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[PMID]:28453684
[Au] Autor:Gupta S; De Puysseleyr V; Van der Heyden J; Maddelein D; Lemmens I; Lievens S; Degroeve S; Tavernier J; Martens L
[Ad] Endereço:Medical Biotechnology Center, VIB, Ghent, Belgium.
[Ti] Título:MAPPI-DAT: data management and analysis for protein-protein interaction data from the high-throughput MAPPIT cell microarray platform.
[So] Source:Bioinformatics;33(9):1424-1425, 2017 May 01.
[Is] ISSN:1367-4811
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Summary: Protein-protein interaction (PPI) studies have dramatically expanded our knowledge about cellular behaviour and development in different conditions. A multitude of high-throughput PPI techniques have been developed to achieve proteome-scale coverage for PPI studies, including the microarray based Mammalian Protein-Protein Interaction Trap (MAPPIT) system. Because such high-throughput techniques typically report thousands of interactions, managing and analysing the large amounts of acquired data is a challenge. We have therefore built the MAPPIT cell microArray Protein Protein Interaction-Data management & Analysis Tool (MAPPI-DAT) as an automated data management and analysis tool for MAPPIT cell microarray experiments. MAPPI-DAT stores the experimental data and metadata in a systematic and structured way, automates data analysis and interpretation, and enables the meta-analysis of MAPPIT cell microarray data across all stored experiments. Availability and Implementation: MAPPI-DAT is developed in Python, using R for data analysis and MySQL as data management system. MAPPI-DAT is cross-platform and can be ran on Microsoft Windows, Linux and OS X/macOS. The source code and a Microsoft Windows executable are freely available under the permissive Apache2 open source license at https://github.com/compomics/MAPPI-DAT. Contact: jan.tavernier@vib-ugent.be or lennart.martens@vib-ugent.be. Supplementary information: Supplementary data are available at Bioinformatics online.
[Mh] Termos MeSH primário: Análise Serial de Proteínas/métodos
Mapeamento de Interação de Proteínas/métodos
Software
[Mh] Termos MeSH secundário: Animais
Ensaios de Triagem em Larga Escala/métodos
Seres Humanos
Mamíferos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/bioinformatics/btx014


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[PMID]:28460635
[Au] Autor:Chen I; Mathews-Greiner L; Li D; Abisoye-Ogunniyan A; Ray S; Bian Y; Shukla V; Zhang X; Guha R; Thomas C; Gryder B; Zacharia A; Beane JD; Ravichandran S; Ferrer M; Rudloff U
[Ad] Endereço:Thoracic and Gastrointestinal Oncology Branch, National Cancer Institute, National Institutes for Health, CCR 4 West/4-3740, 10 Center Drive, Bethesda, MD, 20892-0001, USA.
[Ti] Título:Transcriptomic profiling and quantitative high-throughput (qHTS) drug screening of CDH1 deficient hereditary diffuse gastric cancer (HDGC) cells identify treatment leads for familial gastric cancer.
[So] Source:J Transl Med;15(1):92, 2017 May 01.
[Is] ISSN:1479-5876
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Patients with hereditary diffuse gastric cancer (HDGC), a cancer predisposition syndrome associated with germline mutations of the CDH1 (E-cadherin) gene, have few effective treatment options. Despite marked differences in natural history, histopathology, and genetic profile to patients afflicted by sporadic gastric cancer, patients with HDGC receive, in large, identical systemic regimens. The lack of a robust preclinical in vitro system suitable for effective drug screening has been one of the obstacles to date which has hampered therapeutic advances in this rare disease. METHODS: In order to identify therapeutic leads selective for the HDGC subtype of gastric cancer, we compared gene expression profiles and drug phenotype derived from an oncology library of 1912 compounds between gastric cancer cells established from a patient with metastatic HDGC harboring a c.1380delA CDH1 germline variant and sporadic gastric cancer cells. RESULTS: Unsupervised hierarchical cluster analysis shows select gene expression alterations in c.1380delA CDH1 SB.mhdgc-1 cells compared to a panel of sporadic gastric cancer cell lines with enrichment of ERK1-ERK2 (extracellular signal regulated kinase) and IP3 (inositol trisphosphate)/DAG (diacylglycerol) signaling as the top networks in c.1380delA SB.mhdgc-1 cells. Intracellular phosphatidylinositol intermediaries were increased upon direct measure in c.1380delA CDH1 SB.mhdgc-1 cells. Differential high-throughput drug screening of c.1380delA CDH1 SB.mhdgc-1 versus sporadic gastric cancer cells identified several compound classes with enriched activity in c.1380 CDH1 SB.mhdgc-1 cells including mTOR (Mammalian Target Of Rapamycin), MEK (Mitogen-Activated Protein Kinase), c-Src kinase, FAK (Focal Adhesion Kinase), PKC (Protein Kinase C), or TOPO2 (Topoisomerase II) inhibitors. Upon additional drug response testing, dual PI3K (Phosphatidylinositol 3-Kinase)/mTOR and topoisomerase 2A inhibitors displayed up to >100-fold increased activity in hereditary c.1380delA CDH1 gastric cancer cells inducing apoptosis most effectively in cells with deficient CDH1 function. CONCLUSION: Integrated pharmacological and transcriptomic profiling of hereditary diffuse gastric cancer cells with a loss-of-function c.1380delA CDH1 mutation implies various pharmacological vulnerabilities selective to CDH1-deficient familial gastric cancer cells and suggests novel treatment leads for future preclinical and clinical treatment studies of familial gastric cancer.
