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Pesquisa : A11.284.149.165.420 [Categoria DeCS]
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  1 / 8880 MEDLINE  
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[PMID]:28467903
[Au] Autor:Vaahtomeri K; Brown M; Hauschild R; De Vries I; Leithner AF; Mehling M; Kaufmann WA; Sixt M
[Ad] Endereço:Institute of Science and Technology Austria (IST Austria), Am Campus 1, 3400 Klosterneuburg, Austria; Wihuri Research Institute and Translational Cancer Biology Program, Research Program Unit, University of Helsinki, Biomedicum Helsinki, Haartmaninkatu 8, 00290 Helsinki, Finland. Electronic address:
[Ti] Título:Locally Triggered Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.
[So] Source:Cell Rep;19(5):902-909, 2017 May 02.
[Is] ISSN:2211-1247
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Trafficking cells frequently transmigrate through epithelial and endothelial monolayers. How monolayers cooperate with the penetrating cells to support their transit is poorly understood. We studied dendritic cell (DC) entry into lymphatic capillaries as a model system for transendothelial migration. We find that the chemokine CCL21, which is the decisive guidance cue for intravasation, mainly localizes in the trans-Golgi network and intracellular vesicles of lymphatic endothelial cells. Upon DC transmigration, these Golgi deposits disperse and CCL21 becomes extracellularly enriched at the sites of endothelial cell-cell junctions. When we reconstitute the transmigration process in vitro, we find that secretion of CCL21-positive vesicles is triggered by a DC contact-induced calcium signal, and selective calcium chelation in lymphatic endothelium attenuates transmigration. Altogether, our data demonstrate a chemokine-mediated feedback between DCs and lymphatic endothelium, which facilitates transendothelial migration.
[Mh] Termos MeSH primário: Quimiocina CCL21/metabolismo
Células Dendríticas/fisiologia
Células Endoteliais/fisiologia
Endotélio Linfático/citologia
Migração Transendotelial e Transepitelial
[Mh] Termos MeSH secundário: Animais
Sinalização do Cálcio
Quimiocina CCL21/secreção
Células Dendríticas/metabolismo
Células Endoteliais/metabolismo
Endotélio Linfático/fisiologia
Feminino
Junções Intercelulares/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chemokine CCL21)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


  2 / 8880 MEDLINE  
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[PMID]:29183938
[Au] Autor:Heer NC; Martin AC
[Ad] Endereço:Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
[Ti] Título:Tension, contraction and tissue morphogenesis.
[So] Source:Development;144(23):4249-4260, 2017 Dec 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:D'Arcy Thompson was a proponent of applying mathematical and physical principles to biological systems, an approach that is becoming increasingly common in developmental biology. Indeed, the recent integration of quantitative experimental data, force measurements and mathematical modeling has changed our understanding of morphogenesis - the shaping of an organism during development. Emerging evidence suggests that the subcellular organization of contractile cytoskeletal networks plays a key role in force generation, while on the tissue level the spatial organization of forces determines the morphogenetic output. Inspired by D'Arcy Thompson's , we review our current understanding of how biological forms are created and maintained by the generation and organization of contractile forces at the cell and tissue levels. We focus on recent advances in our understanding of how cells actively sculpt tissues and how forces are involved in specific morphogenetic processes.
[Mh] Termos MeSH primário: Morfogênese/fisiologia
[Mh] Termos MeSH secundário: Actinas/fisiologia
Animais
Fenômenos Biomecânicos
Movimento Celular/fisiologia
Células Epiteliais/fisiologia
Seres Humanos
Junções Intercelulares/fisiologia
Modelos Biológicos
Proteínas Motores Moleculares/fisiologia
Contração Muscular/fisiologia
Miosinas/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Actins); 0 (Molecular Motor Proteins); EC 3.6.4.1 (Myosins)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171204
[Lr] Data última revisão:
171204
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.1242/dev.151282


  3 / 8880 MEDLINE  
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[PMID]:28747440
[Au] Autor:Sharma P; Ng C; Jana A; Padhi A; Szymanski P; Lee JSH; Behkam B; Nain AS
[Ad] Endereço:School of Biomedical Engineering and Sciences, Virginia Tech, Blacksburg, VA 24061.
[Ti] Título:Aligned fibers direct collective cell migration to engineer closing and nonclosing wound gaps.
[So] Source:Mol Biol Cell;28(19):2579-2588, 2017 Sep 15.
