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Pesquisa : A11.284.430.214.190.750.050.830 [Categoria DeCS]
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  1 / 1166 MEDLINE  
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[PMID]:29274784
[Au] Autor:Miyazawa A; Ito S; Asano S; Tanaka I; Sato M; Kondo M; Hasegawa Y
[Ad] Endereço:Department of Respiratory Medicine, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
[Ti] Título:Regulation of PD-L1 expression by matrix stiffness in lung cancer cells.
[So] Source:Biochem Biophys Res Commun;495(3):2344-2349, 2018 01 15.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Expression of programmed death-ligand 1 (PD-L1) in tumor cells such as lung cancer cells plays an important role in mechanisms underlying evasion of an immune check point system. Lung cancer tissue with increased deposition of extracellular matrix is much stiffer than normal lung tissue. There is emerging evidence that the matrix stiffness of cancer tissue affects the phenotypes and properties of cancer cells. Nevertheless, the effects of substrate rigidity on expression of PD-L1 in lung cancer cells remain elusive. We evaluated the effects of substrate stiffness on PD-L1 expression in HCC827 lung adenocarcinoma cells by using polyacrylamide hydrogels with stiffnesses of 2 and 25 kPa. Expression of PD-L1 protein was higher on the stiffer substrates (25 kPa gel and plastic dish) than on the soft 2 kPa gel. PD-L1 expression was reduced by detachment of cells adhering to the substrate. Interferon-γ enhanced expression of PD-L1 protein cultured on stiff (25 kPa gel and plastic dishes) and soft (2 kPa gel) substrates and in the cell adhesion-free condition. As the stiffness of substrates increased, formation of actin stress fiber and cell growth were enhanced. Transfection of the cells with short interfering RNA for PD-L1 inhibited cell growth without affecting stress fiber formation. Treatment of the cells with cytochalasin D, an inhibitor of actin polymerization, significantly reduced PD-L1 protein levels. Taken together, a stiff substrate enhanced PD-L1 expression via actin-dependent mechanisms in lung cancer cells. It is suggested that stiffness as a tumor environment regulates PD-L1 expression, which leads to evasion of the immune system and tumor growth.
[Mh] Termos MeSH primário: Antígeno B7-H1/metabolismo
Matriz Extracelular/metabolismo
Neoplasias Pulmonares/fisiopatologia
Fibras de Estresse/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Força Compressiva
Módulo de Elasticidade
Matriz Extracelular/patologia
Regulação Neoplásica da Expressão Gênica
Dureza
Seres Humanos
Neoplasias Pulmonares/patologia
Fibras de Estresse/fisiologia
Estresse Mecânico
Resistência à Tração
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (B7-H1 Antigen); 0 (CD274 protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171225
[St] Status:MEDLINE


  2 / 1166 MEDLINE  
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[PMID]:28741790
[Au] Autor:Wang HC; Chu YL; Hsieh SC; Sheen LY
[Ad] Endereço:Department of Cosmetics Applications and Management, Cardinal Tien Junior College of Healthcare and Management, No. 112, Minzu Road, Sindian District, New Taipei, Taiwan.
[Ti] Título:Diallyl trisulfide inhibits cell migration and invasion of human melanoma a375 cells via inhibiting integrin/facal adhesion kinase pathway.
[So] Source:Environ Toxicol;32(11):2352-2359, 2017 Nov.
[Is] ISSN:1522-7278
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Melanoma is the leading cause of death from skin disease due to its propensity for metastasis. Studies have shown that integrin-mediated focal adhesion kinase (FAK) signal pathway is implicated in cell proliferation, survival and metastasis of tumor cells. Our previous results indicated that diallyl trisulfide (DATS) provided its antimelanoma activity via inducing cell cycle arrest and apoptosis. The aim of this study was to explore DATS mediated antimetastatic effect and the corresponding mechanism in human melanoma A375 cells. We found that DATS exhibited an inhibitory effect on the abilities of migration and invasion in A375 cells under noncytotoxic concentrations analyzed by wound healing assays and Matrigel invasion chamber system. DATS attenuated invasion of A375 cells with characteristic of decreased activities and protein expressions of matrix metalloproteinase-2 (MMP-2) and MMP-9. Moreover, DATS exerted an inhibitory effect on cell adhesion of A375 cells, which is in correlation with the change in integrin signaling pathway. Results of Western blotting showed that DATS decreased the levels of several integrin subunits, including α4, α5, αv, ß1, ß3 and ß4. Subsequently, DATS induced a strong decrease in total FAK, phosphorylated FAK Tyr-397,-576, -577, and disorganized F-actin stress fibers, resulting in a nonmigratory phenotype. These results suggest that the antimetastatic potential of DATS for human melanoma cells might be due to the disruption of integrin/FAK signaling pathway.