[Mh] Termos MeSH primário: Caderinas/deficiência
Avaliação Pré-Clínica de Medicamentos
Perfilação da Expressão Gênica
Ensaios de Triagem em Larga Escala
Neoplasias Gástricas/tratamento farmacológico
Neoplasias Gástricas/genética
[Mh] Termos MeSH secundário: Adulto
Caderinas/genética
Linhagem Celular Tumoral
Diglicerídeos/metabolismo
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Feminino
Regulação Neoplásica da Expressão Gênica
Predisposição Genética para Doença
Mutação em Linhagem Germinativa/genética
Seres Humanos
Fosfatos de Inositol/metabolismo
Masculino
Linhagem
Reprodutibilidade dos Testes
Neoplasias Gástricas/patologia
Regulação para Cima/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDH1 protein, human); 0 (Cadherins); 0 (Diglycerides); 0 (Inositol Phosphates); 0 (inositol 3,4,5-trisphosphate); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
[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:10.1186/s12967-017-1197-5


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[PMID]:28460441
[Au] Autor:Arora J; Sauer SJ; Tarpley M; Vermeulen P; Rypens C; Van Laere S; Williams KP; Devi GR; Dewhirst MW
[Ad] Endereço:Duke Cancer Institute, Duke University, Durham, NC, USA.
[Ti] Título:Inflammatory breast cancer tumor emboli express high levels of anti-apoptotic proteins: use of a quantitative high content and high-throughput 3D IBC spheroid assay to identify targeting strategies.
[So] Source:Oncotarget;8(16):25848-25863, 2017 Apr 18.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inflammatory breast cancer (IBC) is one of the most lethal breast cancer variants; with existing therapy, 5-yr survival rate is only 35%. Current barriers to successful treatment of IBC include frequent infiltration and the presence of tumor cell clusters, termed tumor emboli, within the breast parenchyma and lymphatics. Prior studies have identified the role of anti-apoptotic signaling, in particular hyperactivation of NFκB and its target genes, in IBC pathobiology and therapeutic resistance. The objectives of this study were to: (1) determine if IBC tumor emboli express anti-apoptotic proteins and (2) develop a high content, multiparametric assay to assess the morphology of the IBC 3D spheroids and to optimize a high throughput format to screen for compounds that can inhibit the formation of the IBC tumor clusters/embolic structures. Immunohistochemical analysis of IBC patient tumor samples with documented tumor emboli revealed high NFκB (p65) staining along with expression of XIAP, a potent anti-apoptotic protein known to interact with NFκB signaling in enhancing survival of malignant cells. Subsequently, the high content assay developed allowed for simultaneous imaging and morphometric analysis, including count and viability of spheroids derived from SUM149, rSUM149 and SUM190 cells and its application to evaluate XIAP and NFκB inhibitory agents. We demonstrate the efficacy of the off-patent drug disulfiram when chelated with copper, which we had previously reported to inhibit NFκB signaling, was highly effective in disrupting both IBC spheroids and emboli grown in vitro. Taken together, these results identify a high-throughput approach to target tumor spheroid formation for drug discovery. Finally, disulfiram is a safe and approved drug for management of alcohol abuse, warranting its evaluation for repurposing in IBC therapy.
