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3,126 results for “epithelial cells”
Data from: ESCRT-III-dependent adhesive and mechanical changes are triggered by a mechanism detecting alteration of Septate Junction integrity in Drosophila epithelial cells
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Data from: Dynamics of the CD9 interactome during bacterial infection of epithelial cells by proximity labelling proteomics
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Culture media strongly influences primary human bronchial epithelial cells' transcriptomic response to ozone exposure
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Data from: Fibroblasts modulate epithelial cell behavior within the proliferative niche and differentiated cell zone within a human colonic crypt model
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Data from: Ovarian BDNF promotes survival, migration, and attachment of tumor precursors originated from p53 mutant fallopian tube epithelial cells
<p class="CxSpFirst"><span>High-grade serous ovarian carcinoma (HGSOC) is the most lethal gynecological malignancy. New evidence supports a hypothesis that HGSOC can originate from fallopian tube epithelium (FTE). It is unclear how genetic alterations and pathophysiological processes drive the progression of FTE tumor precursors into widespread HGSOCs. In this study, we uncovered that brain-derived neurotrophic factor (BDNF) in the follicular fluid stimulates the tropomyosin receptor kinase B (TrkB)-expressing FTE cells to promote their survival, migration, and attachment. Using <i>in vitro</i> and <i>in vivo</i> models, we further identified that the acquisition of common TP53 gain-of-function (GOF) mutations in FTE cells led to enhanced BDNF/TrkB signaling comparing to that of FTE cells with <i>TP53</i> loss-of-function (LOF) mutations. Different mutant p53 proteins can either increase TrkB transcription or enhance TrkB endocytic recycling. Our findings have demonstrated possible interplays between genetic alterations in FTE tumor precursors (i.e., p53 gain-of-function mutations) and pathophysiological processes (i.e., the release of follicular fluid upon ovulation) during the initiation of HGSOC from the fallopian tube. Our data revealed molecular events underlying the link between HGSOC tumorigenesis and ovulation, a physiological process that has been associated with risk factors of HGSOC. </span></p>
RNAseq raw counts FLCN positive vs. FLCN negative renal proximal tubular epithelial cells (RPTEC)
<p>Germline inactivating mutations in Folliculin (FLCN) cause Birt–Hogg–Dubé (BHD) syndrome, a rare autosomal dominant disorder predisposing to kidney tumors. FLCN is a conserved, essential gene linked to diverse cellular processes but the mechanisms by which FLCN prevents kidney cancer remain unknown. Here we show that deleting FLCN activates TFE3, upregulating its downstream E-box genes in human renal tubular epithelial cells (RPTEC/TERT1), including RRAGD and GPNMB, without modifying mTORC1 activity. Surprisingly, deletion of FLCN or its binding partners FNIP1/FNIP2 also induces interferon response genes, but independently of interferon. Mechanistically, FLCN loss promotes STAT2 recruitment to chromatin and slows cellular proliferation. Our integrated analysis identifies STAT1/2 signaling as a novel target of FLCN in renal cells and BHD tumors. STAT1/2 activation appears to counterbalance TFE3-directed hyper-proliferation and may influence the immune response. These findings shed light on unique roles of FLCN in human renal tumorigenesis and pinpoint candidate prognostic biomarkers.</p>
Data from: Early mechanistic events induced by low molecular weight polycyclic aromatic hydrocarbons in mouse lung epithelial cells: a role for eicosanoid signaling
Low molecular weight polycyclic aromatic hydrocarbons (LMW PAHs; <206.3 g/mol) are under regulated environmental contaminants (e.g., secondhand smoke) that lead to gap junction dysregulation, p38 MAPK activation, and increased mRNA production of inflammatory mediators, such as cytokines and cyclooxygenase (COX2), in lung epithelial cells. However, the early mechanisms involving lipid signaling through the arachidonic acid pathway and subsequent eicosanoid production leading to these downstream events are not known. Common human exposures are to mixtures of LMW PAH's, thus C10 cells (a mouse lung epithelial cell line) were exposed to a representative binary PAH mixture, 1-methylanthracene (1-MeA) and fluoranthene (Flthn), for 30 min – 24 h with and without p38 and cytosolic phospholipase A2 (cPLA2) inhibitors. cPLA2 inhibition reversed PAH-induced phospho-p38 MAPK activation and gap junction dysregulation at 30 min. A significant biphasic increase of cPLA2 protein was observed at 30 min, 2, & 4 h, as well as COX2 protein at 2 & 8 h. Untargeted metabolomics demonstrated a similar trend with significantly changing metabolites at 30 min & 4 h of exposure relative to 1 h; a "cPLA2-like" subset of metabolites within the biphasic response were predominately phospholipids. argeted metabolomics showed several eicosanoids (e.g., prostaglandin D2 (PGD2), PGE2α) were significantly increased at 4, 8, and 12 h following exposure to the binary PAH mixture and this effect was p38-dependent. Lastly, PAH metabolism was not observed until after 8 h. These results indicate an early lipid signaling mechanism of PAH toxicity in lung epithelial cells due to parent PAH compounds.
