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Referências encontradas : 650 [refinar]
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[PMID]:29317646
[Au] Autor:Rao L; Qian Y; Khodabukus A; Ribar T; Bursac N
[Ad] Endereço:Department of Biomedical Engineering, Duke University, Durham, NC, 27708, USA.
[Ti] Título:Engineering human pluripotent stem cells into a functional skeletal muscle tissue.
[So] Source:Nat Commun;9(1):126, 2018 01 09.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The generation of functional skeletal muscle tissues from human pluripotent stem cells (hPSCs) has not been reported. Here, we derive induced myogenic progenitor cells (iMPCs) via transient overexpression of Pax7 in paraxial mesoderm cells differentiated from hPSCs. In 2D culture, iMPCs readily differentiate into spontaneously contracting multinucleated myotubes and a pool of satellite-like cells endogenously expressing Pax7. Under optimized 3D culture conditions, iMPCs derived from multiple hPSC lines reproducibly form functional skeletal muscle tissues (iSKM bundles) containing aligned multi-nucleated myotubes that exhibit positive force-frequency relationship and robust calcium transients in response to electrical or acetylcholine stimulation. During 1-month culture, the iSKM bundles undergo increased structural and molecular maturation, hypertrophy, and force generation. When implanted into dorsal window chamber or hindlimb muscle in immunocompromised mice, the iSKM bundles survive, progressively vascularize, and maintain functionality. iSKM bundles hold promise as a microphysiological platform for human muscle disease modeling and drug development.
[Mh] Termos MeSH primário: Músculo Esquelético/citologia
Mioblastos/citologia
Células-Tronco Pluripotentes/citologia
Engenharia Tecidual/métodos
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Células Cultivadas
Células HEK293
Seres Humanos
Células-Tronco Pluripotentes Induzidas/citologia
Células-Tronco Pluripotentes Induzidas/metabolismo
Camundongos Endogâmicos NOD
Camundongos Knockout
Camundongos Nus
Camundongos SCID
Fibras Musculares Esqueléticas/citologia
Fibras Musculares Esqueléticas/metabolismo
Músculo Esquelético/metabolismo
Mioblastos/metabolismo
Fator de Transcrição PAX7/metabolismo
Células-Tronco Pluripotentes/metabolismo
Transplante de Células-Tronco/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (PAX7 Transcription Factor)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02636-4


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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]:28942144
[Au] Autor:Hosoyama T; Ichida S; Kanno M; Ishihara R; Hatashima T; Ueno K; Hamano K
[Ad] Endereço:Department of Surgery and Clinical Science, Yamaguchi University Graduate School of Medicine, Yamaguchi, Japan; Department of Regenerative Medicine, National Center for Geriatrics and Gerontology, Aichi, Japan. Electronic address: toruhoso@ncgg.go.jp.
[Ti] Título:Microgravity influences maintenance of the human muscle stem/progenitor cell pool.
[So] Source:Biochem Biophys Res Commun;493(2):998-1003, 2017 Nov 18.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Microgravity induces skeletal muscle atrophy; however, the underlying mechanism is not clarified. In particular, the influence of microgravity on human skeletal muscle stem/progenitor cells (SMPCs) is not well understood. In this study, we used induced pluripotent stem cell-derived human SMPCs to investigate the effect of microgravity on maintenance of the stem/progenitor cell pool. Human SMPCs were induced by free-floating spherical aggregation culture, and derivatized-SMPC spheres were maintained in a microgravity condition (10 G) for 2 weeks using a clinostat rotation system. Microgravity culture deformed the SMPC spheres, with no signs of apoptosis. The most obvious change from microgravity culture was a significant decrease in the expression level of Pax7 in the SMPC spheres, with reduced numbers of myotubes in adhesion culture. Pax7 expression also decreased in the presence of the proteasome inhibitor MG132, indicating that the proteasomal degradation of Pax7 protein is not critical for its reduced expression in microgravity culture. Moreover, microgravity culture decreased the expression level of tumor necrosis factor receptor-associated factor 6 (TRAF6) and phosphorylation of its downstream molecule extracellular-related kinase (ERK) in SMPC spheres. Therefore, microgravity negatively regulates Pax7 expression in human SMPCs possibly through inhibition of the TRAF6/ERK pathway to consequently dysregulate SMPC pool maintenance. Overall, these results suggest that skeletal muscle atrophy is caused by microgravity-induced exhaustion of the stem cell pool.
