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Pesquisa : A11.284.430.214.190.750 [Categoria DeCS]
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[PMID]:28460469
[Au] Autor:Lam CS; Ng L; Chow AK; Wan TM; Yau S; Cheng NS; Wong SK; Man JH; Lo OS; Foo DC; Poon JT; Pang RW; Law WL
[Ad] Endereço:Division of Colorectal Surgery, Department of Surgery, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong.
[Ti] Título:Identification of microRNA 885-5p as a novel regulator of tumor metastasis by targeting CPEB2 in colorectal cancer.
[So] Source:Oncotarget;8(16):26858-26870, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Colorectal cancer is the third most common cancer in the world and liver is the most frequent site of distant metastasis with poor prognosis. The aim of this study is to investigate microRNAs leading to liver metastasis. We applied microarray analysis and quantitative PCR to identify and validate dysregulated miRNAs in liver metastases when compared to primary CRCs. Functional significance and the underlying molecular mechanism of selected miRNA was demonstrated by a series of in vitro and in vivo assays. Our microarray analysis and subsequent quantitative PCR validation revealed that miR-885-5p was strongly up-regulated in liver metastases and in CRC cell-lines derived from distant metastases. Overexpression of miR-885-5p significantly induced cell migration, cell invasion, formation of stress fibre in vitro and development of liver and lung metastases in vivo. MiR-885-5p induced metastatic potential of CRC by repressing cytoplasmic polyadenylation element binding protein 2 transcription through directly binding to two binding sites on its 3' untranslated region, and consequently led to up-regulation of TWIST1 and hence epithelial-mesenchymal transition. Our findings demonstrated the overexpression of miR-885-5p in liver metastasis and its roles in inducing CRC metastasis, potentiating development of miR-885-5p inhibitor to treat advanced CRC in the future.
[Mh] Termos MeSH primário: Neoplasias Colorretais/genética
Neoplasias Colorretais/patologia
Regulação Neoplásica da Expressão Gênica
MicroRNAs/genética
Interferência de RNA
Proteínas de Ligação a RNA/genética
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Animais
Linhagem Celular Tumoral
Movimento Celular/genética
Citoesqueleto/metabolismo
Modelos Animais de Doenças
Transição Epitelial-Mesenquimal/genética
Xenoenxertos
Seres Humanos
Neoplasias Hepáticas/secundário
Masculino
Camundongos
Metástase Neoplásica
Estadiamento de Neoplasias
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (CPEB2 protein, human); 0 (MIRN885 microRNA, human); 0 (MicroRNAs); 0 (RNA-Binding Proteins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15844


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[PMID]:28453955
[Au] Autor:Xue X; Hong X; Li Z; Deng CX; Fu J
[Ad] Endereço:Department of Mechanical Engineering, University of Michigan, Ann Arbor, MI 48109, USA.
[Ti] Título:Acoustic tweezing cytometry enhances osteogenesis of human mesenchymal stem cells through cytoskeletal contractility and YAP activation.
[So] Source:Biomaterials;134:22-30, 2017 Jul.
[Is] ISSN:1878-5905
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Human mesenchymal stem cells (hMSCs) have great potential for cell-based therapies for treating degenerative bone diseases. It is known that mechanical cues in the cell microenvironment play an important role in regulating osteogenic (bone) differentiation of hMSCs. However, mechanoregulation of lineage commitment of hMSCs in conventional two-dimensional (2D) monocultures or bioengineered three-dimensional (3D) tissue constructs remains suboptimal due to complex biomaterial design criteria for hMSC culture. In this study, we demonstrate the feasibility of a novel cell mechanics and mechanobiology tool, acoustic tweezing cytometry (ATC), for mechanical stimulation of hMSCs. ATC utilizes ultrasound (US) pulses to actuate functionalized lipid microbubbles (MBs) which are covalently attached to hMSCs via integrin binding to exert forces to the cells. ATC stimulation increases cytoskeletal contractility of hMSCs regardless of the cell area. Furthermore, ATC application rescues osteogenic differentiation of hMSCs in culture conditions that are intrinsically repressive for hMSC osteogenesis (e.g., soft cell culture surfaces). ATC application activates transcriptional regulator YAP to enhance hMSC osteogenesis. Our data further show that F-actin, myosin II, and RhoA/ROCK signaling functions upstream of YAP activity in mediating ATC-stimulated hMSC osteogenesis. With the capability of applying controlled dynamic mechanical stimuli to cells, ATC provides a powerful tool for mechanoregulation of stem cell behaviors in tissue engineering and regenerative medicine applications.