[Mh] Termos MeSH primário: Compostos Alílicos/farmacologia
Antineoplásicos/farmacologia
Proteína-Tirosina Quinases de Adesão Focal/metabolismo
Integrinas/metabolismo
Melanoma/tratamento farmacológico
Neoplasias Cutâneas/tratamento farmacológico
Sulfetos/farmacologia
[Mh] Termos MeSH secundário: Adesão Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Seres Humanos
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Fosforilação
Transdução de Sinais
Fibras de Estresse/efeitos dos fármacos
Fibras de Estresse/ultraestrutura
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Allyl Compounds); 0 (Antineoplastic Agents); 0 (Integrins); 0 (Sulfides); 0ZO1U5A3XX (diallyl trisulfide); EC 2.7.10.2 (Focal Adhesion Protein-Tyrosine Kinases); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.35 (Matrix Metalloproteinase 9)
[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:170726
[St] Status:MEDLINE
[do] DOI:10.1002/tox.22445


  3 / 1166 MEDLINE  
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[PMID]:28542912
[Au] Autor:Tocco VJ; Li Y; Christopher KG; Matthews JH; Aggarwal V; Paschall L; Luesch H; Licht JD; Dickinson RB; Lele TP
[Ad] Endereço:Department of Chemical Engineering, University of Florida, Gainesville, Florida.
[Ti] Título:The nucleus is irreversibly shaped by motion of cell boundaries in cancer and non-cancer cells.
[So] Source:J Cell Physiol;233(2):1446-1454, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Actomyosin stress fibers impinge on the nucleus and can exert compressive forces on it. These compressive forces have been proposed to elongate nuclei in fibroblasts, and lead to abnormally shaped nuclei in cancer cells. In these models, the elongated or flattened nuclear shape is proposed to store elastic energy. However, we found that deformed shapes of nuclei are unchanged even after removal of the cell with micro-dissection, both for smooth, elongated nuclei in fibroblasts and abnormally shaped nuclei in breast cancer cells. The lack of shape relaxation implies that the nuclear shape in spread cells does not store any elastic energy, and the cellular stresses that deform the nucleus are dissipative, not static. During cell spreading, the deviation of the nucleus from a convex shape increased in MDA-MB-231 cancer cells, but decreased in MCF-10A cells. Tracking changes of nuclear and cellular shape on micropatterned substrata revealed that fibroblast nuclei deform only during deformations in cell shape and only in the direction of nearby moving cell boundaries. We propose that motion of cell boundaries exert a stress on the nucleus, which allows the nucleus to mimic cell shape. The lack of elastic energy in the nuclear shape suggests that nuclear shape changes in cells occur at constant surface area and volume.
[Mh] Termos MeSH primário: Neoplasias da Mama/patologia
Movimento Celular
Forma do Núcleo Celular
Núcleo Celular/patologia
Forma Celular
Fibroblastos/citologia
Fibras de Estresse/patologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Transferência de Energia
Feminino
Seres Humanos
Mecanotransdução Celular
Camundongos
Células NIH 3T3
Estresse Mecânico
Fatores de Tempo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[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:170526
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.26031


  4 / 1166 MEDLINE  
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[PMID]:28701425
[Au] Autor:Shutova MS; Asokan SB; Talwar S; Assoian RK; Bear JE; Svitkina TM
[Ad] Endereço:Department of Biology, University of Pennsylvania, Philadelphia, PA.
[Ti] Título:Self-sorting of nonmuscle myosins IIA and IIB polarizes the cytoskeleton and modulates cell motility.
