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Single cell transcriptomics and chromatin accessibility profiling elucidate the kidney protective mechanism of mineralocorticoid receptor antagonism [bulk RNA-seq]

ABSTRACT: Single cell transcriptomics and chromatin accessibility profiling elucidate the kidney protective mechanism of mineralocorticoid receptor antagonism [bulk RNA-seq]

PROVIDER: PRJNA762176 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15833600_1.fastq.gz	Fastqsanger.gz
	SRR15833600_2.fastq.gz	Fastqsanger.gz
	SRR15833601_1.fastq.gz	Fastqsanger.gz
	SRR15833601_2.fastq.gz	Fastqsanger.gz
	SRR15833602_1.fastq.gz	Fastqsanger.gz

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Single cell transcriptomics and chromatin accessibility profiling elucidate the kidney protective mechanism of mineralocorticoid receptor antagonism

Project description:Single cell transcriptomics and chromatin accessibility profiling elucidate the kidney protective mechanism of mineralocorticoid receptor antagonism

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Single cell transcriptomics and chromatin accessibility profiling elucidate the kidney protective mechanism of mineralocorticoid receptor antagonism [snATAC-seq]

Project description:Single cell transcriptomics and chromatin accessibility profiling elucidate the kidney protective mechanism of mineralocorticoid receptor antagonism [snATAC-seq]

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Single cell transcriptomics and chromatin accessibility profiling elucidate the kidney protective mechanism of mineralocorticoid receptor antagonism [snRNA-seq]

Project description:Single cell transcriptomics and chromatin accessibility profiling elucidate the kidney protective mechanism of mineralocorticoid receptor antagonism [snRNA-seq]

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Single cell transcriptomics and chromatin accessibility profiling elucidate the kidney protective mechanism of mineralocorticoid receptor antagonism [snATAC-seq]

Project description:Mineralocorticoids play a critical role in maintaining sodium and potassium homeostasis and pathophysiological processes including hypertrophy, inflammation and fibrosis. Mineralocorticoid antagonists (MRAs) have shown to protect from kidney and heart disease, however, their molecular mechanism of action is poorly understood. Here we performed single nuclei and bulk transcriptomics and chromatin accessibility analysis to characterize the mode of kidney protection by steroidal and non-steroidal MRA treatment in a rat model of mineralocorticoid-induced cardiorenal end-organ damage. We define mineralocorticoid sensitive cell types and gene network in the kidney. We show that in diseased kidneys specific proximal tubule cells develop an injured profibrotic phenotype expressing Spp1 and Il34. Nonsteroidal finerenone protects from profibrotic differentiation of proximal tubule cells. Profibrotic gene signature can classify human kidney tissue samples and predict prognosis. Our multi-omics approach elucidates target cell types and potential mechanisms of renal protection by finerenone.

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Single cell transcriptomics and chromatin accessibility profiling elucidate the kidney protective mechanism of mineralocorticoid receptor antagonism [snRNA-seq]

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Single cell transcriptomics and chromatin accessibility profiling elucidate the kidney protective mechanism of mineralocorticoid receptor antagonism [bulk RNA-seq]

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Single cell transcriptomics and chromatin accessibility profiling elucidate the kidney protective mechanism of mineralocorticoid receptor antagonism

Project description:This SuperSeries is composed of the SubSeries listed below.

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Aldosterone-inducible genes in mineralocorticoid receptor expressed human endothelial cell lines

Project description:To elucidate the aldosterone-regulated genes in vascular endothelial cells, we developed human endothelial cell line (EAhy926) stably expressing human mineralocorticoid receptor by retroviral system (MR-EAhy). Then gene expression profile of MR-EAhy stimulated with or without aldosterone was compared using DNA microarray analysis.

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Project description:Non-steroidal mineralocorticoid receptor antagonism by finerenone is sufficient to improve function in preclinical muscular dystrophy

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Non-steroidal mineralocorticoid receptor antagonism by finerenone is sufficient to improve function in preclinical muscular dystrophy

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