[Mh] Termos MeSH primário: Técnicas de Cultura de Células/métodos
Músculo Esquelético/citologia
Células-Tronco/citologia
Ausência de Peso
[Mh] Termos MeSH secundário: Técnicas de Cultura de Células/instrumentação
Linhagem Celular
Desenho de Equipamento
Seres Humanos
Células-Tronco Pluripotentes Induzidas/citologia
Células-Tronco Pluripotentes Induzidas/metabolismo
Sistema de Sinalização das MAP Quinases
Músculo Esquelético/metabolismo
Fator de Transcrição PAX7/análise
Fator de Transcrição PAX7/metabolismo
Células-Tronco/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (PAX7 Transcription Factor); 0 (PAX7 protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170925
[St] Status:MEDLINE


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[PMID]:28919490
[Au] Autor:Zhang P; Wang G; Lin Z; Wu Y; Zhang J; Liu M; Lee KKH; Chuai M; Yang X
[Ad] Endereço:Key Laboratory for Regenerative Medicine of the Ministry of Education, Division of Histology & Embryology, Medical College, Jinan University, Guangzhou 510632, China.
[Ti] Título:Alcohol exposure induces chick craniofacial bone defects by negatively affecting cranial neural crest development.
[So] Source:Toxicol Lett;281:53-64, 2017 Nov 05.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Excess alcohol consumption during pregnancy could lead to fetal alcohol syndrome (FAS). However, the molecular mechanism leading to craniofacial abnormality, a feature of FAS, is still poorly understood. The cranial neural crest cells (NCCs) contribute to the formation of the craniofacial bones. Therefore, NCCs exposed to ethanol was investigated - using chick embryos and in vitro explant culture as experimental models. We demonstrated that exposure to 2% ethanol induced craniofacial defects, which includes parietal defect, in the developing chick fetus. Immunofluorescent staining revealed that ethanol treatment downregulated Ap-2É‘, Pax7 and HNK-1 expressions by cranial NCCs. Using double-immunofluorescent stainings for Ap-2É‘/pHIS3 and Ap-2É‘/c-Caspase3, we showed that ethanol treatment inhibited cranial NCC proliferation and increased NCC apoptosis, respectively. Moreover, ethanol treatment of the dorsal neuroepithelium increased Laminin, N-Cadherin and Cadherin 6B expressions while Cadherin 7 expression was repressed. In situ hybridization also revealed that ethanol treatment up-regulated Cadherin 6B expression but down-regulated slug, Msx1, FoxD3 and BMP4 expressions. In summary, our experimental results demonstrated that ethanol treatment interferes with the production of cranial NCCs by affecting the proliferation and apoptosis of these cells. In addition, ethanol affected the delamination, epithelial-mesenchymal transition (EMT) and cell migration of cranial NCCs, which may have contributed to the etiology of the craniofacial defects.
