Thematische Bibliographien / Transwell test

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Auswahl der wissenschaftlichen Literatur zum Thema „Transwell test“

Autor: Grafiati

Veröffentlicht am 28. Juni 2021

Zuletzt aktualisiert am 18. Februar 2022

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Zeitschriftenartikel zum Thema "Transwell test"

Bates, Amber, Carol Fischer, Vrushali Abhyankar, Georgia Johnson, Janet Guthmiller, Ann Progulske-Fox und Kim Brogden. „Matrix Metalloproteinase Response of Dendritic Cell, Gingival Epithelial Keratinocyte, and T-Cell Transwell Co-Cultures Treated with Porphyromonas gingivalis Hemagglutinin-B“. International Journal of Molecular Sciences 19, Nr. 12 (07.12.2018): 3923. http://dx.doi.org/10.3390/ijms19123923.

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Matrix metalloproteinases (MMPs) are enzymes involved in periodontal tissue destruction. Hemagglutinin B (HagB) from the periodontal pathogen Porphyromonas gingivalis induces an elevated MMP response in dendritic cells, but responses from cultures of single-cell types do not reflect the local tissue environment. The objective of this study was to measure HagB-induced MMP responses in a transwell co-culture system containing dendritic cells, gingival epithelial (GE) keratinocytes, and CD4+ T-cells. Transwell co-cultures were assembled and treated with or without HagB. Immunoassays were used to determine production of MMP1, MMP7, MMP9, and MMP12 in response to HagB up to 64 h. Control responses were subtracted from HagB-induced responses. A two-way fixed effect ANOVA was fit to log-transformed concentrations and pairwise group comparisons were conducted (p < 0.05). At 64 h, dendritic cells produced elevated MMP1 and MMP9 responses, which were attenuated in the 3-cell co-culture (p < 0.05). There were also significant differences in MMP7 and MMP12 production between single-cell cultures and co-cultures. These results support the need to use multiple cell types in culture models to evaluate a more representative response to proinflammatory agonists. This three-cell transwell co-culture model may help us better understand the inflammatory process in periodontal disease and test novel therapeutic approaches.

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Hua, Li, und Han Zhengxue. „The chemotaxis study of adipose derived stem cells (ADSCs) to adenoid cystic carcinoma (ACC) cells.“ Journal of Clinical Oncology 31, Nr. 15_suppl (20.05.2013): e17000-e17000. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e17000.

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e17000 Background: Adenoid cystic carcinoma (ACC) has some properties such as neurotropic, angiotropic and early metastasis, recurrence and metastasis is the leading cause of poor prognosis in sACC. The current theory is that the invasion and metastasis were related to tumor stem cells, and the stem cell microenvironment play an important role in this process. According to the stem cell theory, we hypothesized that normal tissue stem cells may also produce chemotactic migration to tumor stem cell microenvironment, therefore this research was to explore the possibility of adipose derived stem cells as a therapy vector targeted to the microenvironment of ACC. Methods: Conventionally culture ACC cells to logarithmic growth phase, then collected them and cultured in serum-free medium. After 48 h, the culture supernatant was collected, filtered and prewarmed, and then added to each well (24-well plate, the lower chamber of the transwell chamber), 600-800 ul for each. Using the same method, the culture supernatant of T293 cells were joined into the lower chamber as a control. Then, the transwell membrane was gently placed into the well, and 100 ~ 150μl suspension of adipose derived stem cells in the logarithmic growth phase (serum-free media) were added into the upper chamber. After cultured under routine conditions for 24 hours, the transwell chamber were removed , fixed and stained. Under bright field microscope, cells invasived and attached to the transwell membrane were observed and counted, results were statistically analyzed by student test. Results: Selecte five high-power microscopic field randomly, counted the number of adipose derived stem cells migrated to transwell membrane of different cell lines. Results showed that migrated cell number of SACC-LM group was 64.3 ± 7.6, the number of SACC-83 group was 52.3 ± 6.1, both higher than the T293 group (31.8 ± 6.3), and the difference between them was statistically significant (p <0.05). Conclusions: Adipose derived stem cells have obvious chemotaxis to adenoid cystic carcinoma cell culture supernatants, so we can propose that adipose derived stem cells has the possibility and feasibiliy of being used as a targeted therapy vectors for ACC.

