Ontology highlight
ABSTRACT:
PROVIDER: PRJNA799138 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17687042_1.fastq.gz | Fastqsanger.gz | |||
| SRR17687042_2.fastq.gz | Fastqsanger.gz | |||
| SRR17687043_1.fastq.gz | Fastqsanger.gz | |||
| SRR17687043_2.fastq.gz | Fastqsanger.gz | |||
| SRR17687044_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 24 |
Similar Datasets
Project description:We constructed single-cell atlases of AKI induced by different etiologies, revealed potential homogeneity of injury patterns and heterogeneity between models in AKI. Extensive cell death and cytoskeletal remodeling events in proximal tubular cells (PTCs) as well as aberrant proliferation and inflammation of endothelial cells (ECs) in AKI are common injury patterns across different AKI models. However, there are differences in injury outcomes in PTCs with different etiologies, and ECs also have distinct transcriptional profiles.
2022-04-30 | GSE197266 | GEO
Project description:Inflammation plays a crucial role in the development of acute kidney injury (AKI) and subsequent chronic kidney disease (CKD) following renal ischemia-reperfusion (IR). It has been demonstrated that metabolites from the gut microbiota can trigger inflammatory responses and modulate renal damage induced by IR. However, the exact driving factors and underlying mechanisms of this process remain unclear. Trimethylamine N-oxide (TMAO), a choline metabolite derived from the gut, has been observed to increase in AKI and CKD patients. Our study reveals that glycyrrhizic acid (GA) exacerbates IR-induced AKI and subsequent CKD through TMAO. To delve into the underlying mechanisms, we employed single-cell sequencing to construct a molecular map of kidney cells.
2024-09-09 | GSE244890 | GEO
Project description:It has been widely recognized that Acute kidney injury (AKI)represents a multifactorial, heterogeneous syndrome, or a spectrum of diseases. AKI is associated with prolonged hospitalization and high mortality, and it predisposes individuals to chronic kidney disease. To date, no effective AKI treatments have been established. This study used single-cell RNA sequencing (scRNA-seq) to explore novel molecular mechanisms and gene targets for AKI. We identifies a distinct cell-specific gene expression profile, pathogenic signaling pathways and potential cell-cell communications in the pathogenesis of AKI. These findings will provide a promising novel landscape for mechanisms and treatment of AKI.
2022-05-04 | GSE174220 | GEO
Project description:Background: Acute kidney injury (AKI) occurs frequently in critically ill patients and is associated with adverse outcomes. Cellular mechanisms underlying AKI and kidney cell responses to injury remain incompletely understood. Methods: We performed single-nuclei transcriptomics, bulk transcriptomics, molecular imaging studies, and conventional histology on kidney tissues from 8 individuals with severe AKI (stage 2 or 3 according to Kidney Disease: Improving Global Outcomes (KDIGO) criteria). Specimens were obtained within 1-2 hours after individuals had succumbed to critical illness associated with respiratory infections, with 4 of 8 individuals diagnosed with COVID-19. Control kidney tissues were obtained post-mortem or after nephrectomy from individuals without AKI. Results: High-depth single cell-resolved gene expression data of human kidneys affected by AKI revealed enrichment of novel injury-associated cell states within the major cell types of the tubular epithelium, in particular in proximal tubules, thick ascending limbs and distal convoluted tubules. Four distinct, hierarchically interconnected injured cell states were distinguishable and characterized by transcriptome patterns associated with oxidative stress, hypoxia, interferon response, and epithelial-to-mesenchymal transition, respectively. Transcriptome differences between individuals with AKI were driven primarily by the cell type-specific abundance of these four injury subtypes rather than by private molecular responses. AKI-associated changes in gene expression between individuals with and without COVID-19 were similar. Conclusions: The study provides an extensive resource of the cell type-specific transcriptomic responses associated with critical illness-associated AKI in humans, highlighting recurrent disease-associated signatures and inter-individual heterogeneity. Personalized molecular disease assessment in human AKI may foster the development of tailored therapies.
2022-09-08 | GSE210622 | GEO
Project description:Human neurons engineered from induced pluripotent stem cells (iPSCs) through Neurogenin 2 (Ngn2) overexpression are widely used to study neuronal differentiation mechanisms and to model neurological diseases. However, the differentiation paths and heterogeneity of emerged neurons have not been fully explored. Here we used single-cell transcriptomics to dissect the cell states that emerge during Ngn2 overexpression across a time course from pluripotency to neuron functional maturation. We find a substantial molecular heterogeneity in the neuron types generated, with at least two populations that express genes associated with neurons of the peripheral nervous system. Neuron heterogeneity is observed across multiple iPSC clones and lines from different individuals. We find that neuron fate acquisition is sensitive to Ngn2 expression level and the duration of Ngn2 forced expression. Our data reveals that Ngn2 dosage can regulate neuron fate acquisition, and that Ngn2-iN heterogeneity can confound results that are sensitive to neuron type.
