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3,584 results for “Fibroblasts”
Single-cell RNA sequencing of sclerotome-derived fibroblasts in zebrafish
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Data from: Reverse plasticity underlies rapid evolution by clonal selection within populations of fibroblasts propagated on a novel soft substrate
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Human adenovirus serotype 5 infection dysregulates cysteine, purine, and unsaturated fatty acid metabolism in fibroblasts
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AnnData files for "Human dermal fibroblast subpopulations are conserved across single-cell RNA sequencing studies"
<p>AnnData files for "Human dermal fibroblast subpopulations are conserved across single-cell RNA sequencing studies". </p> <p>Includes Joined dataset with all four datasets at once.</p>
Data from: Controlled release of basic fibroblast growth factor from a peptide biomaterial for bone regeneration
<p>Self-assembled peptide scaffolds based on D-RADA16 (D16) are an important matrix for controlled drug release and 3D cell culture. In this work, D16 peptide hydrogels were coated on artificial bone composed of nano-hydroxyapatite/polyamide 66 (NHA/PA66) to obtain a porous drug-releasing structure for treating bone defects. The developed materials were characterized via transmission electron microscopy (TEM), scanning electron microscopy (SEM). The proliferation and adhesion of bone mesenchymal stem cells (BMSCs) were examined by Confocal laser microscopy (CLS) and CCK-8 experiments. The osteogenic ability of the porous materials towards bone BMSCs was examined in vitro by staining with Alizarin Red S and alkaline phosphatase (ALP) and bioactivity were evaluated in vivo. The results revealed that NHA/PA66/D-RADA16/bFGF reduce the degradation rate of D16 hydrogels and prolong sustained release of bFGF, which would promote BMSCs proliferation, adhesion and osteogenesis in vitro and bone repair in vivo. Thus, it deserves more attention and is worthy of further research.</p>
V79 fibroblasts loaded with 50 nm PVP-coated gold nanoparticles
<p>Hamster fibroblasts were perfused with 50nm PVP-coated gold nanoparticles and captured by CytoViva darkfield micorscopy (30 FPS, 160nm),</p>
V79 fibroblasts loaded with 50 nm PVP coated gold particles captures by confocal laser scanning microscopy
<p>Data was recorded continuously in a region of 41x41 μm² at a scan rate of 1400 Hz resulting in a frame duration of 94 ms; the pinhole was set to 600 μm (5.778 μm layer), image resolution was 256x256 pixel. (11 FPS)</p>
Data from: Mouse gingival single cell transcriptomic atlas identified a novel fibroblast subpopulation activated to guide oral barrier immunity in periodontitis
<p>Periodontitis, one of the most common non-communicable diseases, is characterized by chronic oral inflammation and uncontrolled tooth supporting alveolar bone resorption. Its underlying mechanism to initiate aberrant oral barrier immunity has yet to be delineated. Here, we report a unique fibroblast subpopulation activated to guide oral inflammation (AG fibroblasts) identified in a single-cell RNA sequencing gingival cell atlas constructed from the mouse periodontitis models. AG fibroblasts localized beneath the gingival epithelium and in the cervical periodontal ligament responded to the ligature placement and to the discrete topical application of Toll-like receptor stimulants to mouse maxillary tissue. The upregulated chemokines and ligands of AG fibroblasts linked to the putative receptors of neutrophils in the early stages of periodontitis. In the established chronic inflammation, neutrophils together with AG fibroblasts appeared to induce type 3 innate lymphoid cells (ILC3s) that were the primary source of interleukin-17 cytokines. The comparative analysis of <em>Rag2-/-</em> and <em>Rag2gc-/-</em> mice suggested that ILC3 contributed to the cervical alveolar bone resorption interfacing the gingival inflammation. We propose that the AG fibroblast–neutrophil–ILC3 axis as a previously unrecognized mechanism which could be involved in the complex interplay between oral barrier immune cells contributing to pathological inflammation in periodontitis.</p>
