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1,276
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Dataset results
1,276 results for “Stromal cells”
RNA-seq of healthy CD34+ HSPCs after co-culture with myelodyplastic syndrome patient-derived mesenchymal stromal cells
GEO Series GSE119916. Homo sapiens. 9 samples. Type: Expression profiling by high throughput sequencing.
In vivo isolated HER2/neu-Prim1 Primary, Residual, and Recurrent Tumor Cells, and Recurrent Tumor Stromal Cells
GEO Series GSE60609. Mus musculus. 12 samples. Type: Expression profiling by array.
Expression data from monocyte-derived macrophages co-cultured in the presence of multiple myeloma (MM) cell line and/or MM-bone marrow stromal cell (BMSC)
GEO Series GSE122160. Homo sapiens. 10 samples. Type: Expression profiling by array.
Single-cell analysis of stromal AR deletion on the progression of mouse prostate tumors induced by hormonal carcinogenesis
GEO Series GSE186114. Mus musculus. 4 samples. Type: Expression profiling by high throughput sequencing.
Spleen vs SDF1 alpha (Stromal cell derived factor-1) Treated B cell
GEO Series GSE397. Mus musculus. 12 samples. Type: Expression profiling by array.
Molecular profiling of adipose tissue-derived stromal cells cultured in hepatogenic medium
GEO Series GSE12399. Homo sapiens. 4 samples. Type: Expression profiling by array.
Expression data from human cornea epithelial and stromal cells and tissue-engineered anterior lamelar corneas
GEO Series GSE86584. Homo sapiens. 6 samples. Type: Expression profiling by array.
Metabolic adaptation of stromal cells to fatty acid drives metastasis of oral squamous cell carcinoma
GEO Series GSE312946. Homo sapiens. 16 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
Landscape profiling of small RNAs in extracellular vesicles secreted by senescent human stromal cells after DNA damage treatment
GEO Series GSE128927. Homo sapiens. 6 samples. Type: Non-coding RNA profiling by high throughput sequencing.
Gene expression profiling of uterine stromal and epithelial cells isolated from Msx1Msx2 floxed and Msx1Msx2 ablated mice on day 4 of pregnancy
GEO Series GSE30969. Mus musculus. 4 samples. Type: Expression profiling by array.
Dataset related to the article "Neuropeptide Y promotes adipogenesis of human cardiac mesenchymal stromal cells in arrhythmogenic cardiomyopathy"
<p>This record contains raw data related to the article “Neuropeptide Y promotes adipogenesis of human cardiac mesenchymal stromal cells in arrhythmogenic cardiomyopathy"</p> <p><strong>Background: </strong>Arrhythmogenic Cardiomyopathy (AC) is a familial cardiac disease, mainly caused by mutations in desmosomal genes. AC hearts show fibro-fatty myocardial replacement, which favors stress-related life-threatening arrhythmias, predominantly in the young and athletes. AC lacks effective therapies, as its pathogenesis is poorly understood. Recently, we showed that cardiac Mesenchymal Stromal Cells (cMSCs) contribute to adipose tissue in human AC hearts, although the underlying mechanisms are still unclear.</p> <p><strong>Purpose: </strong>We hypothesize that the sympathetic neurotransmitter, Neuropeptide Y (NPY), participates to cMSC adipogenesis in human AC.</p> <p><strong>Methods: </strong>For translation of our findings, we combined in vitro cytochemical, molecular and pharmacologic assays on human cMSCs, from myocardial biopsies of healthy controls and AC patients, with the use of existing drugs to interfere with the predicted AC mechanisms. Sympathetic innervation was inspected in human autoptic heart samples, and NPY plasma levels measured in healthy and AC subjects.</p> <p><strong>Results: </strong>AC cMSCs expressed higher levels of pro-adipogenic isotypes of NPY-receptors (i.e. Y1-R, Y5-R). Consistently, NPY enhanced adipogenesis in AC cMSCs, which was blocked by FDA-approved Y1-R and Y5-R antagonists. AC-associated PKP2 reduction directly caused NPY-dependent adipogenesis in cMSCs. In support of the involvement of sympathetic neurons (SNs) and NPY in AC myocardial remodeling, patients had elevated NPY plasma levels and, in human AC hearts, SNs accumulated in fatty areas and were close to cMSCs.</p> <p><strong>Conclusions: </strong>Independently from the disease origin, AC causes in cMSCs a targetable gain of responsiveness to NPY, which leads to increased adipogenesis, thus playing a role in AC myocardial remodeling.</p>
Dataset related to the article " Nicotinic Acid Adenine Dinucleotide Phosphate Induces Intracellular Ca2+ Signalling and Stimulates Proliferation in Human Cardiac Mesenchymal Stromal Cells"