[Mh] Termos MeSH primário: Técnicas Citológicas/métodos
Citoesqueleto/metabolismo
Células Mesenquimais Estromais/citologia
Osteogênese/fisiologia
[Mh] Termos MeSH secundário: Western Blotting
Diferenciação Celular/fisiologia
Células Cultivadas
Seres Humanos
Células Mesenquimais Estromais/fisiologia
Microbolhas
Osteogênese/genética
Reação em Cadeia da Polimerase em Tempo Real
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


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[PMID]:29384604
[Au] Autor:Mao Z; Yao M; Xu B; Ji X; Jiang H; Han X; Tang Q; Zhou Z; Chen R; Li X; Xia Y
[Ti] Título:Cytoskeletons of Two Reproductive Germ Cell Lines Response Differently to Titanium Dioxide Nanoparticles Mediating Vary Reproductive Toxicity.
[So] Source:J Biomed Nanotechnol;13(4):409-16, 2017 Apr.
[Is] ISSN:1550-7033
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Titanium dioxide nanoparticles (TiO2 NPs) have been widely used for many years. Their toxic effects on the male reproductive system had been reported, but the underlying mechanisms were still not clear. Here we utilized two germ cell lines (GC-2 and TM4) to explore the possible toxic effects of TiO2 NPs on male reproductive system. Our results showed that TiO2 NPs did not affect cell viability but induced cell apoptosis of both GC-2 and TM4 cells up to 100 µg/ml. Microtubule networks and microtubule dynamics of GC-2 but not TM4 cells were changed. The microfilaments arrangement of TM4 cells altered after treated with TiO2 NPs, and the phagocytosis activity of TM4 cells decreased significantly. Although the microfilament network of GC-2 cells seemed normal, the migration ability of GC-2 cells was significantly impaired. Totally TiO2 NPs is toxic to GC-2 cells by inducing cell apoptosis, disturbing microtubule arrangement and microtubule dynamic, and impairing cell migration ability. In addition, they altered the microfilament network and reduced the phagocytic activity of TM4 cells. We firstly reported that cytoskeletons (microtubules and microfilaments) in different cells showed different responses to TiO2 NPs, which might mediate different toxic mechanisms.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Nanopartículas Metálicas/toxicidade
Células de Sertoli/efeitos dos fármacos
Células de Sertoli/fisiologia
Espermatozoides/efeitos dos fármacos
Espermatozoides/fisiologia
Titânio/toxicidade
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Citoesqueleto
Relação Dose-Resposta a Droga
Masculino
Nanopartículas Metálicas/administração & dosagem
Nanopartículas Metálicas/ultraestrutura
Camundongos
Reprodução/efeitos dos fármacos
Células de Sertoli/patologia
Espermatozoides/patologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
15FIX9V2JP (titanium dioxide); D1JT611TNE (Titanium)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE


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[PMID]:29370163
[Au] Autor:Loison-Robert LS; Tassin M; Bonte E; Berbar T; Isaac J; Berdal A; Simon S; Fournier BPJ
[Ad] Endereço:School of Dentistry, Paris Descartes University, Sorbonne Paris Cité, Paris, France.
[Ti] Título:In vitro effects of two silicate-based materials, Biodentine and BioRoot RCS, on dental pulp stem cells in models of reactionary and reparative dentinogenesis.
[So] Source:PLoS One;13(1):e0190014, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Calcium silicate-based cements are biomaterials with calcium oxide and carbonate filler additives. Their properties are close to those of dentin, making them useful in restorative dentistry and endodontics. The aim of this study was to evaluate the in vitro biological effects of two such calcium silicate cements, Biodentine (BD) and Bioroot (BR), on dental stem cells in both direct and indirect contact models. The two models used aimed to mimic reparative dentin formation (direct contact) and reactionary dentin formation (indirect contact). An original aspect of this study is the use of an interposed thin agarose gel layer to assess the effects of diffusible components from the materials. RESULTS: The two biomaterials were compared and did not modify dental pulp stem cell (DPSC) proliferation. BD and BR showed no significant cytotoxicity, although some cell death occurred in direct contact. No apoptosis or inflammation induction was detected. A striking increase of mineralization induction was observed in the presence of BD and BR, and this effect was greater in direct contact. Surprisingly, biomineralization occurred even in the absence of mineralization medium. This differentiation was accompanied by expression of odontoblast-associated genes. Exposure by indirect contact did not stimulate the induction to such a level. CONCLUSION: These two biomaterials both seem to be bioactive and biocompatible, preserving DPSC proliferation, migration and adhesion. The observed strong mineralization induction through direct contact highlights the potential of these biomaterials for clinical application in dentin-pulp complex regeneration.
