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Pesquisa : D12.776.543.940.200.400 [Categoria DeCS]
Referências encontradas : 499 [refinar]
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  1 / 499 MEDLINE  
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[PMID]:28856683
[Au] Autor:Kojima T; Kohno T; Kubo T; Kaneko Y; Kakuki T; Kakiuchi A; Kurose M; Takano KI; Ogasawara N; Obata K; Nomura K; Miyata R; Konno T; Ichimiya S; Himi T
[Ad] Endereço:Department of Cell Science, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
[Ti] Título:Regulation of claudin-4 via p63 in human epithelial cells.
[So] Source:Ann N Y Acad Sci;1405(1):25-31, 2017 Oct.
[Is] ISSN:1749-6632
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:P63 is a regulator of cell-cell junction complexes in the epidermis. Claudin-4 is regulated via various factors in normal epithelial cells and diseases. We found that claudin-4 was directly regulated via p63 (TAp63 and ΔNp63) in human keratinocytes and nasal epithelial cells. In the epidermis of atopic dermatitis (AD), which contains ΔNp63-deficient keratinocytes, high expression of claudin-4 was observed. In primary keratinocytes, downregulation of ΔNp63 by treatment with short interfering RNA (siRNA)-p63 induced claudin-4 expression. In nasal epithelial cells in the context of rhinitis or nasal polyps, upregulation of TAp63 and downregulation of claudin-4 were observed. In primary nasal epithelial cells transfected with the human telomerase reverse transcriptase gene, knockdown of p63 by siRNAs induced claudin-4 expression. Taken together, these findings indicate that p63 is a negative regulator of claudin-4 expression. Understanding the regulation of claudin-4 via p63 in human epithelial cells may be important for developing therapies for allergies and drug delivery systems.
[Mh] Termos MeSH primário: Claudina-4/metabolismo
Células Epiteliais/metabolismo
Queratinócitos/metabolismo
Fatores de Transcrição/metabolismo
Proteínas Supressoras de Tumor/metabolismo
[Mh] Termos MeSH secundário: Claudina-4/genética
Regulação para Baixo
Seres Humanos
Pólipos Nasais/genética
Pólipos Nasais/metabolismo
Rinite/genética
Rinite/metabolismo
Fatores de Transcrição/genética
Ativação Transcricional
Proteínas Supressoras de Tumor/genética
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Claudin-4); 0 (TP63 protein, human); 0 (Transcription Factors); 0 (Tumor Suppressor Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1111/nyas.13456


  2 / 499 MEDLINE  
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[PMID]:28777806
[Au] Autor:Tokuda S; Hirai T; Furuse M
[Ad] Endereço:Department of Respiratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
[Ti] Título:Claudin-4 knockout by TALEN-mediated gene targeting in MDCK cells: Claudin-4 is dispensable for the permeability properties of tight junctions in wild-type MDCK cells.
[So] Source:PLoS One;12(8):e0182521, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Epithelia act as a barrier between the internal and external environments, and the movement of substances via the paracellular pathway is regulated by tight junctions (TJs). Claudins are major determinants of TJ permeability. Claudin-4 was the first claudin whose involvement in the TJ permeability in cultured cells was directly demonstrated, but the permeability properties of individual claudins including claudin-4 are still incompletely clarified. In this study, we established claudin-4 knockout cells using transcription activator-like effector nucleases (TALENs), a recently developed method for genome editing, and investigated the permeability property of claudin-4 in MDCK II cells. We found that claudin-4 knockout has no apparent effect on the localization of other claudins and electrophysiological properties in MDCK II cells. Therefore we further established claudin-2 and claudin-4 double knockout clones and investigated the effects on TJs. Claudin-4 knockout in addition to claudin-2 knockout slightly increased the localization of other claudins at TJs but showed no obvious effects on the electrophysiological properties in MDCK II cells. These results indicate that claudin-4 is dispensable for the barrier property of TJs in wild-type as well as claudin-2 knockout MDCK II cells. Our results suggest the need for further knockout analysis to reveal the permeability properties of individual claudins.