Datasets generated for the manuscript: The basement membrane regulates the cellular localization and the cytoplasmic interactome of Yes-Associated Protein (YAP) in mammary epithelial cells
<p><strong>File proteinGroups-CoIP-Yap1:</strong> Dataset of co-Immunoprecipitation followed of Yes-associated protein (YAP) followed by proteomics to identify YAP interactants.</p> <p><strong>File Gene_set_file_YAP: </strong>Gene sets used for gene set enrichment analysis.</p> <p><strong>Files enrichr_x: </strong>output of the EnrichR tool</p>
Data from: Despite high levels of expression in thymic epithelial cells, miR-181a1 and miR-181b1 are not required for thymic development
MicroRNAs (miRNAs) have been shown to be key modulators of post-transcriptional gene silencing in many cellular processes. In previous studies designed to understand the role of miRNAs in thymic development, we globally deleted miRNA exclusively in thymic epithelial cells (TECs), which are critical in thymic selection. This resulted in the loss of stromal cells that instruct T cell lineage commitment and affect thymocyte positive selection, required for mature T cell development. Since murine miR-181 is expressed in the thymus and miR-181 deficiency disrupts thymocyte development, we first quantified and thereby demonstrated that miR181a1 and miR181b1 are expressed in purified TECs. By generating mice with TEC targeted loss of miR-181a1 and miR-181b1 expression, we observed that neither TEC cellularity nor thymocyte number nor differentiation was adversely affected. Thus, disrupted thymopoiesis in miR-181 deficient mice was not due to miR-181 loss of expression in TECs. Importantly, in mice with restricted TEC deficiency of miR-181a1 and miR-181b1, there were similar numbers of mature T cells in the periphery in regards to frequencies, differentiation, and function as compared to controls. Moreover miR-181a1 and miR-181b1 were not required for maintenance of thymus integrity over time, as thymic involution was not accelerated in gene-targeted mice. Taken together our data indicate that miR-181a1 and miR-181b1 are dispensable for TEC differentiation, their control of thymocyte development and mature T cell export to and homeostasis within the periphery.
CompareRhythms data in healthy and asthmatic airway epithelial cells
<p><strong>Rationale: </strong>Cellular circadian rhythms regulate multiple cellular processes and have been hypothesized to influence epithelial function in asthma. Airway resistance has circadian variability in patients with asthma, profiling of circadian rhythms of gene expression in human airway epithelia has not been performed. Organotypic cultures of primary human airway epithelial cells differentiated at an air-liquid interface recapitulate the major cell types of human airway epithelia to allow for evaluation of gene expression not possible <em>in vivo</em> and demonstrate rhythmicity of core circadian genes after temperature synchronization.</p> <p><strong>Methods:</strong> Primary human airway epithelial cells from 6 healthy children and 6 children with asthma were differentiated an air-liquid interface and circadian rhythms were synchronized using cycled incubator temperature. RNA was harvested every 4 hours and RNA-sequencing performed to measure transcriptome-wide expression, with differential rhythmicity of genes identified using CompareRhythms.</p> <p><strong>Results:</strong> Core circadian genes <em>ARNTL</em> and <em>NR1D1</em> demonstrated rhythmicity in both healthy and asthmatic airway epithelial cells with maintained phase relationships. In RNAseq data from healthy and asthmatic airway epithelial cells, 646 (4%) of protein-coding genes were rhythmic, with 110 genes exhibiting differential rhythmicity in asthma. Gene set enrichment analysis using EnrichR revealed that genes in circadian rhythm, nuclear receptor, and cell adhesion pathways were rhythmic. Neutrophil chemotaxis, cytokine mediated signaling, and viral protein interactions with cytokine receptor pathways demonstrated differential (gain, loss, or change) rhythmicity in asthma.</p> <p><strong>Conclusions: </strong>Core circadian rhythm genes maintain rhythmicity in healthy and asthmatic human airway epithelia, and regulate cytokine mediated signaling and neutrophil chemotaxis pathways in asthmatic human airway epithelia.</p>
Nasal organoids as optimal models for studying structure and function of primary nasal epithelial cell cultures - DIA-MS Dataset
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NSD3-Short Represses E-cadherin Expression in A549 Lung Epithelial Cancer Cells
