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Single cell resolution regulatory landscape of the mouse kidney highlights cellular differentiation programs and renal disease targets

ABSTRACT: Single cell resolution regulatory landscape of the mouse kidney highlights cellular differentiation programs and renal disease targets

PROVIDER: PRJNA660027 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12541202.fastq.gz	Fastqsanger.gz
	SRR12541203.fastq.gz	Fastqsanger.gz
	SRR12541204.fastq.gz	Fastqsanger.gz
	SRR12541205.fastq.gz	Fastqsanger.gz
	SRR12541206.fastq.gz	Fastqsanger.gz

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Single cell resolution regulatory landscape of the mouse kidney highlights cellular differentiation programs and renal disease targets

Project description:Determining the epigenetic program that generates unique cell types in the kidney is critical for understanding cell-type heterogeneity during tissue homeostasis and injury response. Here, we profiled open chromatin and gene expression in developing and adult mouse kidneys at single cell resolution. We show critical reliance of gene expression on distal regulatory elements (enhancers). We define key cell type-specific transcription factors and major gene-regulatory circuits for kidney cells. Dynamic chromatin and expression changes during nephron progenitor differentiation demonstrated that podocyte commitment occurs early and is associated with sustained Foxl1 expression. Renal tubule cells followed a more complex differentiation, where Hfn4a was associated with proximal and Tfap2b with distal fate. Mapping single nucleotide variants associated with human kidney disease identified critical cell types, developmental stages, genes, and regulatory mechanisms. We provide a global single cell resolution view of chromatin accessibility of kidney development. The dataset is available via interactive public websites.

2020-08-29 | GSE157079 | GEO

Single cell regulatory landscape of the mouse kidney highlights cellular differentiation programs and disease targets.

Project description:Determining the epigenetic program that generates unique cell types in the kidney is critical for understanding cell-type heterogeneity during tissue homeostasis and injury response. Here, we profile open chromatin and gene expression in developing and adult mouse kidneys at single cell resolution. We show critical reliance of gene expression on distal regulatory elements (enhancers). We reveal key cell type-specific transcription factors and major gene-regulatory circuits for kidney cells. Dynamic chromatin and expression changes during nephron progenitor differentiation demonstrates that podocyte commitment occurs early and is associated with sustained Foxl1 expression. Renal tubule cells follow a more complex differentiation, where Hfn4a is associated with proximal and Tfap2b with distal fate. Mapping single nucleotide variants associated with human kidney disease implicates critical cell types, developmental stages, genes, and regulatory mechanisms. The single cell multi-omics atlas reveals key chromatin remodeling events and gene expression dynamics associated with kidney development.

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Plasminogen activator inhibitor-2 regulates immune response in kidney injury and renal aging mpact of plasminogen activator inhibitor-2 in kidney injury and renal aging

Project description:The plasminogen activator inhibitor-2 (PAI-2; encoded by the SerpinB2 gene) has been described in the context of macrophage activation and in cellular senescence. As both mechanisms are important in kidney disease we tested a possible role of PAI-2 in renal injury and repair. Methods:Aging, ischemia/reperfusion injury and unilateral ureteral obstruction were performed on the mice. Bone marrow was transplantefrom SerpinB2-/- to wild-type littermates and vice versa. Primary tubular cells and macrophages from SerpinB2-/- and wildtype mice were used for functional studies and transcriptional profiling. Results: PAI-2 expression was up-regulated in cultured senescent tubular cells and in kidneys of aged mice. In the lack of PAI-2 in SerpinB2-/- mice was associated with enhanced renal fibrosis and an inflammatory phenotype during aging and in kidney injury models. While acute injury was associated with fewer monocytes/macrophages in SerpinB2-/- kidneys the subsequent resolution of inflammation seen in wildtype kidneys was lacking in knockout mice. Conclusion: PAI-2 regulates renal aging, tubular damage, and resolution of inflammation. PAI-2 is crucial for kidney repair in mice .

2019-10-22 | GSE139156 | GEO

ST2+ T-regulatory Cells in Renal Inflammation and Fibrosis following Ischemic Kidney Injury

Project description:The role of IL-33 and its receptor ST2 in kidney injury is not well understood. This study demonstrates the importance of ST2 expression on the T-regulatory cells (Tregs) for the resolution of renal injury by suppressing inflammation and fibrosis. Treg-specific deletion of ST2, detrimentally impacted late outcomes of renal injury worsening the impairment of kidney function, inflammation, and fibrosis.