[Mh] Termos MeSH primário: Anormalidades Craniofaciais/patologia
Etanol/toxicidade
Regulação da Expressão Gênica no Desenvolvimento
Crista Neural/efeitos dos fármacos
Organogênese/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Proteína Morfogenética Óssea 4/genética
Proteína Morfogenética Óssea 4/metabolismo
Antígenos CD57/genética
Antígenos CD57/metabolismo
Caderinas/genética
Caderinas/metabolismo
Embrião de Galinha
Anormalidades Craniofaciais/induzido quimicamente
Modelos Animais de Doenças
Regulação para Baixo
Transtornos do Espectro Alcoólico Fetal/fisiopatologia
Laminina/genética
Laminina/metabolismo
Crista Neural/patologia
Fator de Transcrição PAX7/genética
Fator de Transcrição PAX7/metabolismo
Fator de Transcrição AP-2/genética
Fator de Transcrição AP-2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bone Morphogenetic Protein 4); 0 (CD57 Antigens); 0 (Cadherins); 0 (Laminin); 0 (PAX7 Transcription Factor); 0 (Transcription Factor AP-2); 3K9958V90M (Ethanol)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE


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[PMID]:28887016
[Au] Autor:Roy SD; Williams VC; Pipalia TG; Li K; Hammond CL; Knappe S; Knight RD; Hughes SM
[Ad] Endereço:Randall Division of Cell and Molecular Biophysics, New Hunt's House, Guy's Campus, King's College London, London SE1 1UL, UK.
[Ti] Título:Myotome adaptability confers developmental robustness to somitic myogenesis in response to fibre number alteration.
[So] Source:Dev Biol;431(2):321-335, 2017 11 15.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Balancing the number of stem cells and their progeny is crucial for tissue development and repair. Here we examine how cell numbers and overall muscle size are tightly regulated during zebrafish somitic muscle development. Muscle stem/precursor cell (MPCs) expressing Pax7 are initially located in the dermomyotome (DM) external cell layer, adopt a highly stereotypical distribution and thereafter a proportion of MPCs migrate into the myotome. Regional variations in the proliferation and terminal differentiation of MPCs contribute to growth of the myotome. To probe the robustness of muscle size control and spatiotemporal regulation of MPCs, we compared the behaviour of wild type (wt) MPCs with those in mutant zebrafish that lack the muscle regulatory factor Myod. Myod mutants form one third fewer multinucleate fast muscle fibres than wt and show a significant expansion of the Pax7 MPC population in the DM. Subsequently, myod mutant fibres generate more cytoplasm per nucleus, leading to recovery of muscle bulk. In addition, relative to wt siblings, there is an increased number of MPCs in myod mutants and these migrate prematurely into the myotome, differentiate and contribute to the hypertrophy of existing fibres. Thus, homeostatic reduction of the excess MPCs returns their number to normal levels, but fibre numbers remain low. The GSK3 antagonist BIO prevents MPC migration into the deep myotome, suggesting that canonical Wnt pathway activation maintains the DM in zebrafish, as in amniotes. BIO does not, however, block recovery of the myod mutant myotome, indicating that homeostasis acts on fibre intrinsic growth to maintain muscle bulk. The findings suggest the existence of a critical window for early fast fibre formation followed by a period in which homeostatic mechanisms regulate myotome growth by controlling fibre size. The feedback controls we reveal in muscle help explain the extremely precise grading of myotome size along the body axis irrespective of fish size, nutrition and genetic variation and may form a paradigm for wider matching of organ size.
[Mh] Termos MeSH primário: Desenvolvimento Muscular
Fibras Musculares Esqueléticas/metabolismo
Somitos/metabolismo
Peixe-Zebra/embriologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Movimento Celular
Núcleo Celular/metabolismo
Proliferação Celular
Quinase 3 da Glicogênio Sintase/metabolismo
Proteínas de Fluorescência Verde/metabolismo
Larva/metabolismo
Fibras Musculares Esqueléticas/citologia
Mutação/genética
Fator de Transcrição PAX7/metabolismo
Somitos/embriologia
Proteínas de Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (PAX7 Transcription Factor); 0 (Zebrafish Proteins); 147336-22-9 (Green Fluorescent Proteins); EC 2.7.11.26 (Glycogen Synthase Kinase 3)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171115
[Lr] Data última revisão:
171115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170910
[St] Status:MEDLINE


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[PMID]:28790171
[Au] Autor:Kamizaki K; Doi R; Hayashi M; Saji T; Kanagawa M; Toda T; Fukada SI; Ho HH; Greenberg ME; Endo M; Minami Y
[Ad] Endereço:From the Division of Cell Physiology, Department of Physiology and Cell Biology, and.