[So] Source:J Cell Biol;216(9):2877-2889, 2017 Sep 04.
[Is] ISSN:1540-8140
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nonmuscle myosin II (NMII) is uniquely responsible for cell contractility and thus defines multiple aspects of cell behavior. To generate contraction, NMII molecules polymerize into bipolar minifilaments. Different NMII paralogs are often coexpressed in cells and can copolymerize, suggesting that they may cooperate to facilitate cell motility. However, whether such cooperation exists and how it may work remain unknown. We show that copolymerization of NMIIA and NMIIB followed by their differential turnover leads to self-sorting of NMIIA and NMIIB along the front-rear axis, thus producing a polarized actin-NMII cytoskeleton. Stress fibers newly formed near the leading edge are enriched in NMIIA, but over time, they become progressively enriched with NMIIB because of faster NMIIA turnover. In combination with retrograde flow, this process results in posterior accumulation of more stable NMIIB-rich stress fibers, thus strengthening cell polarity. By copolymerizing with NMIIB, NMIIA accelerates the intrinsically slow NMIIB dynamics, thus increasing cell motility and traction and enabling chemotaxis.
[Mh] Termos MeSH primário: Polaridade Celular
Quimiotaxia
Citoesqueleto/metabolismo
Miosina não Muscular Tipo IIA/metabolismo
Miosina não Muscular Tipo IIB/metabolismo
[Mh] Termos MeSH secundário: Animais
Células COS
Cercopithecus aethiops
Citoesqueleto/genética
Microscopia de Fluorescência
Microscopia de Vídeo
Miosina não Muscular Tipo IIA/genética
Miosina não Muscular Tipo IIB/genética
Multimerização Proteica
Estabilidade Proteica
Interferência de RNA
Ratos
Transdução de Sinais
Fibras de Estresse/metabolismo
Fatores de Tempo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; VIDEO-AUDIO MEDIA
[Nm] Nome de substância:
EC 3.6.1.- (Nonmuscle Myosin Type IIA); EC 3.6.1.- (Nonmuscle Myosin Type IIB)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170714
[St] Status:MEDLINE
[do] DOI:10.1083/jcb.201705167


  5 / 1166 MEDLINE  
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[PMID]:28671960
[Au] Autor:Dornhof R; Maschowski C; Osipova A; Gieré R; Seidl M; Merfort I; Humar M
[Ad] Endereço:Institute of Pharmaceutical Sciences, Pharmaceutical Biology and Biotechnology, Albert-Ludwigs University Freiburg, Freiburg, Germany.
[Ti] Título:Stress fibers, autophagy and necrosis by persistent exposure to PM2.5 from biomass combustion.
[So] Source:PLoS One;12(7):e0180291, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Fine particulate matter (PM2.5) can adversely affect human health. Emissions from residential energy sources have the largest impact on premature mortality globally, but their pathological and molecular implications on cellular physiology are still elusive. In the present study potential molecular consequences were investigated during long-term exposure of human bronchial epithelial BEAS-2B cells to PM2.5, collected from a biomass power plant. Initially, we observed that PM2.5 did not affect cellular survival or proliferation. However, it triggered an activation of the stress response p38 MAPK which, along with RhoA GTPase and HSP27, mediated morphological changes in BEAS-2B cells, including actin cytoskeletal rearrangements and paracellular gap formation. The p38 inhibitor SB203580 prevented phosphorylation of HSP27 and ameliorated morphological changes. During an intermediate phase of long-term exposure, PM2.5 triggered proliferative regression and activation of an adaptive stress response necessary to maintain energy homeostasis, including AMPK, repression of translational elongation, and autophagy. Finally, accumulation of intracellular PM2.5 promoted lysosomal destabilization and cell death, which was dependent on lysosomal hydrolases and p38 MAPK, but not on the inflammasome and pyroptosis. TEM images revealed formation of protrusions and cellular internalization of PM2.5, induction of autophagosomes, amphisomes, autophagosome-lysosomal fusion, multiple compartmental fusion, lysosomal burst, swollen mitochondria and finally necrosis. In consequence, persistent exposure to PM2.5 may impair epithelial barriers and reduce regenerative capacity. Hence, our results contribute to a better understanding of PM-associated lung and systemic diseases on the basis of molecular events.