[Mh] Termos MeSH primário: Materiais Dentários
Polpa Dentária/efeitos dos fármacos
Dentina/efeitos dos fármacos
Silicatos/farmacologia
Células-Tronco/efeitos dos fármacos
[Mh] Termos MeSH secundário: Materiais Biocompatíveis
Proliferação Celular/efeitos dos fármacos
Citoesqueleto/efeitos dos fármacos
Polpa Dentária/citologia
Polpa Dentária/metabolismo
Matriz Extracelular/efeitos dos fármacos
Seres Humanos
Concentração de Íons de Hidrogênio
Técnicas In Vitro
Microscopia Eletrônica de Varredura
Modelos Biológicos
Estresse Oxidativo/efeitos dos fármacos
RNA Mensageiro/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Células-Tronco/citologia
Células-Tronco/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biocompatible Materials); 0 (Dental Materials); 0 (RNA, Messenger); 0 (Silicates)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180126
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190014


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[PMID]:29342173
[Au] Autor:Gautam M; Bhattacharya I; Rai U; Majumdar SS
[Ad] Endereço:Department of Zoology, University of Delhi, Delhi, India.
[Ti] Título:Hormone induced differential transcriptome analysis of Sertoli cells during postnatal maturation of rat testes.
[So] Source:PLoS One;13(1):e0191201, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sertoli cells (Sc) are unique somatic cells of testis that are the target of both FSH and testosterone (T) and regulate spermatogenesis. Although Sc of neonatal rat testes are exposed to high levels of FSH and T, robust differentiation of spermatogonial cells becomes conspicuous only after 11-days of postnatal age. We have demonstrated earlier that a developmental switch in terms of hormonal responsiveness occurs in rat Sc at around 12 days of postnatal age during the rapid transition of spermatogonia A to B. Therefore, such "functional maturation" of Sc, during pubertal development becomes prerequisite for the onset of spermatogenesis. However, a conspicuous difference in robust hormone (both T and FSH) induced gene expression during the different phases of Sc maturation restricts our understanding about molecular events necessary for the spermatogenic onset and maintenance. Here, using microarray technology, we for the first time have compared the differential transcriptional profile of Sc isolated and cultured from immature (5 days old), maturing (12 days old) and mature (60 days old) rat testes. Our data revealed that immature Sc express genes involved in cellular growth, metabolism, chemokines, cell division, MAPK and Wnt pathways, while mature Sc are more specialized expressing genes involved in glucose metabolism, phagocytosis, insulin signaling and cytoskeleton structuring. Taken together, this differential transcriptome data provide an important resource to reveal the molecular network of Sc maturation which is necessary to govern male germ cell differentiation, hence, will improve our current understanding of the etiology of some forms of idiopathic male infertility.
[Mh] Termos MeSH primário: Células de Sertoli/metabolismo
Testículo/crescimento & desenvolvimento
Testículo/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/genética
Diferenciação Celular/efeitos dos fármacos
Quimiocinas/genética
Citocinas/genética
Citoesqueleto/genética
Hormônio Foliculoestimulante/metabolismo
Hormônio Foliculoestimulante/farmacologia
Perfilação da Expressão Gênica
Substâncias de Crescimento/genética
Sistema de Sinalização das MAP Quinases/genética
Masculino
Proteínas Monoméricas de Ligação ao GTP/genética
Análise de Sequência com Séries de Oligonucleotídeos
Fagocitose/genética
Ratos
Ratos Wistar
Células de Sertoli/citologia
Células de Sertoli/efeitos dos fármacos
Espermatogênese/efeitos dos fármacos
Espermatogênese/genética
Espermatogênese/fisiologia
Testículo/efeitos dos fármacos
Testosterona/metabolismo
Testosterona/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chemokines); 0 (Cytokines); 0 (Growth Substances); 3XMK78S47O (Testosterone); 9002-68-0 (Follicle Stimulating Hormone); EC 3.6.5.2 (Monomeric GTP-Binding Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191201


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[PMID]:29317486
[Au] Autor:Foster CT; Gualdrini F; Treisman R
[Ad] Endereço:Signalling and Transcription Group, Francis Crick Institute, London NW1 1AT, United Kingdom.