Charting the cellular biogeography in colitis reveals fibroblast trajectories and coordinated spatial remodeling
<p>Scripts associated with the analysis and plotting of data for the Cell paper: Charting the cellular biogeography in colitis reveals fibroblast trajectories and coordinated spatial remodeling</p>
Data for the paper titled 'Dynamic Molecular Atlas for Cardiac Fibrosis at Single-Cell and Spatial Resolution: CD248 in Orchestrating Fibroblast-Immune Interaction'
<p>The deposited data were employed to generate the figures concerning single-cell RNA (scRNA) and spatial transcriptomic analyses in the paper titled 'Dynamic Molecular Atlas for Cardiac Fibrosis at Single-Cell and Spatial Resolution: CD248 in Orchestrating Fibroblast-Immune Interaction'.</p>
Overexpression of VEGF in dermal fibroblast cells accelerates the angiogenesis and wound healing function: in vitro and in vivo studies
<p>Human dermal fibroblasts (Hu02) were transfected by pcDNA3.1(-)-VEGF vector. Following selecting fibroblast cells with hygromycin, recombinant cells were investigated in terms of VEGF expression by quantifying method. We used Real-Time PCR assay to quantitate gene expression of vascular endothelial growth factor from manipulated cells and represented VEGF overexpression.</p> <p>Reverse transcription was performed from 1 μg of total RNA transcribed to complementary DNA (cDNA) through 1 μL of random hexamer primer. The reactions were incubated at 70°C for 5 minutes. After that, 5X RT-buffer, dNTP, and RT-enzyme were added, and the mixtures were incubated at 42°C for 60 minutes and 70°C for 10 minutes. Reverse transcription was performed from 500 ng total RNA using the RT2 First Strand Kit (SA Biosciences). Quantitative real-time PCR was performed (Ampliqon, Denmark) with 40 cycles at 95 oC for 15 seconds and 60 oC for 60 seconds.</p> <p>The normalization and all the data analysis were performed according to RESR and Graph pad-Prism 8 software.<br> For the normalization, it uses the housekeeping gene: β-Actin.<br> Target gene signals normalized to housekeeping genes; 2^-deltaCt, where deltaCt = (Ct_Target − Ct_HKG)].<br> </p>
Dataset related to article "'Understanding fibrosis pathogenesis via modelling macrophage-fibroblast interplay in immune-metabolic context"
<p>This record contains raw data related to article “ 'Understanding fibrosis pathogenesis via modelling macrophage-fibroblast interplay in immune-metabolic context"</p> <p>Abstract not avaible at the moment</p>
ROS-specific Huntingtin Interactions: G418 kill curve in TruHD fibroblasts
<p>Optimization step in the development of an inducible system expressing YFP-tagged huntingtin-specific intrabodies for stable transfection in TruHD fibroblasts.</p>
ROS-specific Huntingtin Interactions: GFP reactivation assay in HD patient fibroblasts
<p>Optimization step in the lead up to phenotypic analysis of ROS-dependent huntingtin interacting proteins. </p>
The effect of extracellular vesicles derived from oral squamous cell carcinoma on the metabolic profile of oral fibroblasts
<p><span>Oral cancer is one of the most common forms of head and neck cancers. Oral squamous cell carcinoma (OSCC) accounts for more than 90% of the oral malignancies. The molecular pathogenesis of OSCC is complex as it involves altered expression of specific genes and proteins, but also comprises changes in metabolic processes. It is suggested that extracellular vesicles (EVs) released by cancer cells may contribute to cancer development and metastasis by recruiting and changing phenotype of normal cells that surround the tumor. The aim of the project was to characterize the effect of OSCC EVs on the metabolic profile of normal oral fibroblasts (NOFs). Targeted </span><span>liquid chromatography-mass spectrometry metabolic profiling was performed on control cells and NOFs exposed to OSCC EVs for 24 and 48 h. Analysis of detected metabolites revealed that OSCC EVs affected NOFs the most after 24 h of exposure. Among metabolites that were significantly altered at 24 h, </span><span>pyruvate, ATP, UTP, coenzyme A, and dihydroxyacetone phosphate were upregulated, while fatty acids such as nervonic acid, linoleate, oleate, palmitoleic acid, and docosahexaenoic acid were downregulated. These findings were supported by Western blotting of pyruvate kinase M2 (PKM2). The metabolic pathways of glycolysis, </span><span>citric acid cycle, and </span><span>amino acid metabolism were enriched, suggesting that OSCC EVs cause phenotype switch in NOFs that may contribute to </span><span>acquiring</span><span> a pro-tumorigenic phenotype.</span></p>