<p><strong>SGC Open Notebook Project to Characterize the HMTase NSD3</strong></p> <p><strong>Exp024 Objective: </strong>In a previous experiment (exp023), we show that siRNA-mediated knockdown of NSD3 increases expression of E-cadherin, a marker of epithelial cell identity. To determine which isoform of NSD3 is involved in promoting epithelial to mesenchymal transition, I have designed siRNA that targets either the long or short isoform and again use E-cadherin expression as a marker. Additionally, I have started using A549 lung epithelial cancer cells (https://www.atcc.org/Products/All/CCL-185) as my primary model. This cell line proliferates faster and is more amenable to <em>in vitro</em> experimentation than the H1299 cell line I was using previously.</p>
The cat as a naturally occurring model of renal interstitial fibrosis: Characterisation of primary feline proximal tubular epithelial cells and comparative pro-fibrotic effects of TGF-β1
<p>Chronic kidney disease (CKD) is common in both geriatric cats and aging humans, and is pathologically characterised by chronic tubulointerstitial inflammation and fibrosis in both species. Cats with CKD may represent a spontaneously occurring, non-rodent animal model of human disease, however little is known of feline renal cell biology. In other species, TGF-β1 signalling in the proximal tubular epithelium is thought to play a key role in the initiation and progression of renal fibrosis. In this study, we first aimed to isolate and characterise feline proximal tubular epithelial cells (FPTEC), comparing them to human primary renal epithelial cells (HREC) and the human proximal tubular cell line HK-2. Secondly, we aimed to examine and compare the effect of human recombinant TGF-β1 on cell proliferation, pro-apoptotic signalling and genes associated with epithelial-to-mesenchymal transition (EMT) in feline and human renal epithelial cells.</p> <p>FPTEC were successfully isolated from cadaverous feline renal tissue, and demonstrated a marker protein expression profile identical to that of HREC and HK-2. Exposure to TGF-β1 (0-10 ng/ml) induced a concentration-dependent loss of epithelial morphology and alterations in gene expression consistent with the occurrence of partial EMT in all cell types. This was associated with transcription of downstream pro-fibrotic mediators, growth arrest in FPTEC and HREC (but not HK-2), and increased apoptotic signalling at high concentrations of TGF- β1. These effects were inhibited by the ALK5 (TGF-β1RI) antagonist SB431542 (5 µM), suggesting they are mediated via the ALK5/TGF-β1RII receptor complex. Taken together, these results suggest that TGF-β1 may be involved in epithelial cell dedifferentiation, growth arrest and apoptosis in feline CKD as in human disease, and that cats may be a useful, naturally occurring model of human CKD.</p>
Deep learning for rapid analysis of cell divisions in vivo during epithelial morphogenesis and repair
<div> <p>Database for paper:</p> <p><a href="https://doi.org/10.7554/eLife.87949.2">doi.org/10.7554/eLife.87949.2</a></p> <p>The scripts for using our deep learning algrithm to detect cell divisions via a napari plugin can be found here:</p> <p>https://github.com/turleyjm/cell-division-dl-plugin</p> <p>The notebooks and analysis for training and evaluating the model are also given in this repository.</p> </div>
Dataset for "Luminal breast epithelial cells from wildtype and BRCA mutation carriers harbor copy number alterations commonly associated with breast cancer"
<p>Processed single cell whole genome sequencing data from:</p> <p>Luminal breast epithelial cells from wildtype and BRCA mutation carriers harbor copy number alterations commonly associated with breast cancer Williams, Vinci Oliphant et al 2024</p> <p>Included are processed copy number profiles for all cells included in the study.</p>
The lncRNA TUG1 regulates Smac/DIABLO expression by competitively inhibiting miR-29b and modulates the apoptosis of lens epithelial cells in age-related cataracts
<p>As one of the first discovered lncRNAs, TUG1 has been reported to be widely expressed in a variety of tumours. It promotes cell proliferation, differentiation, apoptosis and migration. However, our understanding of its importance in cataracts is limited. This study aims to explore the mechanism by which TUG1 mediates the apoptosis of lens epithelial cells by regulating the miR-29b/Smac axis in age-related cataracts and to identify more strategies for the nonsurgical treatment of cataracts. In this experiment we found TUG1 and Smac were expressed at high levels in age-related cataract (ARC) samples and HLEB3 cells treated with H2O2, while miR-29b expression was decreased. In vitro cell-based experiments confirmed that the downregulation of TUG1 inhibits lens epithelial cell apoptosis. Mechanistically, Smac expression is negatively regulated by miR-29b. TUG1 competitively inhibits miR-29b expression and causes the release of more Smac. In addition, miR-29b reverses the effect of TUG1 on HLE-B3 cells. In conclusion, lncRNATUG1 increases Smac expression by competitively inhibiting miR-29b and promoting the apoptosis of lens epithelial cells in age-related cataracts. This mechanism is the cytological basis of ARC formation. Based on these results, the TUG1-miR29b-Smac axis may be a new molecular pathway to regulate the development of age-related cataracts.</p>
