have the capacity to differentiate not only into skeletal myocytes, but also into brown adipocytes. Epigenetic mechanisms regulating fate decision and differentiation of satellite cells during muscle regeneration are not yet fully understood. Here, we show that elevated levels of lysine-specific demethylase 1 (Kdm1a, also known as Lsd1) have a beneficial effect on muscle regeneration and recovery after injury, since Lsd1 directly regulates key myogenic transcription factor genes. Importantly, selective Lsd1 ablation or inhibition in Pax7-positive satellite cells, not only delays muscle regeneration, but changes cell fate towards brown adipocytes. Lsd1 prevents brown adipocyte differentiation of satellite cells by repressing expression of the novel pro-adipogenic transcription factor Glis1. Together, downregulation of Glis1 and upregulation of the muscle-specific transcription program ensure physiological muscle regeneration.
[Mh] Termos MeSH primário: Adipócitos Marrons/metabolismo
Proteínas de Ligação a DNA/genética
Histona Desmetilases/genética
Fibras Musculares Esqueléticas/metabolismo
Regeneração/genética
Células Satélites de Músculo Esquelético/metabolismo
Fatores de Transcrição/genética
[Mh] Termos MeSH secundário: Adipócitos Marrons/citologia
Animais
Diferenciação Celular
Linhagem Celular
Proliferação Celular
Proteínas de Ligação a DNA/metabolismo
Epigênese Genética
Histona Desmetilases/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Desenvolvimento Muscular/genética
Fibras Musculares Esqueléticas/citologia
Músculo Esquelético/lesões
Músculo Esquelético/metabolismo
Fator de Transcrição PAX7/genética
Fator de Transcrição PAX7/metabolismo
Cultura Primária de Células
Células Satélites de Músculo Esquelético/citologia
Transdução de Sinais
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (Glis1 protein, mouse); 0 (PAX7 Transcription Factor); 0 (Pax7 protein, mouse); 0 (Transcription Factors); EC 1.14.11.- (Aof2 protein, mouse); EC 1.14.11.- (Histone Demethylases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180127
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02740-5


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[PMID]:29261652
[Au] Autor:Vélez EJ; Azizi S; Verheyden D; Salmerón C; Lutfi E; Sánchez-Moya A; Navarro I; Gutiérrez J; Capilla E
[Ad] Endereço:Departament de Biologia Cellular, Fisiologia i Immunologia, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain.
[Ti] Título:Proteolytic systems' expression during myogenesis and transcriptional regulation by amino acids in gilthead sea bream cultured muscle cells.
[So] Source:PLoS One;12(12):e0187339, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Proteolytic systems exert an important role in vertebrate muscle controlling protein turnover, recycling of amino acids (AA) or its use for energy production, as well as other functions like myogenesis. In fish, proteolytic systems are crucial for the relatively high muscle somatic index they possess, and because protein is the most important dietary component. Thus in this study, the molecular profile of proteolytic markers (calpains, cathepsins and ubiquitin-proteasome system (UbP) members) were analyzed during gilthead sea bream (Sparus aurata) myogenesis in vitro and under different AA treatments. The gene expression of calpains (capn1, capn3 and capns1b) decreased progressively during myogenesis together with the proteasome member n3; whereas capn2, capns1a, capns1b and ubiquitin (ub) remained stable. Contrarily, the cathepsin D (ctsd) paralogs and E3 ubiquitin ligases mafbx and murf1, showed a significant peak in gene expression at day 8 of culture that slightly decreased afterwards. Moreover, the protein expression analyzed for selected molecules presented in general the same profile of the mRNA levels, which was confirmed by correlation analysis. These data suggest that calpains seem to be more important during proliferation, while cathepsins and the UbP system appear to be required for myogenic differentiation. Concerning the transcriptional regulation by AA, the recovery of their levels after a short starvation period did not show effects on cathepsins expression, whereas it down-regulated the expression of capn3, capns1b, mafbx, murf1 and up-regulated n3. With regards to AA deficiencies, the major changes occurred at day 2, when leucine limitation suppressed ctsb and ctsl expression. Besides at the same time, both leucine and lysine deficiencies increased the expression of mafbx and murf1 and decreased that of n3. Overall, the opposite nutritional regulation observed, especially for the UbP members, points out an efficient and complementary role of these factors that could be useful in gilthead sea bream diets optimization.
[Mh] Termos MeSH primário: Aminoácidos/farmacologia
Regulação da Expressão Gênica
Desenvolvimento Muscular
Músculos/metabolismo
Transcrição Genética
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Proteínas Musculares/metabolismo
Músculos/citologia
Proteólise
Reação em Cadeia da Polimerase em Tempo Real
Dourada
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acids); 0 (Muscle Proteins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0187339


