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3,584 results for “Fibroblasts”
Immunopeptidomics on T. cruzi – infected MC57G murine fibroblasts
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Data from: Exposure effects beyond the epithelial barrier: trans-epithelial induction of oxidative stress by diesel exhaust particulates in lung fibroblasts in an organotypic human airway model
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Hypoxia preconditioned mesenchymal stem cells prevent cardiac fibroblast activation and collagen production via leptin
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Data from: Primary dermal fibroblasts and pectoralis muscle show similar patterns of oxidative stress in tropical and temperate birds despite differing life-histories
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ROS-Specific Huntingtin Interactions: Testing PARG activity in HD patient fibroblasts round 2
<p>Comparison nuclear PAR levels in wild type and HD (TruHD) fibroblasts in response to a PARG inhibitor concentration gradient (as a measure of PARG activity).</p>
Gene expression counts from fibroblast, strand-specific, BCM UDN
<p><strong>File description:</strong></p> <ol> <li> <p>Gene-level counts using the gtf file from the release 34 of GENCODE <a href="https://www.gencodegenes.org/human/release_34">https://www.gencodegenes.org/human/release_34</a></p> </li> <li> <p>Split counts spanning from one exon to another using an annotation-free algorithm, therefore capturing new splice sites</p> </li> <li> <p>Non-split counts covering exon-intron boundaries</p> </li> <li> <p>Sample annotation describing each sample from the dataset</p> </li> <li> <p>Description file with global information from the dataset</p> </li> </ol> <p><strong>Use: </strong>The count matrices are intended to help researchers that are interested in using RNA-Seq data with the purpose of diagnostics. Researchers can merge their own dataset with the downloaded ones, provided the tissue, genome build, strand, and paired end specifications match. Afterwards, the DROP pipeline can be used to compute expression and splicing outliers (<a href="https://github.com/gagneurlab/drop">https://github.com/gagneurlab/drop</a>).</p> <p><strong>Maintainer: </strong>Vicente A. Yépez, <a href="mailto:yepez@in.tum.de">yepez@in.tum.de</a></p> <p><strong>URL:</strong> <a href="https://github.com/gagneurlab/drop/">https://github.com/gagneurlab/drop/</a><br> </p> <p><strong>Title</strong>: BCM UDN Fibroblast<br> <strong>Number of samples</strong>: 139<br> <strong>Tissue</strong>: Fibroblast<br> <strong>Organism</strong>: Homo sapiens<br> <strong>Genome assembly:</strong> hg19<br> <strong>Gene annotation</strong>: gencode34<br> <strong>Disease (ICD-10: N)</strong>: : D17: 1, D84: 12, E34: 2, G82: 1, H57: 3, K92: 3, M25: 18, NONE: 35, Q02: 1, Q20: 5, Q33: 2, Q89: 12, R62: 44<br> <strong>Strand specific</strong>: TRUE<br> <strong>Paired end</strong>: TRUE<br> <strong>Protocol</strong>: poly(A) enrichment<br> <strong>Dataset contact</strong>: David Murdock, <a href="mailto:david.murdock@bcm.edu">david.murdock@bcm.edu</a></p> <p><strong>Citation:</strong> Cite both the resource using Zenodo's citation and the publication under References</p>
Crosstalk between Mast Cells and Lung Fibroblasts Is Modified by Alveolar Extracellular Matrix and Influences Epithelial Migration
<p>Datasets for the data generated and presented in the article: https://doi.org/10.3390/ijms22020506</p>
Data from: Enhanced store-operated Ca2+ influx and ORAI1 expression in ventricular fibroblasts from human failing heart
Excessive cardiac fibrosis, characterized by increased collagen-rich extracellular matrix (ECM) deposition, is a major predisposing factor for mechanical and electrical dysfunction in heart failure (HF). The human ventricular fibroblast (hVF) remodeling mechanisms that cause excessive collagen deposition in HF are unclear, although reports suggest a role for [Ca2+]i in fibrosis. Therefore, we determined the association of differences in cellular Ca2+ dynamics and collagen secretion/deposition between hVFs from failing and normal (control) hearts. Histology of left ventricle sections (Masson trichrome) confirmed excessive fibrosis in HF vs normal. In vitro, hVFs from HF showed increased secretion/deposition of soluble collagen in 48 hours of culture compared with control [85.9±7.4 μg/106 vs 58.5±8.8 μg/106 cells, P<0.05; (Sircol™ assay)]. However, collagen gene expressions (COL1A1 and COL1A2; rt-PCR) were not different. Ca2+ imaging (fluo-3) of isolated hVFs showed no difference in the thapsigargin-induced intracellular Ca2+ release capacity (control 16±1.4% vs HF 17±1.1%); however, Ca2+ influx via store-operated Ca2+ entry [SOCE /CRAC (Ca2+ release-activated)] channels was significantly (P≤0.05) greater in HF-hVFs (47±3%) compared with non-failing (35±5%). Immunoblotting for ICRAC channel components showed increased ORAI1 expression in HF-hVFs compared with normal without any difference in STIM1 expression. The Pearson's correlation coefficient for co-localization of STIM1/ORAI1 was significantly (P<0.01) greater in HF (0.5±0.01) than control (0.4±0.01) hVFs. The increase in collagen secretion of HF vs control hVFs was eliminated by incubation of hVFs with YM58483 (10 μM), a selective ICRAC inhibitor for 48 hours (66.78±5.87μg/106 cells vs 55.81±7.09 μg/106 cells, P=0.27). In conclusion, hVFs from HF have increased collagen secretion capacity vs non-failing hearts and this is related to increase in Ca2+ entry via SOCE and enhanced expression of ORAI, the pore-forming subunit. Therapeutic inhibition of SOCE may reduce the progression of cardiac fibrosis/HF.
