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Soluble RARRES1 induces podocyte apoptosis to promote glomerular disease progression

ABSTRACT: Soluble RARRES1 induces podocyte apoptosis to promote glomerular disease progression

PROVIDER: PRJNA635932 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11878700.fastq.gz	Fastqsanger.gz
	SRR11878701.fastq.gz	Fastqsanger.gz
	SRR11878702.fastq.gz	Fastqsanger.gz
	SRR11878703.fastq.gz	Fastqsanger.gz
	SRR11878704.fastq.gz	Fastqsanger.gz

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Soluble RARRES1 induces podocyte apoptosis to promote glomerular disease progression

Project description:We try to explore the effect of RARRES1 on human podocyte, so we performed RARRES1 overexpression and knockdown experiments. cell mRNA profiles of human human podocyte cell lines transfected with RARRES1 overexpression vectors orcontrol vectors; and cells transfected with RARRES1 shRNA lentivirus or scramble shRNA lentivirus and stimulated with TNFa (10ng/ml) or without TNFa for 24 hours were generated by deep sequencing, in triplicate, using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript. We found that most differentially expressed genes (DEGs) are enriched with cell migration and apoptosis-related pathways, also DEGs stimulated by TNFα but suppressed by RARRES1 knockdown, were also enriched with cell cycle-related pathways.These data suggest that RARRES1 plays a key role in the regulation of cell cycle and apoptosis, consistent with its role as a tumor suppressor gene.

2020-10-07 | GSE151484 | GEO

Single-cell transcriptional analysis of kidney from aging mice with podocyte specific RARRES1 overexpression

Project description:Retinoic acid receptor responder protein-1 (RARRES1) was identified as a podocyte transmembrane protein whose expression correlates with glomerular disease progression. The cytopathic effect of RARRES1 is carried out only when proteolytically cleaved in its ectodomain into a soluble form (sRARRES1) and subsequently endocytosed by podocytes, as a membrane-bound, cleavage site mutant failed to induce any effect. We investigated the effects of long-term podocyte-derived RARRES1 overexpression on aging-induced kidney injury.

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Soluble RARRES1 induces podocyte apoptosis to promote glomerular disease progression.

Project description:Using the Nephrotic Syndrome Study Network Consortium data set and other publicly available transcriptomic data sets, we identified retinoic acid receptor responder protein 1 (RARRES1) as a gene whose expression positively correlated with renal function decline in human glomerular disease. The glomerular expression of RARRES1, which is largely restricted to podocytes, increased in focal segmental glomerulosclerosis (FSGS) and diabetic kidney disease (DKD). TNF-? was a potent inducer of RARRES1 expression in cultured podocytes, and transcriptomic analysis showed the enrichment of cell death pathway genes with RARRES1 overexpression. The overexpression of RARRES1 indeed induced podocyte apoptosis in vitro. Notably, this effect was dependent on its cleavage in the extracellular domain, as the mutation of its cleavage site abolished the apoptotic effect. Mechanistically, the soluble RARRES1 was endocytosed and interacted with and inhibited RIO kinase 1 (RIOK1), resulting in p53 activation and podocyte apoptosis. In mice, podocyte-specific overexpression of RARRES1 resulted in marked glomerular injury and albuminuria, while the overexpression of RARRES1 cleavage mutant had no effect. Conversely, podocyte-specific knockdown of Rarres1 in mice ameliorated glomerular injury in the setting of adriamycin-induced nephropathy. Our study demonstrates an important role and the mechanism of RARRES1 in podocyte injury in glomerular disease.

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Human podocyte differentiation

Project description:Microarray analysis of the molecular phenotype of the glomerular podocyte during temperature shift-induced differentiation Keywords = glomerular podocyte Keywords = differentiation

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Project description:High fructose diet has been proposed as a major contributor to metabolic syndrome, which is usually accompanied with proteinuria due to glomerular podocyte injury. However, the underlying pathological mechanisms of fructose-induced podocyte injury remain elusive. In this study, we have used an iTRAQ based quantitative proteomic strategy to comprehensively characterize the dynamic proteome changes in glomeruli of high fructose-fed rats, and revealed global fructose-induced glomerular metabolic reprogramming at four different stages during the progression of high fructose modeling.

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