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

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

PROVIDER: PRJNA762078 | 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 [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]

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

Project description: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 [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.

2023-11-17 | GSE183840 | GEO

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

2023-11-17 | GSE183839 | GEO

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

2023-11-17 | GSE183841 | GEO

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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Mineralocorticoid Receptor Antagonism by Finerenone Attenuates Established Pulmonary Hypertension in Rats

Project description:Mineralocorticoid Receptor Antagonism by Finerenone Attenuates Established Pulmonary Hypertension in Rats

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Mineralocorticoid Receptor Antagonism by Finerenone Attenuates Established Pulmonary Hypertension in Rats

Project description:We studied the ability of the non-steroidal Mineralocorticoid Receptor (MR) antagonist finerenone to attenuate vascular remodeling and pulmonary hypertension (PH) using two complementary preclinical models [the monocrotaline (MCT) and Sugen

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Single-cell transcriptomics and chromatin accessibility profiling elucidate the kidney-protective mechanism of mineralocorticoid receptor antagonists.

Project description:Mineralocorticoid excess commonly leads to hypertension (HTN) and kidney disease. In our study, we used single-cell expression and chromatin accessibility tools to characterize the mineralocorticoid target genes and cell types. We demonstrated that mineralocorticoid effects were established through open chromatin and target gene expression, primarily in principal and connecting tubule cells and, to a lesser extent, in segments of the distal convoluted tubule cells. We examined the kidney-protective effects of steroidal and nonsteroidal mineralocorticoid antagonists (MRAs), as well as of amiloride, an epithelial sodium channel inhibitor, in a rat model of deoxycorticosterone acetate, unilateral nephrectomy, and high-salt consumption-induced HTN and cardiorenal damage. All antihypertensive therapies protected against cardiorenal damage. However, finerenone was particularly effective in reducing albuminuria and improving gene expression changes in podocytes and proximal tubule cells, even with an equivalent reduction in blood pressure. We noted a strong correlation between the accumulation of injured/profibrotic tubule cells expressing secreted posphoprotein 1 (Spp1), Il34, and platelet-derived growth factor subunit b (Pdgfb) and the degree of fibrosis in rat kidneys. This gene signature also showed a potential for classifying human kidney samples. Our multiomics approach provides fresh insights into the possible mechanisms underlying HTN-associated kidney disease, the target cell types, the protective effects of steroidal and nonsteroidal MRAs, and amiloride.

| S-EPMC10760974 | biostudies-literature

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