<p>This record contains raw data related to the article “Nicotinic Acid Adenine Dinucleotide Phosphate Induces Intracellular Ca<sup>2+</sup> Signalling and Stimulates Proliferation in Human Cardiac Mesenchymal Stromal Cells"</p> <p>Abstract</p> <p>Nicotinic acid adenine dinucleotide phosphate (NAADP) is a newly discovered second messenger that gates two pore channels 1 (TPC1) and 2 (TPC2) to elicit endo-lysosomal (EL) Ca<sup>2+</sup> release. NAADP-induced lysosomal Ca<sup>2+</sup> release may be amplified by the endoplasmic reticulum (ER) through the Ca<sup>2+</sup>-induced Ca<sup>2+</sup> release (CICR) mechanism. NAADP-induced intracellular Ca<sup>2+</sup> signals were shown to modulate a growing number of functions in the cardiovascular system, but their occurrence and role in cardiac mesenchymal stromal cells (C-MSCs) is still unknown. Herein, we found that exogenous delivery of NAADP-AM induced a robust Ca<sup>2+</sup> signal that was abolished by disrupting the lysosomal Ca<sup>2+</sup> store with Gly-Phe β-naphthylamide, nigericin, and bafilomycin A1, and blocking TPC1 and TPC2, that are both expressed at protein level in C-MSCs. Furthermore, NAADP-induced EL Ca<sup>2+</sup> release resulted in the Ca<sup>2+</sup>-dependent recruitment of ER-embedded InsP<sub>3</sub>Rs and SOCE activation. Transmission electron microscopy revealed clearly visible membrane contact sites between lysosome and ER membranes, which are predicted to provide the sub-cellular framework for lysosomal Ca<sup>2+</sup> to recruit ER-embedded InsP<sub>3</sub>Rs through CICR. NAADP-induced EL Ca<sup>2+</sup> mobilization via EL TPC was found to trigger the intracellular Ca<sup>2+</sup> signals whereby Fetal Bovine Serum (FBS) induces C-MSC proliferation. Furthermore, NAADP-evoked Ca<sup>2+</sup> release was required to mediate FBS-induced extracellular signal-regulated kinase (ERK), but not Akt, phosphorylation in C-MSCs. These finding support the notion that NAADP-induced TPC activation could be targeted to boost proliferation in C-MSCs and pave the way for future studies assessing whether aberrant NAADP signaling in C-MSCs could be involved in cardiac disorders.</p>
Dataset related to the article "Ca2+ dysregulation in cardiac stromal cells sustains fibro-adipose remodeling in Arrhythmogenic Cardiomyopathy and can be modulated by flecainide"
<p>This record contains raw data related to the article "Ca2+ dysregulation in cardiac stromal cells sustains fibro-adipose remodeling in Arrhythmogenic Cardiomyopathy and can be modulated by flecainide" </p> <p>Abstract</p> <p><strong>Background: </strong>Cardiac mesenchymal stromal cells (C-MSC) were recently shown to differentiate into adipocytes and myofibroblasts to promote the aberrant remodeling of cardiac tissue that characterizes arrhythmogenic cardiomyopathy (ACM). A calcium (Ca<sup>2+</sup>) signaling dysfunction, mainly demonstrated in mouse models, is recognized as a mechanism impacting arrhythmic risk in ACM cardiomyocytes. Whether similar mechanisms influence ACM C-MSC fate is still unknown. Thus, we aim to ascertain whether intracellular Ca<sup>2+</sup> oscillations and the Ca<sup>2+</sup> toolkit are altered in human C-MSC obtained from ACM patients, and to assess their link with C-MSC-specific ACM phenotypes.</p> <p><strong>Methods and results: </strong>ACM C-MSC show enhanced spontaneous Ca<sup>2+</sup> oscillations and concomitant increased Ca<sup>2+</sup>/Calmodulin dependent kinase II (CaMKII) activation compared to control cells. This is manly linked to a constitutive activation of Store-Operated Ca<sup>2+</sup> Entry (SOCE), which leads to enhanced Ca<sup>2+</sup> release from the endoplasmic reticulum through inositol-1,4,5-trisphosphate receptors. By targeting the Ca<sup>2+</sup> handling machinery or CaMKII activity, we demonstrated a causative link between Ca<sup>2+</sup> oscillations and fibro-adipogenic differentiation of ACM C-MSC. Genetic silencing of the desmosomal gene PKP2 mimics the remodelling of the Ca<sup>2+</sup> signalling machinery occurring in ACM C-MSC. The anti-arrhythmic drug flecainide inhibits intracellular Ca<sup>2+</sup> oscillations and fibro-adipogenic differentiation by selectively targeting SOCE.</p> <p><strong>Conclusions: </strong>Altogether, our results extend the knowledge of Ca<sup>2+</sup> dysregulation in ACM to the stromal compartment, as an etiologic mechanism of C-MSC-related ACM phenotypes. A new mode of action of flecainide on a novel mechanistic target is unveiled against the fibro-adipose accumulation in ACM.</p>
Expression data from bone marrow stromal cells (CD45.1-Ter119-)
GEO Series GSE120286. Mus musculus. 9 samples. Type: Expression profiling by array.
BMP7 Signaling in TGFb Receptor-2 deficient Stromal Cells Provokes Epithelial Carcinogenesis
GEO Series GSE106442. Mus musculus. 3 samples. Type: Expression profiling by array.
Microarray for density study of mouse Adipose-derived Stromal Cells (ASCs)
GEO Series GSE19924. Mus musculus. 12 samples. Type: Expression profiling by array.
Comparing transcriptional effects of radioprotection with dmPGE2 to that of other EP receptor agonists in both hematopoietic stem cells and bone marrow stromal cells
GEO Series GSE218443. Mus musculus. 52 samples. Type: Expression profiling by high throughput sequencing.
Engineering a haematopoietic stem cell niche by reprogramming mesenchymal stromal cells (ATAC-Seq)
GEO Series GSE112231. Mus musculus. 10 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
Stromal Repair via Long-term Engraftment of Primary Bone Marrow Stroma Improves Hematopoietic Stem Cell Transplantation
GEO Series GSE79091. Mus musculus. 6 samples. Type: Expression profiling by array.
Effect of in vivo culture condition on the proliferation and differentiation of rat adipose-derived stromal cells
GEO Series GSE261680. Rattus norvegicus. 9 samples. Type: Expression profiling by high throughput sequencing.
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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.