[Ti] Título:The Ror1 receptor tyrosine kinase plays a critical role in regulating satellite cell proliferation during regeneration of injured muscle.
[So] Source:J Biol Chem;292(38):15939-15951, 2017 Sep 22.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The Ror family receptor tyrosine kinases, Ror1 and Ror2, play important roles in regulating developmental morphogenesis and tissue- and organogenesis, but their roles in tissue regeneration in adult animals remain largely unknown. In this study, we examined the expression and function of Ror1 and Ror2 during skeletal muscle regeneration. Using an skeletal muscle injury model, we show that expression of Ror1 and Ror2 in skeletal muscles is induced transiently by the inflammatory cytokines, TNF-α and IL-1ß, after injury and that inhibition of TNF-α and IL-1ß by neutralizing antibodies suppresses expression of and in injured muscles. Importantly, expression of , but not , was induced primarily in Pax7-positive satellite cells (SCs) after muscle injury, and administration of neutralizing antibodies decreased the proportion of Pax7-positive proliferative SCs after muscle injury. We also found that stimulation of a mouse myogenic cell line, C2C12 cells, with TNF-α or IL-1ß induced expression of Ror1 via NF-κB activation and that suppressed expression of Ror1 inhibited their proliferative responses in SCs. Intriguingly, SC-specific depletion of decreased the number of Pax7-positive SCs after muscle injury. Collectively, these findings indicate for the first time that Ror1 has a critical role in regulating SC proliferation during skeletal muscle regeneration. We conclude that Ror1 might be a suitable target in the development of diagnostic and therapeutic approaches to manage muscular disorders.
[Mh] Termos MeSH primário: Músculo Esquelético/lesões
Músculo Esquelético/fisiologia
Receptores Órfãos Semelhantes a Receptor Tirosina Quinase/metabolismo
Regeneração
Células Satélites de Músculo Esquelético/citologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Proliferação Celular
Regulação Enzimológica da Expressão Gênica
Interleucina-1beta/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Desenvolvimento Muscular
NF-kappa B/metabolismo
Fator de Transcrição PAX7/metabolismo
Receptores Órfãos Semelhantes a Receptor Tirosina Quinase/genética
Células Satélites de Músculo Esquelético/metabolismo
Transdução de Sinais
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (NF-kappa B); 0 (PAX7 Transcription Factor); 0 (Pax7 protein, mouse); 0 (Tumor Necrosis Factor-alpha); EC 2.7.10.1 (Receptor Tyrosine Kinase-like Orphan Receptors); EC 2.7.10.1 (Ror1 protein, mouse); EC 2.7.10.1 (Ror2 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.785709


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[PMID]:28700649
[Au] Autor:Laggner M; Pollreisz A; Schmidinger G; Schmidt-Erfurth U; Chen YT
[Ad] Endereço:Department of Ophthalmology & Optometry, Medical University of Vienna, Vienna, Austria.
[Ti] Título:Autophagy mediates cell cycle response by regulating nucleocytoplasmic transport of PAX6 in limbal stem cells under ultraviolet-A stress.