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[PMID]:28450151
[Au] Autor:Zhang JL; Laurence Souders C; Denslow ND; Martyniuk CJ
[Ad] Endereço:Henan Open Laboratory of Key Subjects of Environmental and Animal Products Safety, College of Animal Science and Technology, Henan University of Science and Technology, Henan, China; Center for Environmental and Human Toxicology, Department of Physiological Sciences, College of Veterinary Medicine,
[Ti] Título:Quercetin, a natural product supplement, impairs mitochondrial bioenergetics and locomotor behavior in larval zebrafish (Danio rerio).
[So] Source:Toxicol Appl Pharmacol;327:30-38, 2017 07 15.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Quercetin is a natural product that is sold as a supplement in health food stores. While there are reported benefits for this flavonoid as a dietary supplement due to antioxidant properties, the full scope of its biological interactions has not been fully addressed. To learn more about the mechanisms of action related to quercetin, we exposed zebrafish (Danio rerio) embryos to 1 and 10µg/L quercetin for 96h starting at 3h post fertilization. Quercetin up to 10µg/L did not induce significant mortality in developing fish, but did increase prevalence of an upward-curved dorsal plane in hatched larvae. To determine whether this developmental defect was potentially related to mitochondrial bioenergetics during development, we measured oxygen consumption rate in whole embryos following a 24-hour exposure to quercetin. Basal mitochondrial and ATP-linked respiration were decreased at 1 and 10µg/L quercetin, and maximal respiration was decreased at 10µg/L quercetin, suggesting that quercetin impairs mitochondrial bioenergetics. This is proposed to be related to the deformities observed during development. Due to the fact that ATP production was affected by quercetin, larval behaviors related to locomotion were investigated, as well as transcriptional responses of six myogenesis transcripts. Quercetin at 10µg/L significantly reduced the swimming velocity of zebrafish larvae. The expression levels of both myostatin A (mstna) and myogenic differentiation (myoD) were also altered by quercetin. Mstna, an inhibitory factor for myogenesis, was significantly increased at 1µg/L quercetin exposure, while myoD, a stimulatory factor for myogenesis, was significantly increased at 10µg/L quercetin exposure. There were no changes in transcripts related to apoptosis (bcl2, bax, casp3, casp7), but we did observe a decrease in mRNA levels for catalase (cat) in fish exposed to each dose, supporting an oxidative stress response. Our data support the hypothesis that quercetin may affect locomotion and induce deformities in zebrafish larvae by diminishing ATP production and by altering the expression of transcripts related to muscle formation and activity.
[Mh] Termos MeSH primário: Suplementos Nutricionais/toxicidade
Metabolismo Energético/efeitos dos fármacos
Locomoção/efeitos dos fármacos
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Quercetina/toxicidade
[Mh] Termos MeSH secundário: Anormalidades Induzidas por Medicamentos/patologia
Trifosfato de Adenosina/biossíntese
Animais
Comportamento Animal/efeitos dos fármacos
Feminino
Larva
Masculino
Desenvolvimento Muscular/efeitos dos fármacos
Desenvolvimento Muscular/genética
Proteína MyoD/biossíntese
Proteína MyoD/genética
Estresse Oxidativo/efeitos dos fármacos
Consumo de Oxigênio/efeitos dos fármacos
Natação
Transcrição Genética/efeitos dos fármacos
Poluentes Químicos da Água
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (MyoD Protein); 0 (Water Pollutants, Chemical); 8L70Q75FXE (Adenosine Triphosphate); 9IKM0I5T1E (Quercetin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