[Mh] Termos MeSH primário: Permeabilidade da Membrana Celular
Claudina-4/antagonistas & inibidores
Técnicas de Inativação de Genes/métodos
Junções Íntimas/fisiologia
Nucleases dos Efetores Semelhantes a Ativadores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Animais
Claudina-4/genética
Claudina-4/metabolismo
Cães
Células Madin Darby de Rim Canino
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Claudin-4); EC 3.1.- (Transcription Activator-Like Effector Nucleases)
[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:170805
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182521


  3 / 499 MEDLINE  
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[PMID]:28753223
[Au] Autor:Bäsler K; Galliano MF; Bergmann S; Rohde H; Wladykowski E; Vidal-Y-Sy S; Guiraud B; Houdek P; Schüring G; Volksdorf T; Caruana A; Bessou-Touya S; Schneider SW; Duplan H; Brandner JM
[Ad] Endereço:Department of Dermatology and Venerology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
[Ti] Título:Biphasic influence of Staphylococcus aureus on human epidermal tight junctions.
[So] Source:Ann N Y Acad Sci;1405(1):53-70, 2017 Oct.
[Is] ISSN:1749-6632
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bacterial infections (e.g., with Staphylococcus aureus) are serious problems in skin with a compromised barrier, such as in patients with atopic dermatitis. Previously, it was shown that tight junction (TJ) proteins are influenced by staphylococcal infection, and TJ function is impaired after infection of the keratinocyte cell line HaCaT. However, functional studies in cells or models more similar to human skin are missing. Therefore, we investigated bacterial colonialization and infection with live S. aureus in primary human keratinocytes and reconstructed human epidermis (RHE). We show that short-term inoculation results in increased TJ barrier function-which could not be seen in HaCaT cells-hinting at an early protective effect. This is accompanied by occludin phosphorylation and sustained localization of occludin and claudin-4 at cell membranes. Long-term incubation resulted in decreased presence of claudin-1 and claudin-4 at cell membranes and decreased TJ barrier function. The agr regulon of S. aureus plays a role in the increasing but not in the decreasing effect. Proinflammatory cytokines, which are produced as a result of S. aureus inoculation, influence both phases. In summary, we show here that S. aureus can have short-term promoting effects on the TJ barrier, while in the long term it results in disturbance of TJs.
[Mh] Termos MeSH primário: Membrana Celular/microbiologia
Epiderme/microbiologia
Queratinócitos/microbiologia
Staphylococcus aureus
Junções Íntimas/microbiologia
[Mh] Termos MeSH secundário: Membrana Celular/metabolismo
Permeabilidade da Membrana Celular/fisiologia
Claudina-1/metabolismo
Claudina-4/metabolismo
Epiderme/metabolismo
Seres Humanos
Queratinócitos/metabolismo
Ocludina/metabolismo
Fosforilação
Infecções Estafilocócicas/metabolismo
Junções Íntimas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Claudin-1); 0 (Claudin-4); 0 (Occludin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170729
[St] Status:MEDLINE
[do] DOI:10.1111/nyas.13418


  4 / 499 MEDLINE  
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[PMID]:28737509
[Au] Autor:Horng S; Therattil A; Moyon S; Gordon A; Kim K; Argaw AT; Hara Y; Mariani JN; Sawai S; Flodby P; Crandall ED; Borok Z; Sofroniew MV; Chapouly C; John GR
[Ad] Endereço:Friedman Brain Institute.
[Ti] Título:Astrocytic tight junctions control inflammatory CNS lesion pathogenesis.