[Ti] Título:Mutual dependence of the MRTF-SRF and YAP-TEAD pathways in cancer-associated fibroblasts is indirect and mediated by cytoskeletal dynamics.
[So] Source:Genes Dev;31(23-24):2361-2375, 2017 12 01.
[Is] ISSN:1549-5477
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Both the MRTF-SRF and the YAP-TEAD transcriptional regulatory networks respond to extracellular signals and mechanical stimuli. We show that the MRTF-SRF pathway is activated in cancer-associated fibroblasts (CAFs). The MRTFs are required in addition to the YAP pathway for CAF contractile and proinvasive properties. We compared MRTF-SRF and YAP-TEAD target gene sets and identified genes directly regulated by one pathway, the other, or both. Nevertheless, the two pathways exhibit mutual dependence. In CAFs, expression of direct MRTF-SRF genomic targets is also dependent on YAP-TEAD activity, and, conversely, YAP-TEAD target gene expression is also dependent on MRTF-SRF signaling. In normal fibroblasts, expression of activated MRTF derivatives activates YAP, while activated YAP derivatives activate MRTF. Cross-talk between the pathways requires recruitment of MRTF and YAP to DNA via their respective DNA-binding partners (SRF and TEAD) and is therefore indirect, arising as a consequence of activation of their target genes. In both CAFs and normal fibroblasts, we found that YAP-TEAD activity is sensitive to MRTF-SRF-induced contractility, while MRTF-SRF signaling responds to YAP-TEAD-dependent TGFß signaling. Thus, the MRF-SRF and YAP-TEAD pathways interact indirectly through their ability to control cytoskeletal dynamics.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Fibroblastos Associados a Câncer/fisiologia
Citoesqueleto/metabolismo
Proteínas de Ligação a DNA/metabolismo
Neoplasias Mamárias Animais/fisiopatologia
Fosfoproteínas/metabolismo
Transativadores/metabolismo
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/genética
Animais
Linhagem Celular Tumoral
Feminino
Perfilação da Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Camundongos
Fosfoproteínas/genética
Transdução de Sinais
Transativadores/genética
Ativação Transcricional/genética
Fator de Crescimento Transformador beta1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (DNA-Binding Proteins); 0 (MKL1 protein, human); 0 (MKL1 protein, mouse); 0 (Phosphoproteins); 0 (Tead1 protein, mouse); 0 (Trans-Activators); 0 (Transcription Factors); 0 (Transforming Growth Factor beta1); 0 (Yap protein, mouse)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180210
[Lr] Data última revisão:
180210
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1101/gad.304501.117


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[PMID]:29253848
[Au] Autor:McFadden WM; McCall PM; Gardel ML; Munro EM
[Ad] Endereço:Biophysical Sciences Program, University of Chicago, Chicago, Illinois, United States of America.
[Ti] Título:Filament turnover tunes both force generation and dissipation to control long-range flows in a model actomyosin cortex.
[So] Source:PLoS Comput Biol;13(12):e1005811, 2017 12.
[Is] ISSN:1553-7358
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Actomyosin-based cortical flow is a fundamental engine for cellular morphogenesis. Cortical flows are generated by cross-linked networks of actin filaments and myosin motors, in which active stress produced by motor activity is opposed by passive resistance to network deformation. Continuous flow requires local remodeling through crosslink unbinding and and/or filament disassembly. But how local remodeling tunes stress production and dissipation, and how this in turn shapes long range flow, remains poorly understood. Here, we study a computational model for a cross-linked network with active motors based on minimal requirements for production and dissipation of contractile stress: Asymmetric filament compliance, spatial heterogeneity of motor activity, reversible cross-links and filament turnover. We characterize how the production and dissipation of network stress depend, individually, on cross-link dynamics and filament turnover, and how these dependencies combine to determine overall rates of cortical flow. Our analysis predicts that filament turnover is required to maintain active stress against external resistance and steady state flow in response to external stress. Steady state stress increases with filament lifetime up to a characteristic time τm, then decreases with lifetime above τm. Effective viscosity increases with filament lifetime up to a characteristic time τc, and then becomes independent of filament lifetime and sharply dependent on crosslink dynamics. These individual dependencies of active stress and effective viscosity define multiple regimes of steady state flow. In particular our model predicts that when filament lifetimes are shorter than both τc and τm, the dependencies of effective viscosity and steady state stress on filament turnover cancel one another, such that flow speed is insensitive to filament turnover, and shows a simple dependence on motor activity and crosslink dynamics. These results provide a framework for understanding how animal cells tune cortical flow through local control of network remodeling.