Unravelling the metabolic alterations induced by Zika infection in prostate epithelial (PNT1a) and adenocarcinoma (PC-3) cell lines
<p>Unravelling the metabolic alterations induced by Zika infection in prostate epithelial (PNT1a) and adenocarcinoma (PC-3) cell lines</p>
Large-scale annotation dataset for cell/tissue segmentation in H&E-stained images : anti-panCK (epithelial cells)
<p><strong>LICENSE</strong></p> <p>This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (<strong>CC-BY-NC-SA 4.0</strong>)</p> <p>For non-commercial use, please use the dataset under CC-BY-NC-SA.<br> If you would like to use the dataset for commercial purposes, please contact us (ishum-prm@m.u-tokyo.ac.jp).</p> <p>A Tar.gz file contains the following files:</p> <p>- HE image file: {antigen}_{celltype}_{slideID}_{posx}_{posy}_HE.png</p> <p>- Mask image file: {antigen}_{celltype}_{slideID}_{posx}_{posy}_mask.png</p> <p>Each image file is 984x984 px.</p> <p>posX and posY are the leftmost position in WSI coordinate.</p> <p>Mask files store binary segmentation mask (background : 0, target : 1)</p> <p> </p> <p>A csv file contains the following information:</p> <p>antigen : Antibodies for this antigen were used to create the segmentation mask.</p> <p>filename: filename of image or mask file.</p> <p>train_val_test : train, validation, or test sample in the paper.</p> <p> </p> <p><strong>Citation</strong></p> <p>If you use this dataset for your research, please cite our paper.</p> <p>Daisuke Komura, Takumi Onoyama, Koki Shinbo, Hiroto Odaka, Minako Hayakawa, Mieko Ochi, Ranny Rahaningrum Herdiantoputri, Haruya Endo, Hiroto Katoh, Tohru Ikeda, Tetsuo Ushiku, Shumpei Ishikawa,<br> Restaining-based annotation for cancer histology segmentation to overcome annotation-related limitations among pathologists, Patterns, Volume 4, Issue 2, 2023, 100688, https://doi.org/10.1016/j.patter.2023.100688.</p>
Hexanematic crossover in epithelial monolayers depends on cell adhesion and cell density.
<p>Raw data files concerning the publication,</p> <p><strong>Hexanematic crossover in epithelial monolayers depends on cell adhesion and cell density</strong><br>Julia Eckert, Benoit Ladoux, Rene-Marc Mege, Luca Giomi and Thomas Schmidt<br>Nature Communications (2023) <strong>14</strong>:5762.<br>doi: <span>https://doi.org/10.1038/s41467-023-41449-6</span><br><br><strong>Abstract:</strong></p> <p>Changes in tissue geometry during developmental processes are associated with collective migration of cells. Recent experimental and numerical results suggest that these changes could leverage on the coexistence of nematic and hexatic orientational order at different length scales. How this multiscale organization is affected by the material properties of the cells and their substrate is presently unknown. In this study, we address these questions in monolayers of Madin-Darby canine kidney cells having various cell densities and molecular repertoires. At small length scales, confluent monolayers are characterized by a prominent hexatic order, independent of the presence of E-cadherin, monolayer density, and underlying substrate stiffness. However, all three properties affect the meso-scale tissue organization. The length scale at which hexatic order transits to nematic order, the ”hexanematic” crossover scale, strongly depends on cell-cell adhesions and correlates with monolayer density. Our study demonstrates how epithelial organization is affected by mechanical properties, and provides a robust description of tissue organization during developmental processes.</p> <p> </p> <p><strong>Data description:</strong></p> <p>WT.zip - zipped raw image data and extracted vertices of experiments on wild-type cells<br>KO.zip - zipped raw image data and extracted vertices of experiments on eCad KO-cells<br>FigureData.zip - zipped data referring to each of the figures in the paper</p> <p> </p> <p><strong>Software:</strong></p> <p>The software to analyze the data presented here is found on GitHub, [https://github.com/hexanematic/orientation tracker]</p>
Limbal Epithelial Stem Cell Transplantation: a Phase II Multicenter Trial
ClinicalTrials.gov study NCT02318485. IPD Sharing: Not stated. Countries: 1. Publications: 1.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.