[So] Source:J Clin Invest;127(8):3136-3151, 2017 Aug 01.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lesions and neurologic disability in inflammatory CNS diseases such as multiple sclerosis (MS) result from the translocation of leukocytes and humoral factors from the vasculature, first across the endothelial blood-brain barrier (BBB) and then across the astrocytic glia limitans (GL). Factors secreted by reactive astrocytes open the BBB by disrupting endothelial tight junctions (TJs), but the mechanisms that control access across the GL are unknown. Here, we report that in inflammatory lesions, a second barrier composed of reactive astrocyte TJs of claudin 1 (CLDN1), CLDN4, and junctional adhesion molecule A (JAM-A) subunits is induced at the GL. In a human coculture model, CLDN4-deficient astrocytes were unable to control lymphocyte segregation. In models of CNS inflammation and MS, mice with astrocyte-specific Cldn4 deletion displayed exacerbated leukocyte and humoral infiltration, neuropathology, motor disability, and mortality. These findings identify a second inducible barrier to CNS entry at the GL. This barrier may be therapeutically targetable in inflammatory CNS disease.
[Mh] Termos MeSH primário: Astrócitos/citologia
Sistema Nervoso Central/patologia
Inflamação
Doenças do Sistema Nervoso/patologia
Junções Íntimas
[Mh] Termos MeSH secundário: Animais
Barreira Hematoencefálica/patologia
Moléculas de Adesão Celular/metabolismo
Claudina-1/metabolismo
Claudina-4/metabolismo
Técnicas de Cocultura
Citocinas/metabolismo
Modelos Animais de Doenças
Encefalomielite Autoimune Experimental/patologia
Feminino
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Esclerose Múltipla/patologia
Receptores de Superfície Celular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Adhesion Molecules); 0 (Claudin-1); 0 (Claudin-4); 0 (Cldn1 protein, mouse); 0 (Cldn4 protein, mouse); 0 (Cytokines); 0 (F11r protein, mouse); 0 (Receptors, Cell Surface)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170725
[St] Status:MEDLINE


  5 / 499 MEDLINE  
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[PMID]:28719466
[Au] Autor:Makise N; Yoshida A; Komiyama M; Nakatani F; Yonemori K; Kawai A; Fukayama M; Hiraoka N
[Ad] Endereço:Departments of *Pathology and Clinical Laboratories §Urology ∥Musculoskeletal Oncology ¶Medical Oncology, National Cancer Center Hospital ‡Rare Cancer Center, National Cancer Center Hospital †Department of Pathology, the University of Tokyo, Tokyo, Japan.
[Ti] Título:Dedifferentiated Liposarcoma With Epithelioid/Epithelial Features.
[So] Source:Am J Surg Pathol;41(11):1523-1531, 2017 Nov.
[Is] ISSN:1532-0979
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dedifferentiated liposarcoma (DDLPS) demonstrates a variety of growth patterns, and their histologic resemblance to other spindle cell mesenchymal tumors has been widely recognized. However, epithelioid morphology in DDLPS has only rarely been documented. Here, we report 6 cases of DDLPS with striking epithelioid/epithelial features. The patients were 5 men and 1 woman with a median age of 61 years. All tumors were located in the internal trunk. During follow-up of 1 to 41 months, local recurrence, distant metastases, and tumor-related death occurred in 4, 2, and 4 patients, respectively. Beside well-differentiated liposarcoma component and conventional high-grade spindle cell morphology, all tumors focally exhibited growth comprising small or large epithelioid cells in diffuse or sheet-like proliferation. Rhabdoid cells were present in 2 cases. All 5 tumors tested harbored MDM2 amplification. Cytokeratin and/or epithelial membrane antigen were at least focally positive in all 5 tumors tested. One case contained a small focus of novel heterologous epithelial differentiation with acinar structures, wherein cytokeratin, MOC31, and claudin-4 were diffusely expressed and H3K27me3 expression was lost. DDLPS with epithelioid/epithelial features may lead to misdiagnosis of carcinoma or mesothelioma, and their diagnosis should be based on correlation with clinicopathologic and molecular findings. The epithelioid morphology in DDLPS may suggest an aggressive behavior based on this small series. In addition, we document 2 cases of MDM2-amplified undifferentiated neoplasm with epithelioid features in the internal trunk that lacked association with well-differentiated liposarcoma histology and showed rapid clinical course. Whether these latter tumors belong to DDLPS with epithelioid features requires further study.