[Mh] Termos MeSH primário: Autofagia
Biomassa
Exposição Ambiental
Material Particulado
Fibras de Estresse/metabolismo
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/metabolismo
Ciclo Celular
Morte Celular
Linhagem Celular Transformada
Proteínas de Choque Térmico HSP27/metabolismo
Seres Humanos
Microscopia Eletrônica de Transmissão
Necrose
Fosforilação
Proteína rhoA de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HSP27 Heat-Shock Proteins); 0 (Particulate Matter); EC 2.7.11.31 (AMP-Activated Protein Kinases); EC 3.6.5.2 (rhoA GTP-Binding Protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170704
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180291


  6 / 1166 MEDLINE  
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[PMID]:28592635
[Au] Autor:Owen LM; Adhikari AS; Patel M; Grimmer P; Leijnse N; Kim MC; Notbohm J; Franck C; Dunn AR
[Ad] Endereço:Biophysics, Stanford University, Stanford, CA 94305.
[Ti] Título:A cytoskeletal clutch mediates cellular force transmission in a soft, three-dimensional extracellular matrix.
[So] Source:Mol Biol Cell;28(14):1959-1974, 2017 Jul 07.
[Is] ISSN:1939-4586
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The ability of cells to impart forces and deformations on their surroundings underlies cell migration and extracellular matrix (ECM) remodeling and is thus an essential aspect of complex, metazoan life. Previous work has resulted in a refined understanding, commonly termed the molecular clutch model, of how cells adhering to flat surfaces such as a microscope coverslip transmit cytoskeletally generated forces to their surroundings. Comparatively less is known about how cells adhere to and exert forces in soft, three-dimensional (3D), and structurally heterogeneous ECM environments such as occur in vivo. We used time-lapse 3D imaging and quantitative image analysis to determine how the actin cytoskeleton is mechanically coupled to the surrounding matrix for primary dermal fibroblasts embedded in a 3D fibrin matrix. Under these circumstances, the cytoskeletal architecture is dominated by contractile actin bundles attached at their ends to large, stable, integrin-based adhesions. Time-lapse imaging reveals that α-actinin-1 puncta within actomyosin bundles move more quickly than the paxillin-rich adhesion plaques, which in turn move more quickly than the local matrix, an observation reminiscent of the molecular clutch model. However, closer examination did not reveal a continuous rearward flow of the actin cytoskeleton over slower moving adhesions. Instead, we found that a subset of stress fibers continuously elongated at their attachment points to integrin adhesions, providing stable, yet structurally dynamic coupling to the ECM. Analytical modeling and numerical simulation provide a plausible physical explanation for this result and support a picture in which cells respond to the effective stiffness of local matrix attachment points. The resulting dynamic equilibrium can explain how cells maintain stable, contractile connections to discrete points within ECM during cell migration, and provides a plausible means by which fibroblasts contract provisional matrices during wound healing.
[Mh] Termos MeSH primário: Adesões Focais/metabolismo
Adesões Focais/fisiologia
Fibras de Estresse/fisiologia
[Mh] Termos MeSH secundário: Citoesqueleto de Actina/metabolismo
Actinina/metabolismo
Actinas/metabolismo
Actomiosina/metabolismo
Fenômenos Biomecânicos/fisiologia
Adesão Celular
Movimento Celular
Citoesqueleto/metabolismo
Matriz Extracelular/metabolismo
Matriz Extracelular/fisiologia
Fibroblastos/metabolismo
Seres Humanos
Integrinas/metabolismo
Paxilina/metabolismo
Fibras de Estresse/metabolismo
Imagem com Lapso de Tempo/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ACTN1 protein, human); 0 (Actins); 0 (Integrins); 0 (Paxillin); 11003-00-2 (Actinin); 9013-26-7 (Actomyosin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170609
[St] Status:MEDLINE
[do] DOI:10.1091/mbc.E17-02-0102


  7 / 1166 MEDLINE  
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[PMID]:28532442
[Au] Autor:Zhang Z; Xia S; Kanchanawong P
[Ad] Endereço:Mechanobiology Institute, Singapore, 117411, Republic of Singapore.