[Mh] Termos MeSH primário: Proteínas Reguladoras de Apoptose/genética
Neoplasias Inflamatórias Mamárias/genética
Neoplasias Inflamatórias Mamárias/patologia
Células Neoplásicas Circulantes/metabolismo
[Mh] Termos MeSH secundário: Proteínas Reguladoras de Apoptose/metabolismo
Biomarcadores Tumorais
Técnicas de Cultura de Células
Sobrevivência Celular/genética
Cobre/farmacologia
Dissulfiram/farmacologia
Feminino
Expressão Gênica
Ensaios de Triagem em Larga Escala
Seres Humanos
Neoplasias Inflamatórias Mamárias/metabolismo
Mitocôndrias/metabolismo
NF-kappa B/genética
NF-kappa B/metabolismo
Esferoides Celulares
Células Tumorais Cultivadas
Proteínas Inibidoras de Apoptose Ligadas ao Cromossomo X/genética
Proteínas Inibidoras de Apoptose Ligadas ao Cromossomo X/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apoptosis Regulatory Proteins); 0 (Biomarkers, Tumor); 0 (NF-kappa B); 0 (X-Linked Inhibitor of Apoptosis Protein); 0 (XIAP protein, human); 789U1901C5 (Copper); TR3MLJ1UAI (Disulfiram)
[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.15667


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[PMID]:27774815
[Au] Autor:Kassegne K; Abe EM; Chen JH; Zhou XN
[Ad] Endereço:a National Institute of Parasitic Diseases, Chinese Center for Disease Control and Prevention, WHO Collaborating Centre for Tropical Diseases, National Center for International Research on Tropical Diseases, Key Laboratory of Parasite and Vector Biology of the Chinese Ministry of Health , Shanghai ,
[Ti] Título:Immunomic approaches for antigen discovery of human parasites.
[So] Source:Expert Rev Proteomics;13(12):1091-1101, 2016 12.
[Is] ISSN:1744-8387
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Genetics combined with proteomics allows for a better understanding of parasite-host interactions and host immune responses. Immunomics elucidates that antigens are targets of induced or naturally acquired immunity (NAI), a promising solution to the challenge of eradicating human infections. High-throughput protein microarrays enhance rapid antigen discovery for the development of serodiagnostic tests/vaccines. Areas covered: This review systematically analyzes the emergence of protein microarrays as a powerful technology for parasite antigen discovery and subsequently summarizes some of the attributes and disadvantages of these approaches. Major insights on novel/validated serological biomarkers or vaccine candidates against malaria and Neglected Tropical Diseases (NTDs) are highlighted. We conclude with a brief description of the processes involved in immunomic protein microarrays. Expert commentary: Interesting discoveries have been made using protein microarrays. However, there is a need to evaluate targets that elicit strong immunogenicity and correlates of protective efficacy to aid prioritization and guide further clinical development. The goal of parasitic disease elimination will be best achieved through an integrated strategy that will incorporate and implement the different control components.
[Mh] Termos MeSH primário: Antígenos de Helmintos
Parasitos/imunologia
Análise Serial de Proteínas/métodos
Proteômica/métodos
Vacinas
[Mh] Termos MeSH secundário: Animais
Ensaios de Triagem em Larga Escala/métodos
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, Helminth); 0 (Vaccines)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161108
[St] Status:MEDLINE


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[PMID]:29385160
[Au] Autor:Just S; Chenard BL; Ceci A; Strassmaier T; Chong JA; Blair NT; Gallaschun RJ; Del Camino D; Cantin S; D'Amours M; Eickmeier C; Fanger CM; Hecker C; Hessler DP; Hengerer B; Kroker KS; Malekiani S; Mihalek R; McLaughlin J; Rast G; Witek J; Sauer A; Pryce CR; Moran MM
[Ad] Endereço:Boehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
[Ti] Título:Treatment with HC-070, a potent inhibitor of TRPC4 and TRPC5, leads to anxiolytic and antidepressant effects in mice.