[So] Source:PLoS One;12(7):e0180868, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Limbal stem cells (LSC) account for homeostasis and regeneration of corneal epithelium. Solar ultraviolet A (UVA) is the major source causing oxidative damage in the ocular surface. Autophagy, a lysosomal degradation mechanism, is essential for physiologic function and stress defense of stem cells. PAX6, a master transcription factor governing corneal homeostasis by regulating cell cycle and cell fate of LSC, responds to oxidative stress by nucleocytoplasmic shuttling. Impaired autophagy and deregulated PAX6 have been reported in oxidative stress-related ocular surface disorders. We hypothesize a functional role for autophagy and PAX6 in LSC's stress response to UVA. Therefore, human LSC colonies were irradiated with a sub-lethal dose of UVA and autophagic activity and intracellular reactive oxygen species (ROS) were measured by CYTO-ID assay and CM-H2DCFDA live staining, respectively. Following UVA irradiation, the percentage of autophagic cells significantly increased in LSC colonies while intracellular ROS levels remained unaffected. siRNA-mediated knockdown (KD) of ATG7 abolished UVA-induced autophagy and led to an excessive accumulation of ROS. Upon UVA exposure, LSCs displayed nuclear-to-cytoplasmic translocation of PAX6, while ATG7KD or antioxidant pretreatment largely attenuated the intracellular trafficking event. Immunofluorescence showing downregulation of proliferative marker PCNA and induction of cell cycle regulator p21 indicates cell cycle arrest in UVA-irradiated LSC. Abolishing autophagy, adenoviral-assisted restoration of nuclear PAX6 or antioxidant pretreatment abrogated the UVA-induced cell cycle arrest. Adenoviral expression of an ectopic PAX gene, PAX7, did not affect UVA cell cycle response. Furthermore, knocking down PAX6 attenuated the cell cycle progression of irradiated ATG7KD LSC by de-repressing p21 expression. Collectively, our data suggest a crosstalk between autophagy and PAX6 in regulating cell cycle response of ocular progenitors under UVA stress. Autophagy deficiency leads to impaired intracellular trafficking of PAX6, perturbed redox balance and uncurbed cell cycle progression in UVA-stressed LSCs. The coupling of autophagic machinery and PAX6 in cell cycle regulation represents an attractive therapeutic target for hyperproliferative ocular surface disorders associated with solar radiation.
[Mh] Termos MeSH primário: Transporte Ativo do Núcleo Celular/fisiologia
Autofagia/fisiologia
Ciclo Celular/fisiologia
Células-Tronco/citologia
Células-Tronco/metabolismo
Raios Ultravioleta
[Mh] Termos MeSH secundário: Transporte Ativo do Núcleo Celular/genética
Autofagossomos/metabolismo
Autofagossomos/efeitos da radiação
Autofagia/genética
Ciclo Celular/genética
Células Cultivadas
Seres Humanos
Microscopia Confocal
Fator de Transcrição PAX6/genética
Fator de Transcrição PAX6/metabolismo
Fator de Transcrição PAX7/genética
Fator de Transcrição PAX7/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Transdução de Sinais/efeitos da radiação
Células-Tronco/efeitos da radiação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (PAX6 Transcription Factor); 0 (PAX7 Transcription Factor); 0 (PAX7 protein, human); 0 (Reactive Oxygen Species)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170713
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180868


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[PMID]:28535373
[Au] Autor:An Y; Wang G; Diao Y; Long Y; Fu X; Weng M; Zhou L; Sun K; Cheung TH; Ip NY; Sun H; Wang H; Wu Z
[Ad] Endereço:Division of Life Science, Center for Stem Cell Research, Center of Systems Biology and Human Health, State Key Laboratory in Molecular Neuroscience, Hong Kong University of Science & Technology, Clearwater Bay, Kowloon, Hong Kong, China.
[Ti] Título:A Molecular Switch Regulating Cell Fate Choice between Muscle Progenitor Cells and Brown Adipocytes.
[So] Source:Dev Cell;41(4):382-391.e5, 2017 May 22.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:During mouse embryo development, both muscle progenitor cells (MPCs) and brown adipocytes (BAs) are known to derive from the same Pax7 /Myf5 progenitor cells. However, the underlying mechanisms for the cell fate control remain unclear. In Pax7-null MPCs from young mice, several BA-specific genes, including Prdm16 and Ucp1 and many other adipocyte-related genes, were upregulated with a concomitant reduction of Myod and Myf5, two muscle lineage-determining genes. This suggests a cell fate switch from MPC to BA. Consistently, freshly isolated Pax7-null but not wild-type MPCs formed lipid-droplet-containing UCP1 BA in culture. Mechanistically, MyoD and Myf5, both known transcription targets of Pax7 in MPC, potently repress Prdm16, a BA-specific lineage-determining gene, via the E2F4/p107/p130 transcription repressor complex. Importantly, inducible Pax7 ablation in developing mouse embryos promoted brown fat development. Thus, the MyoD/Myf5-E2F4/p107/p130 axis functions in both the Pax7 /Myf5 embryonic progenitor cells and postnatal myoblasts to repress the alternative BA fate.