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[PMID]:29194448
[Au] Autor:Nagata Y; Kiyono T; Okamura K; Goto YI; Matsuo M; Ikemoto-Uezumi M; Hashimoto N
[Ad] Endereço:Department of Regenerative Medicine, National Center for Geriatrics and Gerontology, Morioka, Oobu, Aichi, Japan.
[Ti] Título:Interleukin-1beta (IL-1ß)-induced Notch ligand Jagged1 suppresses mitogenic action of IL-1ß on human dystrophic myogenic cells.
[So] Source:PLoS One;12(12):e0188821, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Duchenne muscular dystrophy (DMD) is a severe X-linked recessive muscle disorder caused by mutations in the dystrophin gene. Nonetheless, secondary processes involving perturbation of muscle regeneration probably exacerbate disease progression, resulting in the fatal loss of muscle in DMD patients. A dysfunction of undifferentiated myogenic cells is the most likely cause for the reduction of regenerative capacity of muscle. To clarify molecular mechanisms in perturbation of the regenerative capacity of DMD muscle, we have established several NCAM (CD56)-positive immortalized human dystrophic and non-dystrophic myogenic cell lines from DMD and healthy muscles. A pro-inflammatory cytokine, IL-1ß, promoted cell cycle progression of non-dystrophic myogenic cells but not DMD myogenic cells. In contrast, IL-1ß upregulated the Notch ligand Jagged1 gene in DMD myogenic cells but not in non-dystrophic myogenic cells. Knockdown of Jagged1 in DMD myogenic cells restored the IL-1ß-promoted cell cycle progression. Conversely, enforced expression of Jagged1-blocked IL-1ß promoted proliferation of non-dystrophic myogenic cells. In addition, IL-1ß prevented myogenic differentiation of DMD myogenic cells depending on Jagged1 but not of non-dystrophic myogenic cells. These results demonstrate that Jagged1 induced by IL-1ß in DMD myogenic cells modified the action of IL-1ß and reduced the ability to proliferate and differentiate. IL-1ß induced Jagged1 gene expression may be a feedback response to excess stimulation with this cytokine because high IL-1ß (200-1000 pg/ml) induced Jagged1 gene expression even in non-dystrophic myogenic cells. DMD myogenic cells are likely to acquire the susceptibility of the Jagged1 gene to IL-1ß under the microcircumstances in DMD muscles. The present results suggest that Jagged1 induced by IL-1ß plays a crucial role in the loss of muscle regeneration capacity of DMD muscles. The IL-1ß/Jagged1 pathway may be a new therapeutic target to ameliorate exacerbation of muscular dystrophy in a dystrophin-independent manner.
[Mh] Termos MeSH primário: Interleucina-1beta/metabolismo
Proteína Jagged-1/metabolismo
Distrofia Muscular de Duchenne/metabolismo
Receptor Notch3/metabolismo
[Mh] Termos MeSH secundário: Diferenciação Celular
Células Cultivadas
Seres Humanos
Desenvolvimento Muscular
Distrofia Muscular de Duchenne/patologia
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (Jagged-1 Protein); 0 (NOTCH3 protein, human); 0 (Receptor, Notch3)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188821


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[PMID]:28177127
[Au] Autor:Bohnert KR; McMillan JD; Kumar A
[Ad] Endereço:Department of Anatomical Sciences Neurobiology, University of Louisville School of Medicine, Louisville, Kentucky.
[Ti] Título:Emerging roles of ER stress and unfolded protein response pathways in skeletal muscle health and disease.
[So] Source:J Cell Physiol;233(1):67-78, 2018 Jan.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Skeletal muscle is the most abundant tissue in the human body and can adapt its mass as a consequence of physical activity, metabolism, growth factors, and disease conditions. Skeletal muscle contains an extensive network of endoplasmic reticulum (ER), called sarcoplasmic reticulum, which plays an important role in the regulation of proteostasis and calcium homeostasis. In many cell types, environmental and genetic factors that disrupt ER function cause an accumulation of misfolded and unfolded proteins in the ER lumen that ultimately leads to ER stress. To alleviate the stress and restore homeostasis, the ER activates a signaling network called the unfolded protein response (UPR). The UPR has three arms, which regulate protein synthesis and expression of many ER chaperone and regulatory proteins. However, the role of individual UPR pathways in skeletal muscle has just begun to be investigated. Recent studies suggest that UPR pathways play pivotal roles in muscle stem cell homeostasis, myogenic differentiation, and regeneration of injured skeletal muscle. Moreover, markers of ER stress and the UPR are activated in skeletal muscle in diverse conditions such as exercise, denervation, starvation, high fat diet, cancer cachexia, and aging. Accumulating evidence also suggests that ER stress may have important roles in the pathogenesis of inflammatory myopathies and genetic muscle disorders. The purpose of this review article is to discuss the role and potential mechanisms by which ER stress and the individual arms of the UPR regulate skeletal muscle formation, plasticity, and function in various physiological and pathophysiological conditions.
[Mh] Termos MeSH primário: Estresse do Retículo Endoplasmático
Retículo Endoplasmático/metabolismo
Proteínas Musculares/metabolismo
Músculo Esquelético/metabolismo
Doenças Musculares/metabolismo
Resposta a Proteínas não Dobradas
[Mh] Termos MeSH secundário: Adaptação Fisiológica
Envelhecimento
Animais
Retículo Endoplasmático/patologia
Metabolismo Energético
Exercício
Homeostase
Seres Humanos
Desenvolvimento Muscular
Músculo Esquelético/patologia
Músculo Esquelético/fisiopatologia
Atrofia Muscular/metabolismo
Atrofia Muscular/patologia
Atrofia Muscular/fisiopatologia
Doenças Musculares/patologia
Doenças Musculares/fisiopatologia
Regeneração
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Muscle Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171212
[Lr] Data última revisão:
171212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170209
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25852