[So] Source:PLoS One;13(1):e0191225, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Forty million adults in the US suffer from anxiety disorders, making these the most common forms of mental illness. Transient receptor potential channel canonical subfamily (TRPC) members 4 and 5 are non-selective cation channels highly expressed in regions of the cortex and amygdala, areas thought to be important in regulating anxiety. Previous work with null mice suggests that inhibition of TRPC4 and TRPC5 may have anxiolytic effects. HC-070 IN VITRO: To assess the potential of TRPC4/5 inhibitors as an avenue for treatment, we invented a highly potent, small molecule antagonist of TRPC4 and TRPC5 which we call HC-070. HC-070 inhibits recombinant TRPC4 and TRPC5 homomultimers in heterologous expression systems with nanomolar potency. It also inhibits TRPC1/5 and TRPC1/4 heteromultimers with similar potency and reduces responses evoked by cholecystokinin tetrapeptide (CCK-4) in the amygdala. The compound is >400-fold selective over a wide range of molecular targets including ion channels, receptors, and kinases. HC-070 IN VIVO: Upon oral dosing in mice, HC-070 achieves exposure levels in the brain and plasma deemed sufficient to test behavioral activity. Treatment with HC-070 attenuates the anxiogenic effect of CCK-4 in the elevated plus maze (EPM). The compound recapitulates the phenotype observed in both null TRPC4 and TRPC5 mice in a standard EPM. Anxiolytic and anti-depressant effects of HC-070 are also observed in pharmacological in vivo tests including marble burying, tail suspension and forced swim. Furthermore, HC-070 ameliorates the increased fear memory induced by chronic social stress. A careful evaluation of the pharmacokinetic-pharmacodynamic relationship reveals that substantial efficacy is observed at unbound brain levels similar to, or even lower than, the 50% inhibitory concentration (IC50) recorded in vitro, increasing confidence that the observed effects are indeed mediated by TRPC4 and/or TRPC5 inhibition. Together, this experimental data set introduces a novel, high quality, small molecule antagonist of TRPC4 and TRPC5 containing channels and supports the targeting of TRPC4 and TRPC5 channels as a new mechanism of action for the treatment of psychiatric symptoms.
[Mh] Termos MeSH primário: Ansiolíticos/farmacologia
Antidepressivos/farmacologia
Compostos Heterocíclicos de 4 ou mais Anéis/farmacologia
Canais de Cátion TRPC/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Ansiolíticos/química
Ansiolíticos/farmacocinética
Antidepressivos/química
Antidepressivos/farmacocinética
Ansiedade/tratamento farmacológico
Ansiedade/metabolismo
Ansiedade/psicologia
Complexo Nuclear Basolateral da Amígdala/efeitos dos fármacos
Complexo Nuclear Basolateral da Amígdala/metabolismo
Comportamento Animal/efeitos dos fármacos
Depressão/tratamento farmacológico
Depressão/metabolismo
Depressão/psicologia
Modelos Animais de Doenças
Medo/efeitos dos fármacos
Medo/fisiologia
Medo/psicologia
Compostos Heterocíclicos de 4 ou mais Anéis/química
Compostos Heterocíclicos de 4 ou mais Anéis/farmacocinética
Ensaios de Triagem em Larga Escala
Seres Humanos
Técnicas In Vitro
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Anxiety Agents); 0 (Antidepressive Agents); 0 (HC-070); 0 (Heterocyclic Compounds, 4 or More Rings); 0 (TRPC Cation Channels); 0 (TRPC4 ion channel); 0 (TRPC5 protein, human); 0 (Trpc5 protein, mouse)
[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:180201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191225


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[PMID]:28470618
[Au] Autor:Black C; Barker JJ; Hitchman RB; Kwong HS; Festenstein S; Acton TB
[Ad] Endereço:Evotec Ltd, 114 Innovation Drive, Milton Park, Abingdon, Oxfordshire, OX14 4RZ, UK.
[Ti] Título:High-Throughput Production of Proteins in E. coli for Structural Studies.
[So] Source:Methods Mol Biol;1586:359-371, 2017.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We have developed a standardized and efficient workflow for high-throughput (HT) protein expression in E. coli and parallel purification which can be tailored to the downstream application of the target proteins. It includes a one-step purification for the purposes of functional assays and a two-step protocol for crystallographic studies, with the option of on-column tag removal.
[Mh] Termos MeSH primário: Clonagem Molecular/métodos
Escherichia coli/genética
Proteínas Recombinantes/genética
[Mh] Termos MeSH secundário: Animais
Eletroforese em Gel de Poliacrilamida/métodos
Ensaios de Triagem em Larga Escala/economia
Ensaios de Triagem em Larga Escala/métodos
Seres Humanos
Conformação Proteica
Proteômica/métodos
Proteínas Recombinantes/química
Proteínas Recombinantes/isolamento & purificação
Transformação Genética
Fluxo de Trabalho
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Recombinant Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-4939-6887-9_24


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[PMID]:29305325
[Au] Autor:Kurokawa YK; Shang MR; Yin RT; George SC
[Ad] Endereço:Department of Biomedical Engineering, Washington University in St. Louis, St. Louis, MO 63130, United States.