[Mh] Termos MeSH primário: Desdiferenciação Celular
Células Epiteliais/patologia
Células Epitelioides/patologia
Lipossarcoma/patologia
[Mh] Termos MeSH secundário: Idoso
Biomarcadores Tumorais/análise
Biomarcadores Tumorais/genética
Biópsia
Claudina-4/análise
Diagnóstico Diferencial
Progressão da Doença
Células Epiteliais/química
Células Epitelioides/química
Feminino
Amplificação de Genes
Histonas/análise
Seres Humanos
Imuno-Histoquímica
Hibridização in Situ Fluorescente
Queratinas/análise
Lipossarcoma/mortalidade
Lipossarcoma/secundário
Lipossarcoma/terapia
Masculino
Metilação
Meia-Idade
Mucina-1/análise
Recidiva Local de Neoplasia
Valor Preditivo dos Testes
Proteínas Proto-Oncogênicas c-mdm2/genética
Fatores de Tempo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (CLDN4 protein, human); 0 (Claudin-4); 0 (Histones); 0 (MUC1 protein, human); 0 (Mucin-1); 68238-35-7 (Keratins); EC 2.3.2.27 (MDM2 protein, human); EC 2.3.2.27 (Proto-Oncogene Proteins c-mdm2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE
[do] DOI:10.1097/PAS.0000000000000910


  6 / 499 MEDLINE  
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[PMID]:28636799
[Au] Autor:Boivin FJ; Schmidt-Ott KM
[Ad] Endereço:Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Canada.
[Ti] Título:Transcriptional mechanisms coordinating tight junction assembly during epithelial differentiation.
[So] Source:Ann N Y Acad Sci;1397(1):80-99, 2017 Jun.
[Is] ISSN:1749-6632
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Epithelial tissues form a selective barrier via direct cell-cell interactions to separate and establish concentration gradients between the different compartments of the body. Proper function and formation of this barrier rely on the establishment of distinct intercellular junction complexes. These complexes include tight junctions, adherens junctions, desmosomes, and gap junctions. The tight junction is by far the most diverse junctional complex in the epithelial barrier. Its composition varies greatly across different epithelial tissues to confer various barrier properties. Thus, epithelial cells rely on tightly regulated transcriptional mechanisms to ensure proper formation of the epithelial barrier and to achieve tight junction diversity. Here, we review different transcriptional mechanisms utilized during embryogenesis and disease development to promote tight junction assembly and maintenance of intercellular barrier integrity. We focus particularly on the Grainyhead-like transcription factors and ligand-activated nuclear hormone receptors, two central families of proteins in epithelialization.
[Mh] Termos MeSH primário: Diferenciação Celular
Células Epiteliais/metabolismo
Epitélio/metabolismo
Junções Íntimas/metabolismo
Transcrição Genética
[Mh] Termos MeSH secundário: Junções Aderentes/metabolismo
Animais
Caderinas/genética
Caderinas/metabolismo
Claudina-4/genética
Claudina-4/metabolismo
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Seres Humanos
Modelos Genéticos
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cadherins); 0 (Claudin-4); 0 (DNA-Binding Proteins); 0 (GRHL2 protein, human); 0 (Transcription Factors)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE
[do] DOI:10.1111/nyas.13367


  7 / 499 MEDLINE  
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[PMID]:28636798
[Au] Autor:Piontek A; Witte C; May Rose H; Eichner M; Protze J; Krause G; Piontek J; Schröder L
[Ad] Endereço:Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP), Structural Bioinformatics and Protein Design, Berlin, Germany.
[Ti] Título:A cCPE-based xenon biosensor for magnetic resonance imaging of claudin-expressing cells.