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Xu, Gang, Lihua Zhu, Yan Wang, Yawei Shi, Aihua Gong und Chaoyang Wu. „Stattic Enhances Radiosensitivity and Reduces Radio-Induced Migration and Invasion in HCC Cell Lines through an Apoptosis Pathway“. BioMed Research International 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/1832494.

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Purpose. Signal transducer and activator of transcription factor 3 (STAT3) is involved in tumorigenesis, development, and radioresistance of many solid tumors. The aim of this study is to investigate the effects of stattic (an inhibitor of STAT3) on the radiosensitivity and radio-induced migration and invasion ability in hepatocellular carcinoma (HCC) cell lines. Methods. HCC cells were treated with stattic, and cell survival rate was analyzed through CCK-8 assay. Radiosensitivity was evaluated using cloning formation analysis; STAT3, p-STAT3, and apoptosis related proteins were detected by western blot. Radio-induced migration and invasion ability in HCC cells were analyzed by wound-healing assay and transwell test. Results. Stattic inhibits the expression of p-STAT3 and reduces cell survival in a dose-dependent manner in HCC cell lines, and the IC50 values for Hep G2, Bel-7402, and SMMC-7721 are 2.94 μM, 2.5 μM, and 5.1 μM, respectively. Cloning formation analysis shows that stattic enhances the radiosensitivity of HCC cells. Wound-healing assay and transwell test show that stattic inhibits radio-induced migration and invasion. Further study indicates that stattic promotes radio-induce apoptosis through regulating the expression of apoptosis related proteins in HCC cells. Conclusion. Stattic enhances radiosensitivity and reduces radio-induced migration and invasion ability in HCC cells probably through apoptosis pathway.

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Liu, Bing, Lili Xu, Xinming Yu, Xuefei Jiao, Junwei Yan, Wei Li und Mingjin Guo. „Genistein Inhibited Estradiol-Induced Vascular Endothelial Cell Injury by Downregulating the FAK/Focal Adhesion Pathway“. Cellular Physiology and Biochemistry 49, Nr. 6 (2018): 2277–92. http://dx.doi.org/10.1159/000493830.

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Background/Aims: In this study, we aimed to investigate the effects of genistein on the focal adhesion signaling pathway through its regulation of FAK. Genistein ultimately restored and alleviated estradiol-induced vascular endothelial injury. Methods: Microarray analysis was used to select differentially expressed genes. MTT assay was performed to detect the cell activity, and ROS test and NO test were performed to detect the degree of damage to HUVECs (human umbilical vein endothelial cells). The relative mRNA expression levels and protein expression levels of FAK were tested by western blot and qRT-PCR. GO functional analysis and KEGG pathway analysis were applied to predict the possible relationship between functions and related pathways, and transwell assay was used to detect cell invasion and migration. Results: FAK was highly expressed in the HUVECs treated with estradiol (HU-ESTs). Cell viability and NO level decreased, whereas ROS level increased in the HU-ESTs. Effective knockdown of FAK in HU-ESTs elevated cell viability and NO levels while suppressing ROS levels. In addition, inhibition of FAK greatly decreased cell invasion and migration, while the overexpression of FAK enhanced cell invasion and migration. KEGG further indicated focal adhesion pathways were activated. Genistein elevated HU-EST viability, and NO and ROS level increased in a concentration dependent manner. Transwell and western blot assays revealed that genistein could reduce the FAK expression levels and alleviate the damage to the HU-ESTs. Conclusion: FAK overexpression promoted invasion and migration of the HU-ESTs. However, genistein greatly suppressed FAK and estradiol-induced vascular endothelial cell injury.

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Zhou, Yunfei, Changqin Zhang, Qidong Zhang, Li Zhang und Wenhu Liu. „Original article. The role of p38MAPK in asymmetric dimethylarginineinduced cytoskeleton and cellular permeability changes in cultured endothelial cells“. Asian Biomedicine 5, Nr. 4 (01.08.2011): 449–57. http://dx.doi.org/10.5372/1905-7415.0504.059.