[Is] ISSN:1939-4586
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cell emergence onto damaged or organized fibrous extracellular matrix (ECM) is a crucial precursor to collective cell migration in wound closure and cancer metastasis, respectively. However, there is a fundamental gap in our quantitative understanding of the role of local ECM size and arrangement in cell emergence-based migration and local gap closure. Here, using ECM-mimicking nanofibers bridging cell monolayers, we describe a method to recapitulate and quantitatively describe these in vivo behaviors over multispatial (single cell to cell sheets) and temporal (minutes to weeks) scales. On fiber arrays with large interfiber spacing, cells emerge (invade) either singularly by breaking cell-cell junctions analogous to release of a stretched rubber band (recoil), or in groups of few cells (chains), whereas on closely spaced fibers, multiple chains emerge collectively. Advancing cells on fibers form cell streams, which support suspended cell sheets (SCS) of various sizes and curvatures. SCS converge to form local gaps that close based on both the gap size and shape. We document that cell stream spacing of 375 µm and larger hinders SCS advancement, thus providing abilities to engineer closing and nonclosing gaps. Altogether we highlight the importance of studying cell-fiber interactions and matrix structural remodeling in fundamental and translational cell biology.
[Mh] Termos MeSH primário: Movimento Celular/fisiologia
Matriz Extracelular/fisiologia
Junções Intercelulares/fisiologia
Cicatrização/fisiologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Camundongos
Células NIH 3T3
Nanofibras/química
Tecidos Suporte
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171130
[Lr] Data última revisão:
171130
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1091/mbc.E17-05-0305


  4 / 8880 MEDLINE  
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[PMID]:28466496
[Au] Autor:Temereva EN
[Ad] Endereço:Biological Faculty, Department of Invertebrate Zoology, Moscow State University, Vorobievi Gory 1-12, Moscow, 119991, Russia.
[Ti] Título:Ultrastructure of the coelom in the brachiopod Lingula anatina.
[So] Source:J Morphol;278(7):997-1011, 2017 Jul.
[Is] ISSN:1097-4687
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The organization of the coelomic system and the ultrastructure of the coelomic lining are used in phylogenetic analysis to establish the relationships between major taxa. Investigation of the anatomy and ultrastructure of the coelomic system in brachiopods, which are poorly studied, can provide answers to fundamental questions about the evolution of the coelom in coelomic bilaterians. In the current study, the organization of the coelom of the lophophore in the brachiopod Lingula anatina was investigated using semithin sectioning, 3D reconstruction, and transmission electron microscopy. The lophophore of L. anatina contains two main compartments: the preoral coelom and the lophophoral coelom. The lining of the preoral coelom consists of ciliated cells. The lophophoral coelom is subdivided into paired coelomic sacs: the large and small sinuses (= canals). The lining of the lophophoral coelom varies in structure and includes monociliate myoepithelium, alternating epithelial and myoepithelial cells, specialized peritoneum and muscle cells, and podocyte-like cells. Connections between cells of the coelomic lining are provided by adherens junctions, tight-like junctions, septate junctions, adhesive junctions, and direct cytoplasmic bridges. The structure of the coelomic lining varies greatly in both of the main stems of the Bilateria, that is, in the Protostomia and Deuterostomia. Because of this great variety, the structure of the coelomic lining cannot by itself be used in phylogenetic analysis. At the same time, the ciliated myoepithelium can be considered as the ancestral type of coelomic lining. The many different kinds of junctions between cells of the coelomic lining may help coordinate the functioning of epithelial cells and muscle cells.
[Mh] Termos MeSH primário: Invertebrados/anatomia & histologia
Invertebrados/ultraestrutura
[Mh] Termos MeSH secundário: Animais
Evolução Biológica
Esôfago/anatomia & histologia
Esôfago/ultraestrutura
Junções Intercelulares/ultraestrutura
Invertebrados/fisiologia
Células Musculares/ultraestrutura
[Pt] Tipo de publicação: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:170504
[St] Status:MEDLINE
[do] DOI:10.1002/jmor.20693


  5 / 8880 MEDLINE  
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[PMID]:28945820
[Au] Autor:Guichard A; Jain P; Moayeri M; Schwartz R; Chin S; Zhu L; Cruz-Moreno B; Liu JZ; Aguilar B; Hollands A; Leppla SH; Nizet V; Bier E
[Ad] Endereço:Section of Cell and Developmental Biology, University of California, San Diego, La Jolla, CA, United States of America.