[Ti] Título:An integrated enhancement and reconstruction strategy for the quantitative extraction of actin stress fibers from fluorescence micrographs.
[So] Source:BMC Bioinformatics;18(1):268, 2017 May 22.
[Is] ISSN:1471-2105
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The stress fibers are prominent organization of actin filaments that perform important functions in cellular processes such as migration, polarization, and traction force generation, and whose collective organization reflects the physiological and mechanical activities of the cells. Easily visualized by fluorescence microscopy, the stress fibers are widely used as qualitative descriptors of cell phenotypes. However, due to the complexity of the stress fibers and the presence of other actin-containing cellular features, images of stress fibers are relatively challenging to quantitatively analyze using previously developed approaches, requiring significant user intervention. This poses a challenge for the automation of their detection, segmentation, and quantitative analysis. RESULT: Here we describe an open-source software package, SFEX (Stress Fiber Extractor), which is geared for efficient enhancement, segmentation, and analysis of actin stress fibers in adherent tissue culture cells. Our method made use of a carefully chosen image filtering technique to enhance filamentous structures, effectively facilitating the detection and segmentation of stress fibers by binary thresholding. We subdivided the skeletons of stress fiber traces into piecewise-linear fragments, and used a set of geometric criteria to reconstruct the stress fiber networks by pairing appropriate fiber fragments. Our strategy enables the trajectory of a majority of stress fibers within the cells to be comprehensively extracted. We also present a method for quantifying the dimensions of the stress fibers using an image gradient-based approach. We determine the optimal parameter space using sensitivity analysis, and demonstrate the utility of our approach by analyzing actin stress fibers in cells cultured on various micropattern substrates. CONCLUSION: We present an open-source graphically-interfaced computational tool for the extraction and quantification of stress fibers in adherent cells with minimal user input. This facilitates the automated extraction of actin stress fibers from fluorescence images. We highlight their potential uses by analyzing images of cells with shapes constrained by fibronectin micropatterns. The method we reported here could serve as the first step in the detection and characterization of the spatial properties of actin stress fibers to enable further detailed morphological analysis.
[Mh] Termos MeSH primário: Actinas/metabolismo
Aumento da Imagem/métodos
Microscopia de Fluorescência/métodos
Fibras de Estresse/metabolismo
[Mh] Termos MeSH secundário: Algoritmos
Anisotropia
Automação
Linhagem Celular Tumoral
Forma Celular
Seres Humanos
Software
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins)
[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:170524
[St] Status:MEDLINE
[do] DOI:10.1186/s12859-017-1684-y


  8 / 1166 MEDLINE  
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[PMID]:28331075
[Au] Autor:Wirshing ACE; Cram EJ
[Ad] Endereço:Department of Biology, Northeastern University, Boston, MA 02115.
[Ti] Título:Myosin activity drives actomyosin bundle formation and organization in contractile cells of the spermatheca.
[So] Source:Mol Biol Cell;28(14):1937-1949, 2017 Jul 07.
[Is] ISSN:1939-4586
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Stress fibers-contractile actomyosin bundles-are important for cellular force production and adaptation to physical stress and have been well studied within the context of cell migration. However, less is known about actomyosin bundle formation and organization in vivo and in specialized contractile cells, such as smooth muscle and myoepithelial cells. The spermatheca is a bag-like organ of 24 myoepithelial cells that houses the sperm and is the site of fertilization. During ovulation, spermathecal cells are stretched by oocyte entry and then coordinately contract to expel the fertilized embryo into the uterus. Here we use four-dimensional confocal microscopy of live animals to observe changes to spermathecal actomyosin network organization during cell stretch and contraction. Oocyte entry is required to trigger cell contraction and concomitant production of parallel actomyosin bundles. Actomyosin bundle size, connectivity, spacing, and orientation are regulated by myosin activity. We conclude that myosin drives actomyosin bundle production and that myosin activity is tightly regulated during ovulation to produce an optimally organized actomyosin network in spermathecae.