[So] Source:Ann N Y Acad Sci;1397(1):195-208, 2017 Jun.
[Is] ISSN:1749-6632
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The majority of malignant tumors originate from epithelial cells, and many of them are characterized by an overexpression of claudins (Cldns) and their mislocalization out of tight junctions. We utilized the C-terminal claudin-binding domain of Clostridium perfringens enterotoxin (cCPE), with its high affinity to specific members of the claudin family, as the targeting unit for a claudin-sensitive cancer biosensor. To overcome the poor sensitivity of conventional relaxivity-based magnetic resonance imaging (MRI) contrast agents, we utilized the superior sensitivity of xenon Hyper-CEST biosensors. We labeled cCPE for both xenon MRI and fluorescence detection. As one readout module, we employed a cryptophane (CrA) monoacid and, as the second, a fluorescein molecule. Both were conjugated separately to a biotin molecule via a polyethyleneglycol chemical spacer and later via avidin linked to GST-cCPE. Nontransfected HEK293 cells and HEK293 cells stably expressing Cldn4-FLAG were incubated with the cCPE-based biosensor. Fluorescence-based flow cytometry and xenon MRI demonstrated binding of the biosensor specifically to Cldn4-expressing cells. This study provides proof of concept for the use of cCPE as a carrier for diagnostic contrast agents, a novel approach for potential detection of Cldn3/-4-overexpressing tumors for noninvasive early cancer detection.
[Mh] Termos MeSH primário: Técnicas Biossensoriais/métodos
Claudina-4/metabolismo
Enterotoxinas/metabolismo
Imagem por Ressonância Magnética/métodos
Xenônio/química
[Mh] Termos MeSH secundário: Avidina/química
Claudina-3/química
Claudina-3/genética
Claudina-3/metabolismo
Claudina-4/química
Claudina-4/genética
Enterotoxinas/química
Enterotoxinas/genética
Citometria de Fluxo
Fluoresceínas/química
Células HEK293
Seres Humanos
Microscopia Confocal
Modelos Moleculares
Compostos Policíclicos/química
Polietilenoglicóis/química
Ligação Proteica
Estrutura Terciária de Proteína
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Claudin-3); 0 (Claudin-4); 0 (Enterotoxins); 0 (Fluoresceins); 0 (Polycyclic Compounds); 0 (cryptophane A); 0 (enterotoxin, Clostridium); 1405-69-2 (Avidin); 30IQX730WE (Polyethylene Glycols); 3H3U766W84 (Xenon)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE
[do] DOI:10.1111/nyas.13363


  8 / 499 MEDLINE  
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[PMID]:28545845
[Au] Autor:Baumholtz AI; Simard A; Nikolopoulou E; Oosenbrug M; Collins MM; Piontek A; Krause G; Piontek J; Greene NDE; Ryan AK
[Ad] Endereço:Department of Human Genetics, McGill University, Canada; The Research Institute of the McGill University Health Centre, Montréal, Québec, Canada. Electronic address: amanda.baumholtz@mail.mcgill.ca.
[Ti] Título:Claudins are essential for cell shape changes and convergent extension movements during neural tube closure.
[So] Source:Dev Biol;428(1):25-38, 2017 08 01.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:During neural tube closure, regulated changes at the level of individual cells are translated into large-scale morphogenetic movements to facilitate conversion of the flat neural plate into a closed tube. Throughout this process, the integrity of the neural epithelium is maintained via cell interactions through intercellular junctions, including apical tight junctions. Members of the claudin family of tight junction proteins regulate paracellular permeability, apical-basal cell polarity and link the tight junction to the actin cytoskeleton. Here, we show that claudins are essential for neural tube closure: the simultaneous removal of Cldn3, -4 and -8 from tight junctions caused folate-resistant open neural tube defects. Their removal did not affect cell type differentiation, neural ectoderm patterning nor overall apical-basal polarity. However, apical accumulation of Vangl2, RhoA, and pMLC were reduced, and Par3 and Cdc42 were mislocalized at the apical cell surface. Our data showed that claudins act upstream of planar cell polarity and RhoA/ROCK signaling to regulate cell intercalation and actin-myosin contraction, which are required for convergent extension and apical constriction during neural tube closure, respectively.