[Ti] Título:Modeling trastuzumab-related cardiotoxicity in vitro using human stem cell-derived cardiomyocytes.
[So] Source:Toxicol Lett;285:74-80, 2018 Mar 15.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Trastuzumab (Herceptin ), a monoclonal antibody against the ErbB2 (HER2) receptor, has significantly improved clinical outcomes for HER2 breast cancer patients. However, the drug also has known cardiotoxic side effects through mechanisms that are not fully understood. Here we utilized human induced pluripotent stem cell-derived cardiomyocytes (iPS-CMs) to model trastuzumab-related cardiotoxicity in vitro. We demonstrate that cardiotoxic effects of ErbB2 inhibition by trastuzumab can be recapitulated only when the cardioprotective effects of ErbB2/4 signaling is observed. We observed no cardioprotective effects of ErbB2/4 signaling without cellular stress (doxorubicin exposure in this study). In addition to neuregulin-1 (NRG-1), we show that heparin-binding epidermal growth factor-like growth factor (HB-EGF) also provides cardioprotective effects for iPS-CMs. Finally, we demonstrate a simple, high-throughput co-culture platform utilizing iPS-CMs and endothelial cells that is capable of detecting trastuzumab-related cardiotoxicity. We conclude that iPS-CMs can recapitulate trastuzumab-related cardiotoxicity, and may be used to elucidate additional modes of toxicity of trastuzumab and related compounds.
[Mh] Termos MeSH primário: Antineoplásicos Imunológicos/toxicidade
Células-Tronco Pluripotentes Induzidas/efeitos dos fármacos
Modelos Biológicos
Miócitos Cardíacos/efeitos dos fármacos
Receptor ErbB-2/antagonistas & inibidores
Trastuzumab/toxicidade
[Mh] Termos MeSH secundário: Cardiotoxicidade
Diferenciação Celular/efeitos dos fármacos
Células Cultivadas
Técnicas de Cocultura
Ensaios de Triagem em Larga Escala
Seres Humanos
Células-Tronco Pluripotentes Induzidas/citologia
Células-Tronco Pluripotentes Induzidas/enzimologia
L-Lactato Desidrogenase/secreção
Miócitos Cardíacos/citologia
Miócitos Cardíacos/enzimologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Immunological); EC 1.1.1.27 (L-Lactate Dehydrogenase); EC 2.7.10.1 (Receptor, ErbB-2); P188ANX8CK (Trastuzumab)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180107
[St] Status:MEDLINE


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[PMID]:28470533
[Au] Autor:Öz S; Breiling A; Maercker C
[Ad] Endereço:German Cancer Research Center (DKFZ), Epigenomics and Cancer Risk Factors, Heidelberg, Germany.
[Ti] Título:Measurement of Cellular Behavior by Electrochemical Impedance Sensing.
[So] Source:Methods Mol Biol;1601:267-273, 2017.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:There is a great demand for label-free in vitro assays in a high-throughput context, in order to measure cell viability and analyze cellular functions like cell migration or cell differentiation under noninvasive conditions. Here, we describe impedance measurement to quantify dynamic changes on cell morphology in real time. In order to monitor physiological changes, cells are grown in tissue culture vessels where gold electrodes are incorporated at the bottom. An alternating current signal of several kHz is applied to the electrodes and the resulting voltage is measured to calculate the cellular impedance. Since impedance is closely related to the area of the electrodes covered by the growing cells, parameters such as cell number, size of the cells attached to the electrodes, and cell-cell and cell-substrate/extracellular matrix interactions contribute to the overall impedance values.
[Mh] Termos MeSH primário: Diferenciação Celular/fisiologia
Movimento Celular/fisiologia
Sobrevivência Celular/fisiologia
Impedância Elétrica
[Mh] Termos MeSH secundário: Adesão Celular/fisiologia
Comunicação Celular/fisiologia
Contagem de Células
Tamanho Celular
Eletrodos
Células-Tronco de Carcinoma Embrionário/química
Matriz Extracelular/química
Ouro/química
Ensaios de Triagem em Larga Escala
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
7440-57-5 (Gold)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-4939-6960-9_21


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[PMID]:28470517
[Au] Autor:Menzner AK; Gilbert DF
[Ad] Endereço:Department of Internal Medicine 5, University Medical Center Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
[Ti] Título:A Protocol for In Vitro High-Throughput Chemical Susceptibility Screening in Differentiating NT2 Stem Cells.