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Abstract Background: Asymmetric dimethylarginine (ADMA) induces endothelial cell barrier dysfunction via cytoskeleton activation and contraction. It is supposed that activated p38 mitogen-activated protein kinase (MAPK) would trigger the formation of stress fibers and increase cellular permeability. Objective: Explore p38 MAPK as a potentially important enzyme in ADMA-mediated endothelial cell contractile response and permeability change. Methods: Human umbilical endothelial cells (HUVECs) were cultured, where ADMA and/or SB203580 (the specific inhibitor of p38MAPK) were used to stimulate HUVECs. Immunofluorescent staining was carried out to examine the expression and distribution of F-actin, flow cytometry was used to quantify F-actin, and Transwell was applied to test cellular permeability with FITC-labelled human serum albumin (HSA). Scanning electronic microscopy (SEM) was utilized to observe the changes of intercellar contact. Results: ADMA induced significant p38MAPK activation in a dose-dependent manner, which correlated with increased stress fibers. SB-203580 attenuated the formation of actin stress fiber and the increase of cellular permeability induced ADMA in the HUVECs (p<0.01, LSCM; p<0.01, cytometry; p<0.05, Transwell). Widened intercellular space induced by ADMA was detected and could be inhibited by SB-203580 (SEM). SB-203580 alone had no effect on cytoskeleton and cellular permeability. Conclusion: p38MAPK activation participated in cytoskeleton and cellular permeability changes induced by ADMA in HUVECs.

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Zhang, Zhenyu, Yan Wang, Mingchao Li, Jiaping Li und Jian Wu. „Fibroblast Growth Factor 18 Increases the Trophic Effects of Bone Marrow Mesenchymal Stem Cells on Chondrocytes Isolated from Late Stage Osteoarthritic Patients“. Stem Cells International 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/125683.

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Coculture of mesenchymal stem cells with chondrocytes increases production of cartilaginous matrix. Chondrocytes isolated from late stage osteoarthritic patients usually lost their phenotype of producing cartilaginous matrix. Fibroblast growth factor 18 is believed to redifferentiate OA chondrocyte into functionally active chondrocytes. The aim of this study is to investigate the supportive effects of MSCs on OA chondrocytes and test if FGF18 could enhance the responsiveness of OA chondrocytes to the support of MSCs in a coculture system. Both pellet and transwell co-cultures were used. GAG quantification, hydroxyproline assay, and qPCR were performed. An ectopic models of cartilage formation was also applied. Our data indicated that, in pellets coculture of MSCs and OA chondrocytes, matrix production was increased in the presence of FGF18, comparing to the monoculture of chondrocytes. Results from transwell coculture study showed that expression of matrix producing genes in OA chondrocytes increased when cocultured with MSCs with FGF18 in culture medium, while hypertrophic genes were not changed by coculture. Finally, coimplantation of MSCs with OA chondrocytes produces more matrix than chondrocytes only. In conclusion, FGF18 can restore the responsiveness of OA chondrocytes to the trophic effects of MSCs. Coimplantation of MSCs and OA chondrocytes treated with FGF18 may be a good alternative cell source for regenerating cartilage tissue that is degraded during OA pathological changes.

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Zhang, Mingjuan, Huaming Deng, Xiajun Yi, Siying Xie und Qingying Zhan. „Study on Chlorogenic Acid Inhibiting the Proliferation and Invasion of Fibroblast-Like Synoviocytes in Rheumatoid Arthritis Model“. Journal of Biomaterials and Tissue Engineering 11, Nr. 11 (01.11.2021): 2192–96. http://dx.doi.org/10.1166/jbt.2021.2797.

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This paper explored Chlorogenic acid regulating the biological behavior of RA FLSs and studied the functional role of microRNAs in it. In vivo experiment: Female DBA/1 J mice were used for model establishment and grouping. HE staining was employed. The damage of ankle cartilage was analyzed in each group of mice. The levels of serum cytokines TNF-α and IL-β were measured by ELISA. In vitro experiment: The cells were counterstained with Hoechst 33342, Transwell was used to detect cell invasion. Western blotting was used to detect the expression of Akt protein. The Akt expression plasmid and miR-23b mimic were co-transfected into RA FLSs, and the luciferase activity was measured using a dual-luciferase detection system. In vivo experiments found that Chlorogenic acid can significantly reduce arthritis index and inhibit TNF-α and IL-β levels. In vitro experiments found that TNF-α-induced proliferation of RA FLSs was significantly inhibited by Chlorogenic acid. Transwell invasion test showed that TNF-α-induced cell invasion was attenuated at the presence of Chlorogenic acid, which significantly inhibited Akt protein expression and phosphorylation. The expression of miR-23b in Chlorogenic acid-treated RA-FLSs increased, and silencing miR-23b enhanced the inhibitory effect of RA FLSs on Chlorogenic acid induction. Chlorogenic acid has potential anti-rheumatoid arthritis activity. Its inhibition of RA FLSs proliferation and invasion is related to the induction of miR-23b and the down-regulation of Akt expression.

