Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Renal Epo producing Sca-1+ interstitial cells are increased in number after treatment with the anemia drug roxadustat

ABSTRACT: Renal Epo producing Sca-1+ interstitial cells are increased in number after treatment with the anemia drug roxadustat

PROVIDER: PRJNA633129 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11797943.fastq.gz	Fastqsanger.gz
	SRR11797944.fastq.gz	Fastqsanger.gz
	SRR11797945.fastq.gz	Fastqsanger.gz
	SRR11797946.fastq.gz	Fastqsanger.gz
	SRR11797947.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 20

Similar Datasets

Renal Epo producing Sca-1+ interstitial cells are increased in number after treatment with the anemia drug roxadustat

Project description:We identify and analyse in detail a specific Sca-1-positive cell population that increases after treatment with the anaemia drug roxadustat and is capable to support Epo production in mice

2021-05-14 | GSE150669 | GEO

Receptor-mediated mitophagy regulates EPO production and protects against renal anemia

Project description:Erythropoietin (EPO) drives erythropoiesis and is secreted mainly by the kidney upon hypoxic or anemic stress. The paucity of EPO production in renal EPO-producing cells (REPs) causes renal anemia, one of the most common complications of chronic nephropathies. Although mitochondrial dysfunction is commonly observed in several renal and hematopoietic disorders, the mechanism by which mitochondrial quality control impacts renal anemia remains elusive. In this study, we showed that FUNDC1, a mitophagy receptor, plays a critical role in EPO-driven erythropoiesis induced by stresses. Mechanistically, EPO production is impaired in REPs in Fundc1-/- mice upon stresses, and the impairment is caused by the accumulation of damaged mitochondria, which consequently leads to the elevation of the reactive oxygen species (ROS) level and triggers inflammatory responses by up-regulating proinflammatory cytokines. These inflammatory factors promote the myofibroblastic transformation of REPs, resulting in the reduction of EPO production. We therefore provide a link between aberrant mitophagy and deficient EPO generation in renal anemia. Our results also suggest that the mitochondrial quality control safeguards REPs under stresses, which may serve as a potential therapeutic strategy for the treatment of renal anemia.

2021-05-07 | GSE158361 | GEO

Receptor-mediated mitophagy regulates EPO production and protects against renal anemia

Project description:Receptor-mediated mitophagy regulates EPO production and protects against renal anemia

| PRJNA664995 | ENA

Epo producing cell lines

Project description:Generation of mouse renal Epo-producing (REP) cell lines by conditional gene tagging

| PRJEB19328 | ENA

RNA-seq of whole blood from pediatric Sickle Cell Anemia (SCA) patients

Project description:RNA-seq of whole blood from pediatric Sickle Cell Anemia (SCA) patients

| PRJNA777971 | ENA

RNA-seq of whole blood from pediatric Sickle Cell Anemia (SCA) patients

Project description:RNA-seq of whole blood from pediatric Sickle Cell Anemia (SCA) patients

| PRJNA777972 | ENA

The transcriptional and regulatory identity of erythropoietin producing cells

Project description:Erythropoietin (Epo) is the master regulator of erythropoiesis and oxygen homeostasis. Despite its physiological importance, the molecular and genomic contexts of the cells responsible for renal Epo production have not yet been resolved, limiting effective cell-based therapies for anemia. Here, we performed single-cell profiling of an Epo reporter mouse to molecularly identify Epo-producing cells under hypoxic conditions. We report that a distinct and homogeneous population of kidney stromal cells, which we name Norn cells, are the sole source of Epo production in vivo. Extensive characterization of the Norn epigenetic and transcriptional landscapes revealed Norn-specific markers, pathways, and transcription factor circuits conserved from mice to humans. These findings open new avenues to functionally dissect EPO gene regulation in human evolution and disease, and pave the way for the next generation of genetic and cell-based approaches for EPO therapies.

2023-03-13 | GSE193321 | GEO

Pre-established chromatin interactions mediate acute transcriptional response to Epo [HiChIP]

Project description:Although chromatin architecture has been established in a variety of cell and tissue types, chromatin contacts’ dynamics in response to hormone stimulation has yet to be fully elucidated. Using the unique anemia-inducing strain of the Friend virus (FVA) murine model system, we show that there are transcriptional and epigenetic changes in response to erythropoietin within an invariant chromatin domain organization. There is an acute transcriptional response, as seen by genes with significant differential RNA polymerase II occupancy. Additionally, we find that YY1 is highly dynamic in response to Epo stimulation and these binding locations are not shared with CTCF. Using HiChIP, which combines Hi-C and ChIP methodologies, we identified enhancer-promoter interactions mediated by H3K27ac and YY1, revealing a subset of invariant chromatin loops. Together, these findings offer new insights into Epo-mediated gene regulation through chromatin organization.

2020-09-28 | GSE142004 | GEO

Pre-established chromatin interactions mediate acute transcriptional response to Epo [ChIPexo-seq]

2020-09-28 | GSE142003 | GEO

Pre-established chromatin interactions mediate acute transcriptional response to Epo [RNA-seq]

2020-09-28 | GSE142005 | GEO