[Ti] Título:Anthrax edema toxin disrupts distinct steps in Rab11-dependent junctional transport.
[So] Source:PLoS Pathog;13(9):e1006603, 2017 Sep.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Various bacterial toxins circumvent host defenses through overproduction of cAMP. In a previous study, we showed that edema factor (EF), an adenylate cyclase from Bacillus anthracis, disrupts endocytic recycling mediated by the small GTPase Rab11. As a result, cargo proteins such as cadherins fail to reach inter-cellular junctions. In the present study, we provide further mechanistic dissection of Rab11 inhibition by EF using a combination of Drosophila and mammalian systems. EF blocks Rab11 trafficking after the GTP-loading step, preventing a constitutively active form of Rab11 from delivering cargo vesicles to the plasma membrane. Both of the primary cAMP effector pathways -PKA and Epac/Rap1- contribute to inhibition of Rab11-mediated trafficking, but act at distinct steps of the delivery process. PKA acts early, preventing Rab11 from associating with its effectors Rip11 and Sec15. In contrast, Epac functions subsequently via the small GTPase Rap1 to block fusion of recycling endosomes with the plasma membrane, and appears to be the primary effector of EF toxicity in this process. Similarly, experiments conducted in mammalian systems reveal that Epac, but not PKA, mediates the activity of EF both in cell culture and in vivo. The small GTPase Arf6, which initiates endocytic retrieval of cell adhesion components, also contributes to junctional homeostasis by counteracting Rab11-dependent delivery of cargo proteins at sites of cell-cell contact. These studies have potentially significant practical implications, since chemical inhibition of either Arf6 or Epac blocks the effect of EF in cell culture and in vivo, opening new potential therapeutic avenues for treating symptoms caused by cAMP-inducing toxins or related barrier-disrupting pathologies.
[Mh] Termos MeSH primário: Antígenos de Bactérias/farmacologia
Toxinas Bacterianas/farmacologia
Edema/metabolismo
Endossomos/efeitos dos fármacos
Junções Intercelulares/efeitos dos fármacos
[Mh] Termos MeSH secundário: Fatores de Ribosilação do ADP/metabolismo
Adenilil Ciclases/metabolismo
Animais
Caderinas/metabolismo
Linhagem Celular
Endossomos/metabolismo
Junções Intercelulares/metabolismo
Transporte Proteico/efeitos dos fármacos
Proteínas rab de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Bacterial); 0 (Bacterial Toxins); 0 (Cadherins); 0 (anthrax toxin); EC 3.6.5.2 (ADP-Ribosylation Factors); EC 3.6.5.2 (ADP-ribosylation factor 6); EC 3.6.5.2 (rab GTP-Binding Proteins); EC 4.6.1.1 (Adenylyl Cyclases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170926
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006603


  6 / 8880 MEDLINE  
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[PMID]:28928095
[Au] Autor:English WR; Siviter RJ; Hansen M; Murphy G
[Ad] Endereço:University of Cambridge Department of Oncology, Cancer Research UK Cambridge Institute, Li Ka Shing Centre, Robinson Way, Cambridge, CB2 0RE, UK; Tumour Microcirculation Group, Department of Oncology and Metabolism, The Medical School, University of Sheffield, Beech Hill Road, Sheffield S10 2RX, UK.
[Ti] Título:ADAM9 is present at endothelial cell - cell junctions and regulates monocyte - endothelial transmigration.
[So] Source:Biochem Biophys Res Commun;493(2):1057-1062, 2017 Nov 18.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We have found that A Disintegrin And Metalloproteinase-9 (ADAM9) localises to cell-cell junctions with VE-Cadherin in confluent endothelial monolayers. Co-cultures of cells separately transfected with ADAM9-EGFP or ADAM9-HA showed expression is required in two adjacent cells for localisation to cell-cell junctions suggesting the ADAM9 ectodomain may self-associate. A direct interaction between ADAM9 ectodomains was confirmed using recombinant proteins and an ELISA based method. As the ADAM9 ectodomain can also exist as a soluble form physiologically, we examined if this could inhibit endothelial functions dependent on cell-cell junctions. The soluble ADAM9 ectodomain could not increase endothelial monolayer permeability or inhibit monocyte-endothelial adhesion, but could inhibit monocyte-endothelial transmigration. These novel findings point to ADAM9 playing an important role in endothelial cell biology that is distinct from the other ADAMs.