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Amini, Elham, Abhinav Kurumaddali, Sharvari Bhagwat, Simon M. Berger und Günther Hochhaus. „Optimization of the Transwell® System for Assessing the Dissolution Behavior of Orally Inhaled Drug Products through In Vitro and In Silico Approaches“. Pharmaceutics 13, Nr. 8 (21.07.2021): 1109. http://dx.doi.org/10.3390/pharmaceutics13081109.

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The aim of this study was to further evaluate and optimize the Transwell® system for assessing the dissolution behavior of orally inhaled drug products (OIDPs), using fluticasone propionate as a model drug. Sample preparation involved the collection of a relevant inhalable dose fraction through an anatomical mouth/throat model, resulting in a more uniform presentation of drug particles during the subsequent dissolution test. The method differed from previously published procedures by (1) using a 0.4 µm polycarbonate (PC) membrane, (2) stirring the receptor compartment, and (3) placing the drug-containing side of the filter paper face downwards, towards the PC membrane. A model developed in silico, paired with the results of in vitro studies, suggested that a dissolution medium providing a solubility of about 5 µg/mL would be a good starting point for the method’s development, resulting in mean transfer times that were about 10 times longer than those of a solution. Furthermore, the model suggested that larger donor/receptor and sampling volumes (3, 3.3 and 2 mL, respectively) will significantly reduce the so-called “mass effect”. The outcomes of this study shed further light on the impact of experimental conditions on the complex interplay of dissolution and diffusion within a volume-limited system, under non-sink conditions.

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Liang, Jianwei, Teng Sun, Guoxiang Wang und Hao Zhang. „Clinical significance and functions of miR-203a-3p/AVL9 axis in human non-small-cell lung cancer“. Personalized Medicine 17, Nr. 4 (01.07.2020): 271–82. http://dx.doi.org/10.2217/pme-2019-0108.

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Aim: We aimed to investigate the clinical significance and biological function of miR-203a-3p in non-small-cell lung cancer (NSCLC). Methods: The association between miR-203a-3p expression and clinicopathological parameters in NSCLC was assessed by χ2 test. Kaplan–Meier method and Cox regression model were applied to evaluate the prognosis value of miR-203a-3p. The biological function of miR-203-3p was explored using CCK-8 and transwell assays. Results: Significantly downregulated miR-203a-3p was associated with TNM stage, lymph node metastasis and poor prognosis. AVL9 was identified as a direct target of miR-203a-3p. Functionally, we found overexpression of miR-203a-3p inhibited cell proliferation, migration and invasion in NSCLC cells by targeting AVL9. Conclusion: Collectively, targeting the miR-203a-3p/ AVL9 axis might help to develop useful therapeutic target for NSCLC.

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Zheng, Jianxing, Daming Cheng, Dongyang Wu, Libing Wang, Fengzhi Qu, Xiaotang Wu, Ling Cheng, Yanbin Wei und Xiaogang Liu. „MiR-452-5p mediates the proliferation, migration and invasion of hepatocellular carcinoma cells via targeting COLEC10“. Personalized Medicine 18, Nr. 2 (März 2021): 97–106. http://dx.doi.org/10.2217/pme-2020-0027.

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Objective: This study explored the potential function of miR-452-5p in hepatocellular carcinoma (HCC) and clarified the mechanism underlying HCC progression. Materials & methods: Real-time quantitative PCR was used to detect miR-452-5p and COLEC10 mRNA expression in HCC, western blot was performed to test COLEC10 protein expression. The regulatory mechanism of miR-452-5p/COLEC10 in HCC cells was explored using CCK-8, wound healing assay, Transwell and dual-luciferase reporter assay. Results: MiR-452-5p was greatly upregulated in HCC cells, and it served as an oncogene playing an active role in HCC cell proliferation, migration and invasion. COLEC10 was identified as the target of miR-452-5p in HCC attenuating the promoting effect of miR-452-5p on HCC cells upon overexpression. Conclusion: MiR-452-5p can promote the progression of HCC via targeting COLEC10.