Emergence of inflammatory fibroblasts with aging in Hermansky-Pudlak syndrome associated pulmonary fibrosis
<p>The longitudinal cellular interactions that drive pulmonary fibrosis are not well understood. To investigate the disease underpinnings associated with fibrosis onset and progression, we generated a scRNAseq atlas of lungs from young and aged mouse models of multiple subtypes of Hermansky-Pudlak syndrome (HPS), a collection of rare autosomal recessive diseases associated with albinism, platelet dysfunction, and pulmonary fibrosis. We identified an age-dependent increase in SAA3<sup>+</sup> inflammatory lung fibroblasts in HPS mice, including in double-mutant HPS1-2 mice which develop spontaneous fibrosis. HPS1 fibroblasts showed increased expression of IL-1R1, whereas alveolar type II epithelial cells from HPS2 mice induced the inflammatory gene signature in co-cultured fibroblasts. scRNAseq of lung tissue from three HPS1 patients similarly showed the presence of inflammatory fibroblasts and increased <em>IL1R1</em> expression on fibroblasts. These data posit complex interactions between dysfunctional epithelial cells, inflammatory fibroblasts, and recruited immune cells, suggesting potential opportunities for mitigation of the fibrotic cascade. </p> <p>This record contains gzipped anndata h5ad (hdf5) files corresponding to the human scRNA-seq data analyzed during this study. One file (`adata_processed_data_generated_in_study_zenodo.h5ad`) contains only data derived from new samples processed in this study. Another file (`adata_processed_combined_zenodo.h5ad`) contains the aforementioned data from new samples, as well as data from previously published studies that are publicly available (Guo et. al., 2023, Tsukui et.al., 2022, Habermann et. al., 2020). Raw gene expression counts, as well as normalized counts, are provided as values in the `layers` attribute of the anndata object. Cell annotations and projection coordinates are similarly provided in the `obs` and `obsm` attributes of the object, respectively. The AnnData and Scanpy python libraries are required to load and re-process these data. </p>
Macrophage Secreted TGF-β1 Contributes to Fibroblast Activation and Ureteral Stricture Following Ablation Injury
<p>Original dataset for figures.</p>
Attenuation of chronic T cell responses through constitutive COX2-dependent prostanoid synthesis by lymph node fibroblasts
<p>Raw data (in microsoft excel format) which were used to generate the figures in this manuscript. One worksheet per figure.</p>
Fibroblast-derived PI16 as a novel regulator of neuropathic pain
<p>Non-neuronal cells, including glia and leukocytes contribute to chronic pain. Here we identify fibroblasts secreting the protein PI16 as novel regulator of neuropathic pain. Mice deficient in PI16, a member of the CAP superfamily of proteases, are protected against neuropathic pain induced by spared nerve injury (SNI) or paclitaxel. SNI increases PI16 in fibroblasts and in vitro myofiborblast differentiation increases PI16 expression and secretion. In vitro, PI16 conditioned medium promotes migration of immune cells across the endothelial layer. Consistently, protection against neuropathic pain in PI16-/- mice was associated with reduced endothelial barrier permeability, lower leukocyte infiltration and reduced activation of the endothelial barrier regulator MLCK. Collectively our findings indicate that the fibroblast- derived protein PI16 promotes neuropathic pain by increasing vascular permeability and cellular infiltration. Due to its key role in pain and limited cellular distribution PI16 is an attractive novel target for pain management.</p>
ROS-Specific Huntingtin Interactions: Testing PARG activity in HD patient fibroblasts
<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>
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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.