[Mh] Termos MeSH primário: Polaridade Celular/fisiologia
Forma Celular/fisiologia
Placa Neural/embriologia
Tubo Neural/embriologia
Neurulação/fisiologia
Junções Íntimas/fisiologia
[Mh] Termos MeSH secundário: Citoesqueleto de Actina/metabolismo
Animais
Moléculas de Adesão Celular/metabolismo
Embrião de Galinha
Claudina-3/genética
Claudina-3/metabolismo
Claudina-4/genética
Claudina-4/metabolismo
Claudinas/genética
Claudinas/metabolismo
Técnicas de Cultura Embrionária
Camundongos
Morfogênese/fisiologia
Proteínas do Tecido Nervoso/metabolismo
Defeitos do Tubo Neural/genética
Transdução de Sinais/fisiologia
Proteína cdc42 de Ligação ao GTP/metabolismo
Proteínas rho de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cdc42 protein, mouse); 0 (Cell Adhesion Molecules); 0 (Claudin-3); 0 (Claudin-4); 0 (Claudins); 0 (Cldn3 protein, mouse); 0 (Cldn4 protein, mouse); 0 (Ltap protein, mouse); 0 (Nerve Tissue Proteins); 0 (Pard3 protein, mouse); 0 (claudin 8); EC 3.6.5.2 (RhoA protein, mouse); EC 3.6.5.2 (cdc42 GTP-Binding Protein); EC 3.6.5.2 (rho GTP-Binding Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170527
[St] Status:MEDLINE


  9 / 499 MEDLINE  
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[PMID]:28493961
[Au] Autor:Molina-Jijón E; Rodríguez-Muñoz R; González-Ramírez R; Namorado-Tónix C; Pedraza-Chaverri J; Reyes JL
[Ad] Endereço:Department of Physiology, Biophysics and Neuroscience, Center for Research and Advanced Studies of the National Polytechnic Institute (CINVESTAV-IPN), Mexico City, México.
[Ti] Título:Aldosterone signaling regulates the over-expression of claudin-4 and -8 at the distal nephron from type 1 diabetic rats.
[So] Source:PLoS One;12(5):e0177362, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hyperglycemia in diabetes alters tight junction (TJ) proteins in the kidney. We evaluated the participation of aldosterone (ALD), and the effect of spironolactone (SPL), a mineralocorticoid receptor antagonist, on the expressions of claudin-2, -4, -5 and -8, and occludin in glomeruli, proximal and distal tubules isolated from diabetic rats. Type 1 diabetes was induced in female Wistar rats by a single tail vein injection of streptozotocin (STZ), and SPL was administrated daily by gavage, from days 3-21. Twenty-one days after STZ injection the rats were sacrificed. In diabetic rats, the serum ALD levels were increased, and SPL-treatment did not have effect on these levels or in hyperglycemia, however, proteinuria decreased in SPL-treated diabetic rats. Glomerular damage, evaluated by nephrin and Wilm's tumor 1 (WT1) protein expressions, and proximal tubular damage, evaluated by kidney injury molecule 1 (Kim-1) and heat shock protein 72 kDa (Hsp72) expressions, were ameliorated by SPL. Also, SPL prevented decrement in claudin-5 in glomeruli, and claudin-2 and occludin in proximal tubules by decreasing oxidative stress, evaluated by superoxide anion (O2●-) production, and oxidative stress markers. In distal tubules, SPL ameliorated increase in mRNA, protein expression, and phosphorylation in threonine residues of claudin-4 and -8, through a serum and glucocorticoid-induced kinase 1 (SGK1), and with-no-lysine kinase 4 (WNK4) signaling pathway. In conclusion, this is the first study that demonstrates that ALD modulates the expression of renal TJ proteins in diabetes, and that the blockade of its actions with SPL, may be a promising therapeutic strategy to prevent alterations of TJ proteins in diabetic nephropathy.