[Mh] Termos MeSH primário: Contração Muscular/fisiologia
Fibras de Estresse/metabolismo
[Mh] Termos MeSH secundário: Citoesqueleto de Actina/metabolismo
Actomiosina/metabolismo
Animais
Caenorhabditis elegans/metabolismo
Proteínas de Caenorhabditis elegans/metabolismo
Movimento Celular
Células Epiteliais/metabolismo
Músculo Liso/metabolismo
Miosinas/metabolismo
Oócitos/metabolismo
Imagem Óptica
Ovulação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Caenorhabditis elegans Proteins); 9013-26-7 (Actomyosin); EC 3.6.4.1 (Myosins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170324
[St] Status:MEDLINE
[do] DOI:10.1091/mbc.E17-01-0029


  9 / 1166 MEDLINE  
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[PMID]:28329735
[Au] Autor:Wei F; Liu S; Luo L; Gu N; Zeng Y; Chen X; Xu S; Zhang D
[Ad] Endereço:Department of Emergency, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, PR China; Department of Intensive Care Unit, Xi'an No. 4 Hospital, PR China.
[Ti] Título:Anti-inflammatory mechanism of ulinastatin: Inhibiting the hyperpermeability of vascular endothelial cells induced by TNF-α via the RhoA/ROCK signal pathway.
[So] Source:Int Immunopharmacol;46:220-227, 2017 May.
[Is] ISSN:1878-1705
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Ulinastatin reduces the high permeability of vascular endothelial cells induced by tumor necrosis factor alpha (TNF-α). This study investigated the molecular mechanism behind this effect, with the aim of understanding the action of ulinastatin in sepsis therapy and exploring novel therapeutic strategies for sepsis patients. METHODS: A TNF-α treated human umbilical vein endothelial cell line (EA.hy926) was employed as an inflammation model. Horseradish peroxidase permeability assays and an epithelial voltmeter method were used to measure the permeability of EA.hy926 cells. Immunocytochemistry was used to assay the expression of p-MYPT1 and the distribution and morphology of F-actin; the expression of the key molecules related to vascular endothelial permeability (RhoA, ROCK2, MYPT1, p-MYPT1 and VE-cadherin) was detected by immunocytochemistry assays, western blotting and quantitative real-time polymerase chain reaction. RESULTS: After incubation with TNF-α or septic serum, the transendothelial electrical resistance of EA.hy926 cells decreased and the permeability of the cells increased significantly (all P<0.05). The expression of p-MYPT1 was higher and VE-cadherin was lower compared with the control group, and F-actin was redistributed, with the formation of additional stress fibers in the cells. Ulinastatin treatment moderated these phenomena. The immunocytochemistry assays and western blots showed that the expression of RhoA and ROCK2 was significantly upregulated in cells treated with TNF-α (P<0.05); however, ulinastatin could inhibit the high expression of these two proteins. Under treatment with TNF-α and ulinastatin, compared with normal EA.hy926 cells, overexpression of RhoA upregulated expression of RhoA, ROCK2 and p-MYPT1, downregulated expression of VE-cadherin, and restored the hyperpermeability of vascular endothelial cells due to TNF-α treatment (P<0.05). CONCLUSIONS: Ulinastatin inhibited the hyperpermeability of vascular endothelial cells induced by TNF-α. This inhibitory effect of ulinastatin may be related to the RhoA/ROCK signaling pathway.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Permeabilidade Capilar/efeitos dos fármacos
Endotélio Vascular/metabolismo
Glicoproteínas/farmacologia
Sepse/metabolismo
Quinases Associadas a rho/metabolismo
Proteína rhoA de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Actinas/metabolismo
Caderinas/metabolismo
Linhagem Celular Transformada
Impedância Elétrica
Endotélio Vascular/efeitos dos fármacos
Endotélio Vascular/patologia
Regulação da Expressão Gênica
Seres Humanos
Lentivirus/genética
Fosfatase de Miosina-de-Cadeia-Leve/genética
Fosfatase de Miosina-de-Cadeia-Leve/metabolismo
Sepse/imunologia
Transdução de Sinais/efeitos dos fármacos
Fibras de Estresse/efeitos dos fármacos
Fibras de Estresse/patologia
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Anti-Inflammatory Agents); 0 (Cadherins); 0 (Glycoproteins); 0 (Tumor Necrosis Factor-alpha); 124671-05-2 (RHOA protein, human); EC 2.7.11.1 (rho-Associated Kinases); EC 3.1.3.53 (Myosin-Light-Chain Phosphatase); EC 3.1.3.53 (PPP1R12A protein, human); EC 3.6.5.2 (rhoA GTP-Binding Protein); OR3S9IF86U (urinastatin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170620
[Lr] Data última revisão:
170620
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170323
[St] Status:MEDLINE


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[PMID]:28315692
[Au] Autor:Ma J; Bishoff B; Mercer RR; Barger M; Schwegler-Berry D; Castranova V
[Ad] Endereço:Health Effects Laboratory Division, NIOSH, Morgantown, WV, United States.