[Mh] Termos MeSH primário: Proteínas ADAM/metabolismo
Células Endoteliais/citologia
Junções Intercelulares/metabolismo
Proteínas de Membrana/metabolismo
Monócitos/citologia
Migração Transendotelial e Transepitelial
[Mh] Termos MeSH secundário: Proteínas ADAM/análise
Animais
Linhagem Celular
Células Endoteliais/metabolismo
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Junções Intercelulares/ultraestrutura
Proteínas de Membrana/análise
Camundongos
Monócitos/metabolismo
Domínios Proteicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Proteins); EC 3.4.24.- (ADAM Proteins); EC 3.4.24.- (ADAM9 protein, human); EC 3.4.24.- (Adam9 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171119
[Lr] Data última revisão:
171119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE


  7 / 8880 MEDLINE  
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[PMID]:28845032
[Au] Autor:Sumitomo T
[Ad] Endereço:Department of Oral and Molecular Microbiology, Osaka University Graduate School of Dentistry.
[Ti] Título:Streptococcus pyogenes translocates across an epithelial barrier.
[So] Source:Nihon Saikingaku Zasshi;72(3):213-218, 2017.
[Is] ISSN:1882-4110
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:Streptococcus pyogenes is a ß-hemolytic organism responsible for a wide variety of human diseases that commonly occur as self-limiting purulent diseases of the pharynx and skin. Although the occurrence of invasive infections by S. pyogenes is rare, mortality rates remain high even with progressive medical therapy. As a prerequisite for causing the severe invasive disease, S. pyogenes must invade underlying sterile tissues by translocating across the epithelial barrier. In this study, streptolysin S and SpeB were identified as the novel factors that facilitate bacterial translocation via degradation of intercellular junctions. Furthermore, we found that S. pyogenes exploits host plasminogen for acceleration of bacterial invasion into deeper tissues via tricellular tight junctions. Here, I would like to show our study on bacterial translocation across the epithelial barrier through paracellular route.
[Mh] Termos MeSH primário: Translocação Bacteriana
Epitélio/microbiologia
Infecções Estreptocócicas/microbiologia
Streptococcus pyogenes/fisiologia
Streptococcus pyogenes/patogenicidade
[Mh] Termos MeSH secundário: Proteínas de Bactérias/fisiologia
Translocação Bacteriana/genética
Células Epiteliais/microbiologia
Células Epiteliais/fisiologia
Epitélio/fisiologia
Exotoxinas/fisiologia
Seres Humanos
Junções Intercelulares/microbiologia
Junções Intercelulares/fisiologia
Plasminogênio/metabolismo
Streptococcus pyogenes/genética
Estreptolisinas/fisiologia
Junções Íntimas/microbiologia
Junções Íntimas/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Exotoxins); 0 (Streptolysins); 0 (erythrogenic toxin); 0 (streptolysin S); 9001-91-6 (Plasminogen)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171015
[Lr] Data última revisão:
171015
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170829
[St] Status:MEDLINE
[do] DOI:10.3412/jsb.72.213


  8 / 8880 MEDLINE  
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[PMID]:28759570
[Au] Autor:Rezaee F; Harford TJ; Linfield DT; Altawallbeh G; Midura RJ; Ivanov AI; Piedimonte G
[Ad] Endereço:Pediatric Research Center and Pediatric Institute, Cleveland Clinic Children's, Cleveland, Ohio, United States of America.
[Ti] Título:cAMP-dependent activation of protein kinase A attenuates respiratory syncytial virus-induced human airway epithelial barrier disruption.
[So] Source:PLoS One;12(7):e0181876, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Airway epithelium forms a barrier to the outside world and has a crucial role in susceptibility to viral infections. Cyclic adenosine monophosphate (cAMP) is an important second messenger acting via two intracellular signaling molecules: protein kinase A (PKA) and the guanidine nucleotide exchange factor, Epac. We sought to investigate effects of increased cAMP level on the disruption of model airway epithelial barrier caused by RSV infection and the molecular mechanisms underlying cAMP actions. Human bronchial epithelial cells were infected with RSV-A2 and treated with either cAMP releasing agent, forskolin, or cAMP analogs. Structure and functions of the Apical Junctional Complex (AJC) were evaluated by measuring transepithelial electrical resistance and permeability to FITC-dextran, and determining localization of AJC proteins by confocal microscopy. Increased intracellular cAMP level significantly attenuated RSV-induced disassembly of AJC. These barrier-protective effects of cAMP were due to the activation of PKA signaling and did not involve Epac activity. Increased cAMP level reduced RSV-induced reorganization of the actin cytoskeleton, including apical accumulation of an essential actin-binding protein, cortactin, and inhibited expression of the RSV F protein. These barrier-protective and antiviral-function of cAMP signaling were evident even when cAMP level was increased after the onset of RSV infection. Taken together, our study demonstrates that cAMP/PKA signaling attenuated RSV-induced disruption of structure and functions of the model airway epithelial barrier by mechanisms involving the stabilization of epithelial junctions and inhibition of viral biogenesis. Improving our understanding of the mechanisms involved in RSV-induced epithelial dysfunction and viral pathogenesis will help to develop novel anti-viral therapeutic approaches.