Data from: New quantitative approaches reveal the spatial preference of nuclear compartments in mammalian fibroblasts
The nuclei of higher eukaryotic cells display compartmentalization and certain nuclear compartments have been shown to follow a degree of spatial organization. To date, the study of nuclear organization has often involved simple quantitative procedures that struggle with both the irregularity of the nuclear boundary and the problem of handling replicate images. Such studies typically focus on inter-object distance, rather than spatial location within the nucleus. The concern of this paper is the spatial preference of nuclear compartments, for which we have developed statistical tools to quantitatively study and explore nuclear organization. These tools combine replicate images to generate 'aggregate maps' which represent the spatial preferences of nuclear compartments. We present two examples of different compartments in mammalian fibroblasts (WI-38 and MRC-5) that demonstrate new knowledge of spatial preference within the cell nucleus. Specifically, the spatial preference of RNA polymerase II is preserved across normal and immortalized cells, whereas PML nuclear bodies exhibit a change in spatial preference from avoiding the centre in normal cells to exhibiting a preference for the centre in immortalized cells. In addition, we show that SC35 splicing speckles are excluded from the nuclear boundary and localize throughout the nucleoplasm and in the interchromatin space in non-transformed WI-38 cells. This new methodology is thus able to reveal the effect of large-scale perturbation on spatial architecture and preferences that would not be obvious from single cell imaging.
Data from: Maintenance of age in human neurons generated by microRNA-based neuronal conversion of fibroblasts
Aging is a major risk factor in many forms of late-onset neurodegenerative disorders. The ability to recapitulate age-related characteristics of human neurons in culture will offer unprecedented opportunities to study the biological processes underlying neuronal aging. Here, we show that using a recently demonstrated microRNA-based cellular reprogramming approach, human fibroblasts from postnatal to near centenarian donors can be efficiently converted into neurons that maintain multiple age-associated signatures. Application of an epigenetic biomarker of aging (referred to as epigenetic clock) to DNA methylation data revealed that the epigenetic ages of fibroblasts were highly correlated with corresponding age estimates of reprogrammed neurons. Transcriptome and microRNA profiles reveal genes differentially expressed between young and old neurons. Further analyses of oxidative stress, DNA damage and telomere length exhibit the retention of age-associated cellular properties in converted neurons from corresponding fibroblasts. Our results collectively demonstrate the maintenance of age after neuronal conversion.
Original pictures of isolation, culture and immunofluorescence staining of primary fibroblasts from cervical tissue in vitro
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Fibroblast cells dataset
<p>High resolution images of fibroblast cell cultures at 10x and 4x magnifications</p>
Random Sample from Keratinocytes, Fibroblasts and Melanocytes
<p>From the ftp genboree.org. Subsample of publicly available data.</p>
ROS-Specific Huntingtin Interactions: Testing PARP activity in HD patient fibroblasts
<p>Comparison of nuclear PAR levels in wild type and HD (TruHD) fibroblasts in response to a PARP inhibitor concentration gradient (as a measure of PARP activity).</p>
Role of Hypoxic Secretome from Mesenchymal Stem Cells in Enhancing Tissue Repair: Regulatory Effects on HIF-1α, VEGF, and Fibroblast in a Sphincterotomy Rat Model
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Human cross-tissue, multi-disease fibrotic disease fibroblast atlas (FDFA)
<p><span>Cross-tissue, Multi-disease Fibrotic Disease Fibroblast Atlas</span></p>
Fibroblast Growth Factor Regeneration of Tympanic Membrane Perforations
ClinicalTrials.gov study NCT02307916. IPD Sharing: NO. Countries: 1. Publications: 0.
Fibroblast Growth Factors 19 and 21 in Gestational Diabetes Mellitus
ClinicalTrials.gov study NCT01858597. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Fibroblast Growth Factor 23 in Chronic Respiratory Failure
ClinicalTrials.gov study NCT05258370. IPD Sharing: YES. Countries: 0. Publications: 4.
Safety and Efficacy Study of Autologous Fibroblasts in the Treatment of Severe Facial Acne Scarring
ClinicalTrials.gov study NCT00642642. IPD Sharing: Not stated. Countries: 1. Publications: 0.
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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)
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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.