[Ti] Título:Role of epithelial-mesenchymal transition (EMT) and fibroblast function in cerium oxide nanoparticles-induced lung fibrosis.
[So] Source:Toxicol Appl Pharmacol;323:16-25, 2017 May 15.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The emission of cerium oxide nanoparticles (CeO ) from diesel engines, using cerium compounds as a catalyst to lower the diesel exhaust particles, is a health concern. We have previously shown that CeO induced pulmonary inflammation and lung fibrosis. The objective of the present study was to investigate the modification of fibroblast function and the role of epithelial-mesenchymal transition (EMT) in CeO -induced fibrosis. Male Sprague-Dawley rats were exposed to CeO (0.15 to 7mg/kg) by a single intratracheal instillation and sacrificed at various times post-exposure. The results show that at 28days after CeO (3.5mg/kg) exposure, lung fibrosis was evidenced by increased soluble collagen in bronchoalveolar lavage fluid, elevated hydroxyproline content in lung tissues, and enhanced sirius red staining for collagen in the lung tissue. Lung fibroblasts and alveolar type II (ATII) cells isolated from CeO -exposed rats at 28days post-exposure demonstrated decreasing proliferation rate when compare to the controls. CeO exposure was cytotoxic and altered cell function as demonstrated by fibroblast apoptosis and aggregation, and ATII cell hypertrophy and hyperplasia with increased surfactant. The presence of stress fibers, expressed as α-smooth muscle actin (SMA), in CeO -exposed fibroblasts and ATII cells was significantly increased compared to the control. Immunohistofluorescence analysis demonstrated co-localization of TGF-ß or α-SMA with prosurfactant protein C (SPC)-stained ATII cells. These results demonstrate that CeO exposure affects fibroblast function and induces EMT in ATII cells that play a role in lung fibrosis. These findings suggest potential adverse health effects in response to CeO nanoparticle exposure.
[Mh] Termos MeSH primário: Células Epiteliais Alveolares/efeitos dos fármacos
Cério/toxicidade
Transição Epitelial-Mesenquimal/efeitos dos fármacos
Fibroblastos/efeitos dos fármacos
Pulmão/efeitos dos fármacos
Nanopartículas Metálicas/toxicidade
Fibrose Pulmonar/induzido quimicamente
[Mh] Termos MeSH secundário: Actinas/metabolismo
Células Epiteliais Alveolares/metabolismo
Células Epiteliais Alveolares/patologia
Animais
Líquido da Lavagem Broncoalveolar/química
Forma Celular/efeitos dos fármacos
Células Cultivadas
Colágeno/metabolismo
Fibroblastos/metabolismo
Fibroblastos/patologia
Hidroxiprolina/metabolismo
Pulmão/metabolismo
Pulmão/patologia
Masculino
Peptídeos/metabolismo
Fibrose Pulmonar/metabolismo
Fibrose Pulmonar/patologia
Ratos Sprague-Dawley
Medição de Risco
Fibras de Estresse/efeitos dos fármacos
Fibras de Estresse/metabolismo
Fibras de Estresse/patologia
Fatores de Tempo
Fator de Crescimento Transformador beta/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Peptides); 0 (Transforming Growth Factor beta); 0 (smooth muscle actin, rat); 133135-52-1 (Sftpc protein, rat); 30K4522N6T (Cerium); 619G5K328Y (ceric oxide); 9007-34-5 (Collagen); RMB44WO89X (Hydroxyproline)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170424
[Lr] Data última revisão:
170424
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170320
[St] Status:MEDLINE



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