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Transcriptional programs in transient embryonic zones of the cerebral cortex defined by high-resolution mRNA-sequencing

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2011-08-22 | E-GEOD-30765 | biostudies-arrayexpress

High-resolution translatome analysis reveals cortical cell programs during early soybean nodulation

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Transcriptional programs define intratumoral heterogeneity of Ewing sarcoma at single cell resolution

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Renal allograft dysfunction (kidney tissue data set)

Project description:The study comprises various components: Samples TD: We aims to screen out different gene expression profile in donor biopsies after revascularization , We aims to predict renal allograft dysfunction early after transplantation. Samples AR, ATN, Tx: We aim to screen out different gene expression profile in acute rejection on the kidney. We aim to screen out different gene expression profile in acute tubular necrosis on the kidney. Results from the various study components can help to diagnose renal allograft dysfunction with different causes by distinct gene expression profile. Keywords: acute rejection, acute tubular necrosis, donor biopsies, renal allograft dysfunction Samples AR1-AR17: This study has been accomplished with 17 patients of acute rejection on the kidney.Technical replicates: 2 replicates Samples ATN1-ATN5: This study has been accomplished with 5 patients of acute tubular necrosis on the kidney. Technical replicates: 2 replicates Samples Tx1-Tx14: This study has been accomplished with 14 patients of stable renal function on the kidney.Tecnical replicates:2 replicates(except Tx12) Samples TD1-TD12: This study has been accomplished with 12 patients of donor tissue with stable function early after transplantation on the kidney.Technical replicates: 2 replicates Samples TD13-TD21: This study has been accomplished with 9 patients of donor tissue with renal dysfunction early after transplantation on the kidney.Technical replicates: 2 replicates

2011-02-02 | E-GEOD-26578 | biostudies-arrayexpress

Integrative analysis demonstrates widespread NOTCH pathway activation in patients with renal cancer and reveals aberrant DNA methylation that targets the regulatory regions of the kidney genome

Project description:Even though mutations in epigenetic regulators have been seen in renal neoplasms, their effects on the epigenome have not been elucidated. High resolution analysis of DNA methylation was performed in clear cell RCCs and matched microdissected renal tubular controls and revealed widespread hypermethylation that preferentially affected gene bodies and CpG shores. Aberrant methylation was particularly enriched in kidney specific enhancer regions associated with H3K4Me1 marks. MOTIF analysis of aberrantly methylated loci revealed enrichment for AHR, HAIRY and HIF-1 transcription factors, reflecting dysregulated hypoxia and NOTCH pathways in RCC. Parallel copy number analysis demonstrated that both genetic and epigenetic alterations led to NOTCH pathway activation in RCC. NOTCH ligands,JAGGED1 and JAGGED2, were overexpressed and associated with hypomethylation and amplification respectively in RCC samples. Examination of TCGA RNA-seq dataset revealed widespread activation of NOTCH pathway in 405 RCC samples. Samples with NOTCH pathway activation were also clinically distinct and were associated with better overall survival. Finally, transgenic expression of NOTCH1 led to dysplastic hyperproliferation of tubular epithelial cells in vivo confirming the procarcinogenic role of NOTCH. In summary, our study is the first global methylome analysis of RCC and reveals that mechanistic basis of NOTCH pathway activation in RCC. We analyzed the methylome of clear cell renal cell cancer (CCRCC) by the HELP assay. 13 cases of histologically verified CCRCC tumor samples were compared to 13 control microdissected proximal tubules from non-tumor part of nephrectomy samples

2014-07-31 | E-GEOD-49420 | biostudies-arrayexpress

Renal congestion exacerbates acute kidney injury in mice

Project description:The number of heart failure (HF) patients is increasing. HF is frequently accompanied by kidney dysfunction and such organ failure is closely related. Recent investigations revealed that increased renal venous pressure, rather than decreased cardiac output, causes the deterioration of kidney function in HF patients; however, the underlying responsible mechanisms are unknown. We demonstrated that reduced blood flow speed in peritubular capillaries (PTCs) by renal congestion and upregulation of nuclear factor-κB (NF-κB) signaling synergistically exacerbate kidney injury. We generated a novel mouse model with unilateral renal congestion by coarctation of the inferior vena cava between renal veins. Intravital imaging highlighted the notable dilatation of PTCs and decreased renal blood flow speed in the congestive kidney. Renal damage after ischemia reperfusion injury was exacerbated in the congestive kidney and accumulation of polymorphonuclear leukocytes (PMNs) within PTCs was observed at the acute phase after injury. Pharmacological inhibition of NF-κB ameliorated renal congestion-mediated exacerbation of kidney injury. In vitro, adhesion of PMNs on the TNFα-stimulated endothelial cells was accelerated by perfusion of PMNs at a slower speed, which was cancelled by the inhibition of NF-κB signaling. Our study demonstrates the importance of slower blood flow accompanying activated NF-κB signaling in the congestive kidney in the exacerbation of renal injury. These mechanisms may explain how increased renal venous pressure in HF patients causes the deterioration of kidney dysfunction. Inhibition of NF-κB signaling may be a therapeutic candidate for the vicious cycle between heart and kidney failure with increased renal venous pressure.

2024-02-16 | GSE166838 | GEO

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