[Mh] Termos MeSH primário: Actomiosina/fisiologia
[Mh] Termos MeSH secundário: Citoesqueleto de Actina/química
Citoesqueleto de Actina/fisiologia
Actomiosina/química
Animais
Fenômenos Biomecânicos
Biologia Computacional
Simulação por Computador
Citoesqueleto/fisiologia
Modelos Biológicos
Proteínas Motores Moleculares/química
Proteínas Motores Moleculares/fisiologia
Morfogênese
Reologia
Estresse Fisiológico
Viscosidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Molecular Motor Proteins); 9013-26-7 (Actomyosin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180210
[Lr] Data última revisão:
180210
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pcbi.1005811


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[PMID]:29303350
[Au] Autor:Dierckx H; Biktasheva IV; Verschelde H; Panfilov AV; Biktashev VN
[Ad] Endereço:Department of Physics and Astronomy, Ghent University, 9000 Ghent, Belgium.
[Ti] Título:Filament Tension and Phase Locking of Meandering Scroll Waves.
[So] Source:Phys Rev Lett;119(25):258101, 2017 Dec 22.
[Is] ISSN:1079-7114
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Meandering spiral waves are often observed in excitable media such as the Belousov-Zhabotinsky reaction and cardiac tissue. We derive a theory for drift dynamics of meandering rotors in general reaction-diffusion systems and apply it to two types of external disturbances: an external field and curvature-induced drift in three dimensions. We find two distinct regimes: with small filament curvature, meandering scroll waves exhibit filament tension, whose sign determines the stability and drift direction. In the regimes of strong external fields or meandering motion close to resonance, however, phase locking of the meander pattern is predicted and observed.
[Mh] Termos MeSH primário: Simulação por Computador
Fenômenos Eletromagnéticos
Coração
Movimento (Física)
[Mh] Termos MeSH secundário: Citoesqueleto
Difusão
Modelos Cardiovasculares
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1103/PhysRevLett.119.258101


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[PMID]:28465423
[Au] Autor:Wagstaff JM; Tsim M; Oliva MA; García-Sanchez A; Kureisaite-Ciziene D; Andreu JM; Löwe J
[Ad] Endereço:MRC Laboratory of Molecular Biology, Cambridge, United Kingdom.
[Ti] Título:A Polymerization-Associated Structural Switch in FtsZ That Enables Treadmilling of Model Filaments.
[So] Source:MBio;8(3), 2017 May 02.
[Is] ISSN:2150-7511
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bacterial cell division in many organisms involves a constricting cytokinetic ring that is orchestrated by the tubulin-like protein FtsZ. FtsZ forms dynamic filaments close to the membrane at the site of division that have recently been shown to treadmill around the division ring, guiding septal wall synthesis. Here, using X-ray crystallography of FtsZ (SaFtsZ), we reveal how an FtsZ can adopt two functionally distinct conformations, open and closed. The open form is found in SaFtsZ filaments formed in crystals and also in soluble filaments of FtsZ as deduced by electron cryomicroscopy. The closed form is found within several crystal forms of two nonpolymerizing SaFtsZ mutants and corresponds to many previous FtsZ structures from other organisms. We argue that FtsZ's conformational switch is polymerization-associated, driven by the formation of the longitudinal intersubunit interfaces along the filament. We show that such a switch provides explanations for both how treadmilling may occur within a single-stranded filament and why filament assembly is cooperative. The FtsZ protein is a key molecule during bacterial cell division. FtsZ forms filaments that organize cell membrane constriction, as well as remodeling of the cell wall, to divide cells. FtsZ functions through nucleotide-driven filament dynamics that are poorly understood at the molecular level. In particular, mechanisms for cooperative assembly (nonlinear dependency on concentration) and treadmilling (preferential growth at one filament end and loss at the other) have remained elusive. Here, we show that most likely all FtsZ proteins have two distinct conformations, a "closed" form in monomeric FtsZ and an "open" form in filaments. The conformational switch that occurs upon polymerization explains cooperativity and, in concert with polymerization-dependent nucleotide hydrolysis, efficient treadmilling of FtsZ polymers.