[Mh] Termos MeSH primário: Adipócitos Marrons/citologia
Adipócitos Marrons/metabolismo
Linhagem da Célula
Músculos/citologia
Células-Tronco/citologia
Células-Tronco/metabolismo
[Mh] Termos MeSH secundário: Tecido Adiposo Marrom/embriologia
Tecido Adiposo Marrom/metabolismo
Animais
Linhagem Celular
Linhagem da Célula/genética
Células Cultivadas
Proteínas de Ligação a DNA/metabolismo
Fator de Transcrição E2F4/metabolismo
Embrião de Mamíferos/metabolismo
Deleção de Genes
Técnicas de Silenciamento de Genes
Camundongos
Proteína MyoD/metabolismo
Fator Regulador Miogênico 5/metabolismo
Fator de Transcrição PAX7/metabolismo
Proteínas Repressoras/metabolismo
Fatores de Transcrição/metabolismo
Transcrição Genética
Regulação para Cima/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (E2F4 Transcription Factor); 0 (MyoD Protein); 0 (Myogenic Regulatory Factor 5); 0 (PAX7 Transcription Factor); 0 (Prdm16 protein, mouse); 0 (Repressor Proteins); 0 (Transcription Factors)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170913
[Lr] Data última revisão:
170913
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170524
[St] Status:MEDLINE


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[PMID]:28498863
[Au] Autor:Sakai H; Fukuda S; Nakamura M; Uezumi A; Noguchi YT; Sato T; Morita M; Yamada H; Tsuchida K; Tajbakhsh S; Fukada SI
[Ad] Endereço:Stem Cells & Development, Department of Developmental & Stem Cell Biology, CNRS UMR 3738, Institut Pasteur, Paris, France.
[Ti] Título:Notch ligands regulate the muscle stem-like state ex vivo but are not sufficient for retaining regenerative capacity.
[So] Source:PLoS One;12(5):e0177516, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Myogenic stem cells are a promising avenue for the treatment of muscular disorders. Freshly isolated muscle stem cells have a remarkable engraftment ability in vivo, but their cell number is limited. Current conventional culture conditions do not allow muscle stem cells to expand in vitro with their bona fide engraftment efficiency, requiring the improvement of culture procedures for achieving successful cell-therapy for muscle disorders. Here we expanded mouse muscle stem cells and human myoblasts with Notch ligands, DLL1, DLL4, and JAG1 to activate Notch signaling in vitro and to investigate whether these cells could retain their engraftment efficiency. Notch signaling promotes the expansion of Pax7+MyoD- mouse muscle stem-like cells and inhibits differentiation even after passage in vitro. Treatment with Notch ligands induced the Notch target genes and generated PAX7+MYOD- stem-like cells from human myoblasts previously cultured on conventional culture plates. However, cells treated with Notch ligands exhibit a stem cell-like state in culture, yet their regenerative ability was less than that of freshly isolated cells in vivo and was comparable to that of the control. These unexpected findings suggest that artificial maintenance of Notch signaling alone is insufficient for improving regenerative capacity of mouse and human donor-muscle cells and suggest that combinatorial events are critical to achieve muscle stem cell and myoblast engraftment potential.