[Mh] Termos MeSH primário: Aldosterona/metabolismo
Claudina-4/metabolismo
Claudinas/metabolismo
Diabetes Mellitus Experimental/metabolismo
Diabetes Mellitus Tipo 1/metabolismo
Néfrons/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Diabetes Mellitus Experimental/sangue
Diabetes Mellitus Experimental/complicações
Diabetes Mellitus Experimental/patologia
Diabetes Mellitus Tipo 1/sangue
Diabetes Mellitus Tipo 1/complicações
Diabetes Mellitus Tipo 1/patologia
Feminino
Hiperglicemia/sangue
Hiperglicemia/tratamento farmacológico
Hiperglicemia/prevenção & controle
Proteínas Imediatamente Precoces/metabolismo
Glomérulos Renais/efeitos dos fármacos
Glomérulos Renais/patologia
Túbulos Renais/efeitos dos fármacos
Túbulos Renais/patologia
Modelos Biológicos
Natriurese/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
Fosforilação/efeitos dos fármacos
Potássio/sangue
Proteínas Serina-Treonina Quinases/metabolismo
Proteinúria/sangue
Proteinúria/complicações
Proteinúria/tratamento farmacológico
Proteinúria/prevenção & controle
Ratos Wistar
Transdução de Sinais/efeitos dos fármacos
Espironolactona/farmacologia
Espironolactona/uso terapêutico
Junções Íntimas/efeitos dos fármacos
Junções Íntimas/metabolismo
Perda de Peso/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Claudin-4); 0 (Claudins); 0 (Immediate-Early Proteins); 0 (claudin 8); 27O7W4T232 (Spironolactone); 4964P6T9RB (Aldosterone); EC 2.7.1.- (Prkwnk4 protein, rat); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (serum-glucocorticoid regulated kinase); RWP5GA015D (Potassium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170512
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0177362


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[PMID]:28415141
[Au] Autor:Hashimoto Y; Fukasawa M; Kuniyasu H; Yagi K; Kondoh M
[Ad] Endereço:Graduate School of Pharmaceutical Sciences, Osaka University, Suita, Osaka, Japan.
[Ti] Título:Claudin-targeted drug development using anti-claudin monoclonal antibodies to treat hepatitis and cancer.
[So] Source:Ann N Y Acad Sci;1397(1):5-16, 2017 Jun.
[Is] ISSN:1749-6632
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The 27-member family of tetraspan membrane proteins known as claudins (CLDNs) is a major component of tight junctions. A series of studies elucidating the relationship between CLDNs and various pathological conditions has provided new insights into drug development. For instance, CLDN-1 may be a potent target for epidermal absorption of drugs and for treating hepatitis C virus (HCV) infection. CLDN-4 may be a target for treating cancer. Because CLDNs are also expressed in various normal tissues, safety and efficacy evaluations are critical for translational research. We previously developed several anti-CLDN antibodies and have established proof of concept for CLDN-targeted drug development using these reagents. Here, we provide an overview of CLDN-1 as a target for improving epidermal drug absorption and preventing HCV infection and of CLDN-4 as a target for anticancer therapeutics.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/uso terapêutico
Claudina-1/metabolismo
Claudina-4/metabolismo
Hepacivirus/efeitos dos fármacos
Hepatite C/tratamento farmacológico
Neoplasias/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Claudina-1/imunologia
Claudina-4/imunologia
Epiderme/metabolismo
Hepacivirus/fisiologia
Hepatite C/virologia
Seres Humanos
Junções Íntimas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Claudin-1); 0 (Claudin-4)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170418
[St] Status:MEDLINE
[do] DOI:10.1111/nyas.13337



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