Ena-DATASET-QCMG-21-04-2021-07:35:14:980-1022 - samples
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00001007533 | EGA |
REPOSITORIES: EGA
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Project description:sn-RNAseq profiling of the impact of a cytokine storm model in human cardiac organoids
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Project description:In order to unravel the impact of intestinal smooth muscle tissue on the intestinal epithelium, we isolated clean smooth muscle, cultured it for 24h in DMEM-F12, and collected the supernatant (muscle-SN). This supernatant was used to treat small intestinal organoids (made of intestinal epithelium), compared to normal ENR treatment. After 5 days of muscle-SN exposure, we disrupted the organoids, and directly isolate the RNA. RNA-seq was performed in this sample to assess the genetic changes induced by muscle products.
2021-09-27 | E-MTAB-9181 | biostudies-arrayexpress
Project description:Human cardiac organoids to model COVID‐19 cytokine storm induced cardiac injuries
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Project description:We use single cell RNA sequencing (scRNA-seq) to analyze the impact of NGB on early neural development based on cerebral organoids model.
2025-03-19 | GSE253940 | GEO
Project description:SARS-CoV2 infection leads to cardiac injury and dysfunction in 20-30% of hospitalized patients and higher rates of mortality in patients with pre-existing cardiovascular disease. Inflammatory factors released as part of the 'cytokine storm' are thought to play a critical role in cardiac dysfunction in severe COVID-19 patients. Here we use human cardiac organoid technology combined with high sensitivity phosphoproteomics and single nuclei RNA sequencing to identify inflammatory targets inducing cardiac dysfunction. This new pipeline allowed rapid progress and identification of putative therapeutics. We identify a novel interferon-gamma driven BRD4 (bromodomain protein 4)-fibrosis/iNOS axis as a key intracellular mediator of inflammation-induced cardiac dysfunction. This axis is therapeutically targetable using BRD4 inhibitors, which promoted full recovery of function in human cardiac organoids and prevented severe inflammation and death in a cytokine-storm mouse model. The BRD inhibitor INCB054329 was the most efficacious, and is a prime candidate for drug repurposing to attenuate cardiac dysfunction and improve COVID-19 mortality in humans.
2022-02-21 | PXD020994 | Pride
Project description:Acute cardiac injuries occur in 20%–25% of hospitalized COVID‐19 patients. Herein, we demonstrate that human cardiac organoids (hCOs) are a viable platform to model the cardiac injuries caused by COVID‐19 hyperinflammation. As IL‐1β is an upstream cytokine and a core COVID‐19 signature cytokine, it was used to stimulate hCOs to induce the release of a milieu of proinflammatory cytokines that mirror the profile of COVID‐19 cytokine storm. The IL‐1β treated hCOs recapitulated transcriptomic, structural, and functional signatures of COVID‐19 hearts. The comparison of IL‐1β treated hCOs with cardiac tissue from COVID‐19 autopsies illustrated the critical roles of hyper‐inflammation in COVID‐19 cardiac insults and indicated the cardioprotective effects of endothelium. The IL‐1β treated hCOs thus provide a defined and robust model to assess the efficacy and potential side effects of immunomodulatory drugs, as well as the reversibility of COVID‐19 cardiac in- juries at baseline and simulated exercise conditions.
2023-12-20 | GSE250520 | GEO
Project description:Kidney organoids are a valuable and innovative model to understand genetic diseases, kidney development and transcriptomic dynamics. However, their proteome has not been analyzed so far. Here, we analyzed the organoid proteome trajectory during differentiation. Genes involved in podocytopathies and cystic kidney diseases were abundantly expressed on protein level, distinguishing organoids from almost every available cell culture model. On their pathway to terminal differentiation, organoids developed increased deposition of extracellular matrix. Single cell transcriptomic analysis suggests that most changes locate to podocytes and early podocyte progenitors. This matrix deposition is different from commonly used animal models of glomerular disease. We grew organoids from two independent batches according to the Freedman protocol, and performed proteomic profiling (Freedman, Brooks et al. 2015, Czerniecki, Cruz et al. 2018). The IPSCs were differentiated for a three-week period until first spheroids from. From day 21 of the culture they were used in our experiments up until day 29, where off-target differentiation of organoids becomes an issue.
2023-05-12 | PXD029716 | Pride
Project description:In this study, we demonstrate the use of human cardiac organoids (comprised of cardiomyocyte, fibroblast, and endothelial origin) to model IR injury through a model of hypoxia and reoxygenation and therapeutic nanovesicle remodelling. Engineered nanovesicles (NVs), generated directly from human stem cells (SC), have been shown to influence cardiac tissue repair, and provide a platform for the reproducible, rapid, and scalable cell free-mediated therapy. Functionally, we demonstrate that administration of NVs (from different human induced pluripotent stem cell (iPSC) origin) during reoxygenation significantly increase cardiomyocyte survival and preserve contractility function (contractile duration, relaxation time, relaxation:contraction velocity). A mass-spectrometry-based proteomics approach was applied to decipher protein dynamics and molecular mechanisms of IR injury in human cardiac organoids following NV treatments
2025-12-10 | MSV000100182 | MassIVE
Project description:Schwann cells (SC) are crucial for normal conduction in peripheral nerves. They produce myelin, provide axonal metabolic support, and activate a reparatory phenotype after nerve injury. During aging, peripheral nerves present abnormal myelin, reduced SC density, and increased senescence. All these changes induce abnormal electrical conduction and consequently impaired function of target tissues, like for example, skeletal muscle weakness and cardiac arrhythmia. In order to understand differences between cardiac and sciatic nerve (SN) SC, as well as to explore age-related changes of function, we characterize two inducible CRE mouse models, Sox10CreERT2 and Plp1CreERT, to genetically trace SC by combining them with TdT reporter mice. To do this, we use FACS to sort tdt (+) cells from the heart and SN, and further perform RNAseq to characterize their gene expression. Complementarily, we confirm protein expression using immunofluorescence. Our data indicates that cardiac SC detected using the Plp1CreERT model are enriched for MPZ (+) myelinating SC. In addition, we describe a novel pro-angiogenic function for cardiac SC in young mice. Furthermore, we found that during aging, SC from SN activate collagen remodeling and secrete pro-inflammatory signals like TNFα. Finally, we detect increased neural-death associated genes in cardiac SC, which also have less expression of the fatty acid co-transporter FABP4, suggesting abnormal myelin formation. Thus, cardiac and musculoskeletal SC have different expression profiles, and undergo different but remarkable changes during aging, which can contribute to abnormal nerve function.
2025-10-03 | GSE282368 | GEO
Project description:HLA-DRB1*11:04:21 differs from HLA-DRB1*11:04:01 by one nucleotide substitution in codon 69 in exon 2.
| S-EPMC9544036 | biostudies-literature