[Mh] Termos MeSH primário: Proteínas de Bactérias/química
Proteínas de Bactérias/metabolismo
Proteínas do Citoesqueleto/química
Proteínas do Citoesqueleto/metabolismo
Citoesqueleto/metabolismo
Staphylococcus aureus/metabolismo
[Mh] Termos MeSH secundário: Divisão Celular
Microscopia Crioeletrônica
Cristalografia por Raios X
Citoesqueleto/química
Escherichia coli/metabolismo
Mutação
Polimerização
Conformação Proteica
Staphylococcus aureus/química
Staphylococcus aureus/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Cytoskeletal Proteins); 0 (FtsZ protein, Bacteria)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180126
[Lr] Data última revisão:
180126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:28743511
[Au] Autor:Yang L; Tang L; Dai F; Meng G; Yin R; Xu X; Yao W
[Ad] Endereço:School of pharmacy, Nantong University, 19 QiXiu Road, Nantong 226001, China.
[Ti] Título:Raf-1/CK2 and RhoA/ROCK signaling promote TNF-α-mediated endothelial apoptosis via regulating vimentin cytoskeleton.
[So] Source:Toxicology;389:74-84, 2017 08 15.
[Is] ISSN:1879-3185
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Both RhoA/ROCK and Raf-1/CK2 pathway play essential roles in cell proliferation, apoptosis, differentiation, and multiple other common cellular functions. We previously reported that vimentin is responsible for TNF-α-induced cell apoptosis. Herein, we investigated the regulation of RhoA/ROCK and Raf-1/CK2 signaling on vimentin filaments and endothelial apoptosis mediated by TNF-α. Treatment with TNF-α significantly induced the activation of RhoA and ROCK, and the expression of ROCK1. RhoA deficiency could obviously inhibit ROCK activation and ROCK1 expression induced by TNF-α. Both RhoA deficiency and ROCK activity inhibition (Y-27632) greatly inhibited endothelial apoptosis and preserved cell viability in TNF-α-induced human umbilical vein endothelial cells (HUVECs). Also vimentin phosphorylation and the remodeling of vimentin or phospho-vimentin induced by TNF-α were obviously attenuated by RhoA suppression and ROCK inhibition. TNF-α-mediated vimentin cleavage was significantly inhibited by RhoA suppression and ROCK inhibition through decreasing the activation of caspase3 and 8. Furthermore, TNF-α treatment greatly enhanced the activation of Raf-1. Suppression of Raf-1 or CK2 by its inhibitor (GW5074 or TBB) blocked vimentin phosphorylation, remodeling and endothelial apoptosis, and preserved cell viability in TNF-α-induced HUVECs. However, Raf-1 inhibition showed no significant effect on TNF-α-induced ROCK expression and activation, suggesting that the regulation of Raf-1/CK2 signaling on vimentin was independent of ROCK. Taken together, these results indicate that both RhoA/ROCK and Raf-1/CK2 pathway are responsible for TNF-α-mediated endothelial cytotoxicity via regulating vimentin cytoskeleton.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Caseína Quinase II/metabolismo
Citoesqueleto/efeitos dos fármacos
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-raf/metabolismo
Fator de Necrose Tumoral alfa/toxicidade
Vimentina/metabolismo
Quinases Associadas a rho/metabolismo
Proteína rhoA de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Caseína Quinase II/antagonistas & inibidores
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Citoesqueleto/enzimologia
Citoesqueleto/patologia
Células Endoteliais da Veia Umbilical Humana/enzimologia
Células Endoteliais da Veia Umbilical Humana/patologia
Seres Humanos
Fosforilação
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas c-raf/antagonistas & inibidores
Interferência de RNA
Transdução de Sinais/efeitos dos fármacos
Transfecção
Proteína cdc42 de Ligação ao GTP/genética
Proteína cdc42 de Ligação ao GTP/metabolismo
Quinases Associadas a rho/antagonistas & inibidores
Proteína rhoA de Ligação ao GTP/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Protein Kinase Inhibitors); 0 (Tumor Necrosis Factor-alpha); 0 (Vimentin); 124671-05-2 (RHOA protein, human); EC 2.7.11.1 (Casein Kinase II); EC 2.7.11.1 (Proto-Oncogene Proteins c-raf); EC 2.7.11.1 (ROCK1 protein, human); EC 2.7.11.1 (rho-Associated Kinases); EC 3.6.5.2 (cdc42 GTP-Binding Protein); EC 3.6.5.2 (rhoA GTP-Binding Protein)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180122
[Lr] Data última revisão:
180122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE



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