[So] Source:Methods Mol Biol;1601:61-70, 2017.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The incidence of neurological diseases including learning and developmental disorders has increased in recent years. Concurrently, the number and volume of worldwide registered and traded chemicals have also increased. There is a broad consensus that the developing brain is particularly sensitive to damage by chemicals and that evaluation of chemicals for developmental toxicity or neurotoxicity is critical to human health. Human pluripotent embryonal carcinoma (NTERA-2 or NT2) cells are increasingly considered as a suitable model for in vitro developmental toxicity and neurotoxicity (DT/DNT) studies as they undergo neuronal differentiation upon stimulation with retinoic acid (RA) and allow toxicity assessment at different stages of maturation. Here we describe a protocol for cell fitness screening in differentiating NT2 cells based on the analysis of intracellular ATP levels allowing for the identification of chemicals which are potentially harmful to the developing brain. The described method is suitable to be adapted to low-, medium-, and high-throughput screening and allows multiplexing with other cell fitness indicators. While the presented protocol focuses on cell fitness screening in human pluripotent stem cells it may also be applied to other in vitro models.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
Encéfalo/embriologia
Sobrevivência Celular/efeitos dos fármacos
Células-Tronco de Carcinoma Embrionário/efeitos dos fármacos
Ensaios de Triagem em Larga Escala/métodos
Células-Tronco Pluripotentes/efeitos dos fármacos
Testes de Toxicidade
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Diferenciação Celular/efeitos dos fármacos
Avaliação Pré-Clínica de Medicamentos
Seres Humanos
Neurônios/citologia
Neurônios/efeitos dos fármacos
Bibliotecas de Moléculas Pequenas/toxicidade
Tretinoína/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Small Molecule Libraries); 5688UTC01R (Tretinoin); 8L70Q75FXE (Adenosine Triphosphate)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-4939-6960-9_5


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[PMID]:28470516
[Au] Autor:Ivanov DP; Grabowska AM; Garnett MC
[Ad] Endereço:Cancer Biology, Division of Cancer and Stem Cells, School of Medicine, Queen's Medical Centre, University of Nottingham, Nottingham, NG7 2UH, UK. delyan.ivanov@nottingham.ac.uk.
[Ti] Título:High-Throughput Spheroid Screens Using Volume, Resazurin Reduction, and Acid Phosphatase Activity.
[So] Source:Methods Mol Biol;1601:43-59, 2017.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mainstream adoption of physiologically relevant three-dimensional models has been slow in the last 50 years due to long, manual protocols with poor reproducibility, high price, and closed commercial platforms. This chapter describes high-throughput, low-cost, open methods for spheroid viability assessment which use readily available reagents and open-source software to analyze spheroid volume, metabolism, and enzymatic activity. We provide two ImageJ macros for automated spheroid size determination-for both single images and images in stacks. We also share an Excel template spreadsheet allowing users to rapidly process spheroid size data, analyze plate uniformity (such as edge effects and systematic seeding errors), detect outliers, and calculate dose-response. The methods would be useful to researchers in preclinical and translational research planning to move away from simplistic monolayer studies and explore 3D spheroid screens for drug safety and efficacy without substantial investment in money or time.
[Mh] Termos MeSH primário: Sobrevivência Celular
Ensaios de Triagem em Larga Escala/métodos
Indicadores e Reagentes/metabolismo
Esferoides Celulares/fisiologia
[Mh] Termos MeSH secundário: Fosfatase Ácida/metabolismo
Encéfalo/citologia
Linhagem Celular Tumoral
Relação Dose-Resposta a Droga
Avaliação Pré-Clínica de Medicamentos
Ensaios de Triagem em Larga Escala/economia
Seres Humanos
Processamento de Imagem Assistida por Computador
Oxazinas/química
Reprodutibilidade dos Testes
Sensibilidade e Especificidade
Software
Esferoides Celulares/citologia
Esferoides Celulares/metabolismo
Fatores de Tempo
Xantenos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Indicators and Reagents); 0 (Oxazines); 0 (Xanthenes); 1FN9YD6968 (resazurin); EC 3.1.3.2 (Acid Phosphatase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-4939-6960-9_4



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