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[PMID]:29183940
[Au] Autor:Felsenthal N; Zelzer E
[Ad] Endereço:Department of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel.
[Ti] Título:Mechanical regulation of musculoskeletal system development.
[So] Source:Development;144(23):4271-4283, 2017 Dec 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:During embryogenesis, the musculoskeletal system develops while containing within itself a force generator in the form of the musculature. This generator becomes functional relatively early in development, exerting an increasing mechanical load on neighboring tissues as development proceeds. A growing body of evidence indicates that such mechanical forces can be translated into signals that combine with the genetic program of organogenesis. This unique situation presents both a major challenge and an opportunity to the other tissues of the musculoskeletal system, namely bones, joints, tendons, ligaments and the tissues connecting them. Here, we summarize the involvement of muscle-induced mechanical forces in the development of various vertebrate musculoskeletal components and their integration into one functional unit.
[Mh] Termos MeSH primário: Desenvolvimento Musculoesquelético/fisiologia
[Mh] Termos MeSH secundário: Animais
Fenômenos Biomecânicos
Desenvolvimento Ósseo/fisiologia
Condrogênese/fisiologia
Seres Humanos
Camundongos
Modelos Biológicos
Desenvolvimento Muscular/fisiologia
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171204
[Lr] Data última revisão:
171204
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.1242/dev.151266


  10 / 8064 MEDLINE  
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[PMID]:28471487
[Au] Autor:Hwang SY; Kang YJ; Sung B; Jang JY; Hwang NL; Oh HJ; Ahn YR; Kim HJ; Shin JH; Yoo MA; Kim CM; Chung HY; Kim ND
[Ad] Endereço:Department of Pharmacy, College of Pharmacy, Pusan National University, Busan, Republic of Korea.
[Ti] Título:Folic acid is necessary for proliferation and differentiation of C2C12 myoblasts.
[So] Source:J Cell Physiol;233(2):736-747, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Folic acid, a water soluble B vitamin, plays an important role in cellular metabolic activities, such as functioning as a cofactor in one-carbon metabolism for DNA and RNA synthesis as well as nucleotide and amino acid biosynthesis in the body. A lack of dietary folic acid can lead to folic acid deficiency and result in several health problems, including macrocytic anemia, elevated plasma homocysteine, cardiovascular disease, birth defects, carcinogenesis, muscle weakness, and walking difficulty. However, the effect of folic acid deficiency on skeletal muscle development and its molecular mechanisms are unknown. We, therefore, investigated the effect of folic acid deficiency on myogenesis in skeletal muscle cells and found that folic acid deficiency induced proliferation inhibition and cell cycle breaking as well as cellular senescence in C2C12 myoblasts, implying that folic acid deficiency influences skeletal muscle development. Folic acid deficiency also inhibited differentiation of C2C12 myoblasts and induced deregulation of the cell cycle exit and many cell cycle regulatory genes. It inhibited expression of muscle-specific marker MyHC as well as myogenic regulatory factor (myogenin). Moreover, immunocytochemistry and Western blot analyses revealed that DNA damage was more increased in folic acid-deficient medium-treated differentiating C2C12 cells. Furthermore, we found that folic acid resupplementation reverses the effect on the cell cycle and senescence in folic acid-deficient C2C12 myoblasts but does not reverse the differentiation of C2C12 cells. Altogether, the study results suggest that folic acid is necessary for normal development of skeletal muscle cells.
[Mh] Termos MeSH primário: Diferenciação Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Deficiência de Ácido Fólico/tratamento farmacológico
Ácido Fólico/farmacologia
Desenvolvimento Muscular/efeitos dos fármacos
Mioblastos Esqueléticos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Ciclo Celular/efeitos dos fármacos
Linhagem Celular
Senescência Celular/efeitos dos fármacos
Dano ao DNA
Deficiência de Ácido Fólico/metabolismo
Deficiência de Ácido Fólico/patologia
Camundongos
Mioblastos Esqueléticos/metabolismo
Mioblastos Esqueléticos/patologia
Miogenina/metabolismo
Cadeias Pesadas de Miosina/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Myog protein, mouse); 0 (Myogenin); 935E97BOY8 (Folic Acid); EC 3.6.4.1 (Myosin Heavy Chains)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25989



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