2021-08-05 | E-MTAB-10632 | biostudies-arrayexpress
Project description:The pathogenesis and molecular signature of human acute kidney injury (AKI) remain incompletely understood, in part, owing to the heterogeneity of the disease. Further, the link between animal models and human AKI is not well characterized. Transcript expression of AKI in 39 native human renal biopsy samples was compared to 9 reference nephrectomies. These data demonstrate that the molecular signature segregates patients with AKI in spite of similar pathological and clinical phenotyping. Such molecular characterization will offer advantages in categorizing and understanding the underlying pathogenesis of phenotypically complex and heterogeneous forms of AKI.
2019-10-28 | GSE139061 | GEO
Project description:Mononuclear phagocytes have important functions in regulating tissue injury and regeneration after AKI. We tested the hypothesis that kidney resident macrophages (R2) and infiltrative mononuclear phagocytes (R1) exist in distinct transcriptional subsets that are resolvable by single cell RNA sequencing. A further objective was to identify transcriptional signatures for those subsets. By cell sorting R2 and R1 cells from quiescent and injured mouse kidneys, we found remarkable heterogeneity among intrarenal innate immune cells. We define four subsets of dendritic cells and six subsets of R2 cells and specify differentially expressed genes that identify these cell types. Additionally, we observed subset-specific transcriptional responses to AKI. R2 cells, which express surface phenotype homogeneity, adopt distinct transcriptional programs in the steady state and after injury. Expression of MHC class II and invariant chain genes are decreased in a predominant subset of R2 cells after AKI. In contrast, other macrophage lineage-defining genes such as C1qa, b, and c, are expressed at similar levels across R2 cell subsets and their expression does not change in response to injury. This study has allowed us to identify R2 and R1 subsets that may prove to be therapeutic targets for inhibiting damaging inflammation and fibrosis or promoting tissue regeneration.
2023-09-01 | GSE157338 | GEO
Project description:Extensive cellular heterogeneity exists within specific immune-cell subtypes classified as a single lineage, but its molecular underpinnings are rarely characterized at a genomic scale. Here, we use single-cell RNA-seq to investigate the molecular mechanisms governing heterogeneity and pathogenicity of Th17 cells isolated from the central nervous system (CNS) and lymph nodes (LN) at the peak of autoimmune encephalomyelitis (EAE) or polarized in vitro under either pathogenic or non-pathogenic differentiation conditions. Computational analysis reveals a spectrum of cellular states in vivo, including a self-renewal state, Th1-like effector/memory states and a dysfunctional/senescent state. Relating these states to in vitro differentiated Th17 cells, unveils genes governing pathogenicity and disease susceptibility. Using knockout mice, we validate four novel genes: Gpr65, Plzp, Toso and Cd5l (in a companion paper). Cellular heterogeneity thus informs Th17 function in autoimmunity, and can identify targets for selective suppression of pathogenic Th17 cells while sparing non-pathogenic tissue-protective ones. Single-cell transcriptional profiling of Th17 cells, harvested at peak of disease in EAE from LN
2015-11-20 | E-GEOD-75108 | biostudies-arrayexpress
Project description:Extensive cellular heterogeneity exists within specific immune-cell subtypes classified as a single lineage, but its molecular underpinnings are rarely characterized at a genomic scale. Here, we use single-cell RNA-seq to investigate the molecular mechanisms governing heterogeneity and pathogenicity of Th17 cells isolated from the central nervous system (CNS) and lymph nodes (LN) at the peak of autoimmune encephalomyelitis (EAE) or polarized in vitro under either pathogenic or non-pathogenic differentiation conditions. Computational analysis reveals a spectrum of cellular states in vivo, including a self-renewal state, Th1-like effector/memory states and a dysfunctional/senescent state. Relating these states to in vitro differentiated Th17 cells, unveils genes governing pathogenicity and disease susceptibility. Using knockout mice, we validate four novel genes: Gpr65, Plzp, Toso and Cd5l (in a companion paper). Cellular heterogeneity thus informs Th17 function in autoimmunity, and can identify targets for selective suppression of pathogenic Th17 cells while sparing non-pathogenic tissue-protective ones. Single-cell transcriptional profiling of Th17 cells, differentiated in vitro for 48h
2015-11-20 | E-GEOD-75109 | biostudies-arrayexpress
Project description:Extensive cellular heterogeneity exists within specific immune-cell subtypes classified as a single lineage, but its molecular underpinnings are rarely characterized at a genomic scale. Here, we use single-cell RNA-seq to investigate the molecular mechanisms governing heterogeneity and pathogenicity of Th17 cells isolated from the central nervous system (CNS) and lymph nodes (LN) at the peak of autoimmune encephalomyelitis (EAE) or polarized in vitro under either pathogenic or non-pathogenic differentiation conditions. Computational analysis reveals a spectrum of cellular states in vivo, including a self-renewal state, Th1-like effector/memory states and a dysfunctional/senescent state. Relating these states to in vitro differentiated Th17 cells, unveils genes governing pathogenicity and disease susceptibility. Using knockout mice, we validate four novel genes: Gpr65, Plzp, Toso and Cd5l (in a companion paper). Cellular heterogeneity thus informs Th17 function in autoimmunity, and can identify targets for selective suppression of pathogenic Th17 cells while sparing non-pathogenic tissue-protective ones. Single-cell transcriptional profiling of Th17 cells, harvested at peak of disease in EAE from CNS
2015-11-20 | E-GEOD-75107 | biostudies-arrayexpress