[Mh] Termos MeSH primário: Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
AMP Cíclico/metabolismo
Epitélio/virologia
Vírus Sincicial Respiratório Humano
Infecções Respiratórias/virologia
[Mh] Termos MeSH secundário: Citoesqueleto de Actina/metabolismo
Brônquios/citologia
Colforsina/farmacologia
Dextranos/química
Células Epiteliais/metabolismo
Células Epiteliais/virologia
Epitélio/patologia
Fluoresceína-5-Isotiocianato/análogos & derivados
Fatores de Troca do Nucleotídeo Guanina/metabolismo
Seres Humanos
Junções Intercelulares/metabolismo
Proteínas dos Microfilamentos/metabolismo
Microscopia Confocal
Permeabilidade
Transdução de Sinais/efeitos dos fármacos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dextrans); 0 (Guanine Nucleotide Exchange Factors); 0 (Microfilament Proteins); 0 (fluorescein isothiocyanate dextran); 1F7A44V6OU (Colforsin); E0399OZS9N (Cyclic AMP); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); I223NX31W9 (Fluorescein-5-isothiocyanate)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170801
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181876


  9 / 8880 MEDLINE  
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[PMID]:28754672
[Au] Autor:Du W; Xu X; Niu Q; Zhang X; Wei Y; Wang Z; Zhang W; Yan J; Ru Y; Fu Z; Li X; Jiang Y; Ma Z; Zhang Z; Yao Z; Liu Z
[Ad] Endereço:Department of Immunology, Biochemistry and Molecular Biology, Collaborative Innovation Center of Tianjin for Medical Epigenetics, Tianjin Key Laboratory of Medical Epigenetics, Tianjin Medical University, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China.
[Ti] Título:Spi-B-Mediated Silencing of Claudin-2 Promotes Early Dissemination of Lung Cancer Cells from Primary Tumors.
[So] Source:Cancer Res;77(18):4809-4822, 2017 Sep 15.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dissociation from epithelial sheets and invasion through the surrounding stroma are critical early events during epithelial cancer metastasis. Here we find that a lymphocyte lineage-restricted transcription factor, Spi-B, is frequently expressed in human lung cancer tissues. The Spi-B-expressing cancer cells coexpressed vimentin but repressed E-cadherin and exhibited invasive behavior. Increased Spi-B expression was associated with tumor grade, lymphatic metastasis, and short overall survival. Mechanistically, Spi-B disrupted intercellular junctions and enhanced invasiveness by reconfiguring the chromatin structure of the tight junction gene claudin-2 ( ) and repressing its transcription. These data suggest that Spi-B participates in mesenchymal invasion, linking epithelial cancer metastasis with a lymphatic transcriptional program. .