[Mh] Termos MeSH primário: Células Musculares/citologia
Receptores Notch/metabolismo
Células-Tronco/citologia
Células-Tronco/metabolismo
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/genética
Diferenciação Celular/fisiologia
Células Cultivadas
Imuno-Histoquímica
Peptídeos e Proteínas de Sinalização Intercelular/genética
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Peptídeos e Proteínas de Sinalização Intracelular/genética
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Proteína Jagged-1/genética
Proteína Jagged-1/metabolismo
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Camundongos
Desenvolvimento Muscular/genética
Desenvolvimento Muscular/fisiologia
Proteína MyoD/genética
Proteína MyoD/metabolismo
Mioblastos/citologia
Mioblastos/metabolismo
Fator de Transcrição PAX7/genética
Fator de Transcrição PAX7/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Receptores Notch/genética
Regeneração/genética
Regeneração/fisiologia
Transdução de Sinais/genética
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dlk1 protein, mouse); 0 (Intercellular Signaling Peptides and Proteins); 0 (Intracellular Signaling Peptides and Proteins); 0 (Jag1 protein, mouse); 0 (Jagged-1 Protein); 0 (Membrane Proteins); 0 (MyoD Protein); 0 (MyoD1 myogenic differentiation protein); 0 (PAX7 Transcription Factor); 0 (Pax7 protein, mouse); 0 (Receptors, Notch); 0 (delta protein)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170513
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0177516


  10 / 650 MEDLINE  
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[PMID]:28441415
[Au] Autor:Lilja KC; Zhang N; Magli A; Gunduz V; Bowman CJ; Arpke RW; Darabi R; Kyba M; Perlingeiro R; Dynlacht BD
[Ad] Endereço:Department of Pathology, New York University Cancer Institute, New York University School of Medicine, New York, New York, United States of America.
[Ti] Título:Pax7 remodels the chromatin landscape in skeletal muscle stem cells.
[So] Source:PLoS One;12(4):e0176190, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pluripotent stem cells (PSC) hold great promise for the treatment of human skeletal muscle diseases. However, it remains challenging to convert PSC to skeletal muscle cells, and the mechanisms by which the master regulatory transcription factor, Pax7, promotes muscle stem (satellite) cell identity are not yet understood. We have taken advantage of PSC-derived skeletal muscle precursor cells (iPax7), wherein the induced expression of Pax7 robustly initiates the muscle program and enables the in vitro generation of precursors that seed the satellite cell compartment upon transplantation. Remarkably, we found that chromatin accessibility in myogenic precursors pre-figures subsequent activation of myogenic differentiation genes. We also found that Pax7 binding is generally restricted to euchromatic regions and excluded from H3K27 tri-methylated regions in muscle cells, suggesting that recruitment of this factor is circumscribed by chromatin state. Further, we show that Pax7 binding induces dramatic, localized remodeling of chromatin characterized by the acquisition of histone marks associated with enhancer activity and induction of chromatin accessibility in both muscle precursors and lineage-committed myoblasts. Conversely, removal of Pax7 leads to rapid reversal of these features on a subset of enhancers. Interestingly, another cluster of Pax7 binding sites is associated with a durably accessible and remodeled chromatin state after removal of Pax7, and persistent enhancer accessibility is associated with subsequent, proximal binding by the muscle regulatory factors, MyoD1 and myogenin. Our studies provide new insights into the epigenetic landscape of skeletal muscle stem cells and precursors and the role of Pax7 in satellite cell specification.
[Mh] Termos MeSH primário: Cromatina/metabolismo
Células Musculares/metabolismo
Desenvolvimento Muscular/fisiologia
Fator de Transcrição PAX7/metabolismo
Células-Tronco Pluripotentes/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Camundongos
Músculo Esquelético/metabolismo
Proteína MyoD/metabolismo
Miogenina/metabolismo
Fator de Transcrição PAX7/genética
Células Satélites de Músculo Esquelético/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chromatin); 0 (MyoD Protein); 0 (Myogenin); 0 (PAX7 Transcription Factor); 0 (Pax7 protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170426
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0176190



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