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Dissertationen zum Thema "Transwell test"

Scholasterová, Viktorie. „Studium migrace mesenchymálních kmenových buněk v extracelulárním matrix na principu chemotaxe“. Master's thesis, Vysoké učení technické v Brně. Fakulta elektrotechniky a komunikačních technologií, 2021. http://www.nusl.cz/ntk/nusl-442488.

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This thesis engages in a study of mesenchymal stem cell migration in extracellular matrix based on principles of chemotaxis. First, attention is focused on a theoretical part associated with a clarification of basic terms such as extracellular matrix, migration, confocal microscopy, mesenchymal stem cells or chemotaxis. There is also included a list and a description of some basic methods for monitoring cell migration and a more detailed description of a method called transwell assay, which has been chosen for an experiment in a practical part of this thesis. This part includes protocols of individual steps for the preparation of the experiment, the procedure of data processing obtained by scanning cells with a confocal microscope and a description of the resulting confluence values.

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Pošustová, Veronika. „Studium migrace mesenchymálních kmenových buněk na principu chemotaxe“. Master's thesis, Vysoké učení technické v Brně. Fakulta elektrotechniky a komunikačních technologií, 2020. http://www.nusl.cz/ntk/nusl-413169.

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The purpose of this Master thesis is to verify migration of mesenchymal stem cells on the principle known as chemotaxis. First part of this study is focused on cell migration in order to explain the whole migration process. Next part describes various chemotaxis methods and selected studies dealing with clinical applications of mesenchymal stem cells in different medical and biomedical fields. The following step describes confocal microscopy, which is used for acquiring images of the cells. The experimental part is focused on cultivation of mesenchymal stem cells in a laboratory, which is necessary for cell vitality. Furthermore, there are designed two main experiments. Firstly there is a 2D experiment with adherent cells for chemotaxis using -Slide Chemotaxis. Secondly Transwell migration test is designed and executed. Finally, the acquired images from confocal microscope are used for image processing, which was done in Matlab R2020a programming environment. The result of this processing is evaluation of cell confluence and migration. In the end, experimental part of this study was optimized according to recommended studies. The results are summarized in the conclusion with proposal for improvements of those methods.

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Buchteile zum Thema "Transwell test"

Christ, Bastian, Christina Fey, Alevtina Cubukova, Heike Walles, Sofia Dembski und Marco Metzger. „Screening Applications to Test Cellular Fitness in Transwell® Models After Nanoparticle Treatment“. In Methods in Molecular Biology, 111–22. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6960-9_10.

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Konferenzberichte zum Thema "Transwell test"

Brayshaw, W. J., A. H. Sherry, M. G. Burke und P. James. „Characterisation of Microstructure and Properties of a Transition Weld“. In ASME 2016 Pressure Vessels and Piping Conference. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/pvp2016-63045.

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Transition welds represent a challenge for the assessment of structural integrity of nuclear plant due to the complexity of the microstructure, properties and local stress state. This paper presents the initial findings of a study aimed at characterising the local microstructure and properties of a transition weld between SA508-4N ferritic steel and SS316LN austenitic stainless steel using a nickel-base filler of Alloy 82. The local microstructures and local composition of the material interfaces are characterised using backscattered electron imaging and Energy-dispersive X-ray spectroscopy. The ferritic steel shows significant grain refinement in the heat affected zone compared to the base metal. This refinement is also observed in the heat affected zone of the austenitic stainless steel although not as significant. Micro-hardness testing has also been incorporated to provide an indication of the influence of local microstructure on flow properties across the weld region. The results indicate a hardness range of between 180–340HV across the weld with the highest value in the heat affected zone of the ferritic steel and the lowest in the austenitic stainless steel. Yield and flow properties derived from flat transweld tensile tests incorporating digital image correlation are related to the micro-hardness results and microstructural characterisation, and an initial assessment of the fracture mechanism performed using fractography.

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