[Mh] Termos MeSH primário: Carcinoma Pulmonar de Lewis/secundário
Claudina-2/metabolismo
Proteínas de Ligação a DNA/metabolismo
Regulação Neoplásica da Expressão Gênica
Neoplasias Pulmonares/patologia
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Adenocarcinoma/genética
Adenocarcinoma/metabolismo
Adenocarcinoma/secundário
Animais
Apoptose
Biomarcadores Tumorais
Carcinoma Pulmonar de Lewis/genética
Carcinoma Pulmonar de Lewis/metabolismo
Carcinoma Pulmonar de Células não Pequenas/genética
Carcinoma Pulmonar de Células não Pequenas/metabolismo
Carcinoma Pulmonar de Células não Pequenas/secundário
Carcinoma de Células Escamosas/genética
Carcinoma de Células Escamosas/metabolismo
Carcinoma de Células Escamosas/secundário
Proliferação Celular
Claudina-2/genética
Proteínas de Ligação a DNA/genética
Seres Humanos
Junções Intercelulares
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Invasividade Neoplásica
Estadiamento de Neoplasias
Prognóstico
Carcinoma de Pequenas Células do Pulmão/genética
Carcinoma de Pequenas Células do Pulmão/metabolismo
Carcinoma de Pequenas Células do Pulmão/secundário
Fatores de Transcrição/genética
Células Tumorais Cultivadas
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Claudin-2); 0 (DNA-Binding Proteins); 0 (Transcription Factors); 148350-00-9 (SPIB protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170730
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-17-0020


  10 / 8880 MEDLINE  
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[PMID]:28705794
[Au] Autor:Hara T; Monguchi T; Iwamoto N; Akashi M; Mori K; Oshita T; Okano M; Toh R; Irino Y; Shinohara M; Yamashita Y; Shioi G; Furuse M; Ishida T; Hirata KI
[Ad] Endereço:From the Division of Cardiovascular Medicine, Department of Internal Medicine (T.H., T.M., K.M., T.O., M.O., T.I., K.-i.H.), Division of Cell Biology, Department of Physiology and Cell Biology (N.I., M.A., M.F.), Department of Oral and Maxillofacial Surgery (M.A.), Division of Evidence-Based Laborat
[Ti] Título:Targeted Disruption of JCAD (Junctional Protein Associated With Coronary Artery Disease)/KIAA1462, a Coronary Artery Disease-Associated Gene Product, Inhibits Angiogenic Processes In Vitro and In Vivo.
[So] Source:Arterioscler Thromb Vasc Biol;37(9):1667-1673, 2017 Sep.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Recent genome-wide association studies newly identified the human KIAA1462 gene as a new locus for coronary artery disease. However, the function of the gene product, named JCAD (junctional protein associated with coronary artery disease), is unknown. Because JCAD is expressed at cell-cell junctions in endothelial cells, we hypothesized and tested whether JCAD regulates angiogenic processes in vitro and in vivo. APPROACH AND RESULTS: Cell culture experiments revealed impaired angiogenic ability (proliferation, migration, and cord formation) by the knockdown of JCAD with siRNA ( <0.05 versus control siRNA). We have generated mice lacking JCAD (mKIAA1462 ) by gene-targeted deletion of JCAD to address in vivo angiogenic function. mKIAA1462 mice did not show morphological differences in development of retinal vasculature. Ex vivo aortic ring model demonstrated impaired neovascularization in aorta from mKIAA1462 mice than control wild-type mice ( <0.05). Tumor growth was assessed by monitoring tumor volume after the subcutaneous injection of melanoma, LLC (Lewis lung carcinoma), and E0771 cells into the mice. mKIAA1462 mice exhibited significantly smaller tumor volume compared with wild-type mice ( <0.001). Histological assessment of the tumor exhibited less smooth muscle actin-positive neovascularization determined by CD31-positive vascular structure in tumor of mKIAA1462 mice than wild-type mice, indicating that knockdown of JCAD inhibited the vascular maturation in pathological angiogenic process. CONCLUSIONS: These in vitro and in vivo studies suggest that JCAD has a redundant functional role in physiological angiogenesis but serves a pivotal role in pathological angiogenic process after birth.
[Mh] Termos MeSH primário: Moléculas de Adesão Celular/metabolismo
Células Endoteliais/metabolismo
Junções Intercelulares/metabolismo
Neovascularização Patológica
Neovascularização Fisiológica
Neovascularização Retiniana
[Mh] Termos MeSH secundário: Animais
Carcinoma Pulmonar de Lewis/irrigação sanguínea
Carcinoma Pulmonar de Lewis/genética
Carcinoma Pulmonar de Lewis/metabolismo
Moléculas de Adesão Celular/deficiência
Moléculas de Adesão Celular/genética
Movimento Celular
Proliferação Celular
Células Cultivadas
Genótipo
Células Endoteliais da Veia Umbilical Humana/metabolismo
Melanoma Experimental/irrigação sanguínea
Melanoma Experimental/genética
Melanoma Experimental/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fenótipo
Interferência de RNA
Transdução de Sinais
Fatores de Tempo
Técnicas de Cultura de Tecidos
Transfecção
Carga Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (9430020K01Rik protein, mouse); 0 (Cell Adhesion Molecules); 0 (KIAA1462 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170715
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.117.309721



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