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Podocyte-specific YAP activation triggers crescentic glomerulonephritis through cross-talk with parietal epithelial cells

ABSTRACT: Podocyte-specific YAP activation triggers crescentic glomerulonephritis through cross-talk with parietal epithelial cells

PROVIDER: PRJNA1138722 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29916202_1.fastq.gz	Fastqsanger.gz
	SRR29916202_2.fastq.gz	Fastqsanger.gz
	SRR29916203_1.fastq.gz	Fastqsanger.gz
	SRR29916203_2.fastq.gz	Fastqsanger.gz
	SRR29916204_1.fastq.gz	Fastqsanger.gz

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Podocyte-specific YAP activation triggers crescentic glomerulonephritis through cross-talk with parietal epithelial cells

Project description:YAP, a transcriptional co-activator, is known to control programs that are both cell- and context-dependent. We report that the overactivation of YAP (YAP5SA) in podocytes has both cell autonomous and non-cell autonomous consequences. RNA-seq analysis of YAP5SA-expressing compared to control podocytes revealed pathways and candidate genes that could explain both these effects.

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CC chemokine ligand 18 (CCL18) is associated with disease activity and relapse in ANCA-associated crescentic glomerulonephritis

Project description:Anti neutrophil cytoplasmic antibody (ANCA) associated vasculitis is the most frequent cause of crescentic glomerulonephritis. Histopathologic features and clinical course of the disease are diverse and judgment of disease activity is often limited due to the lack of reliable activity markers. In order to define potentially new molecular or cellular markers in the kidney which may predict clinical outcome, we performed microarray analyses of renal biopsies from patients with ANCA-associated crescentic glomerulonephritis. We correlated expression profiles with clinical data from our prospective study of patients with renal ANCA disease. The CC chemokine ligand 18 (CCL18) was one of the most up-regulated proteins in kidneys of patients with ANCA-associated crescentic glomerulonephritis. CCL18 producing cells in the kidneys were identified as CD68 and CD209 positive myeloid dendritic cells. The density of CCL18 positive cells correlated with the severity of acute tubular injury and with the impairment of renal function. CCL18 protein levels were elevated in serum samples of patients with renal ANCA disease when compared with patients with non- ANCA-associated crescentic glomerulonephritis. Persistence of high CCL18 serum levels correlated with impairment of renal function and the risk of relapsing disease. Therefore, CCL18 might serve as a marker for persistent disease activity and renal relapses in ANCA-associated vasculitis.

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Transcription profiling by array of rat macrophages from WKY/NCrl and LEW/Crl strains to determine susceptibility to glomerulonephritis

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Primary cultures of glomerular parietal epithelial cells or podocytes with proven origin

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Project description:The second messenger cyclic AMP (cAMP) is involved in many aspects of renal physiology and disease. Epac is an effector of cAMP and its pathophysiological role in the development of chronic kidney diseases (CKD) has yet to be determined. Here, we show that total Epac1 isoform genetic deletion does not cause any baseline renal abnormalities but remarkably potentiates the deterioration of renal structure and function during the progression of the nephrotoxic serum (NTS)-induced glomerular nephritis (GN). Similarly, podocyte Epac1 deletion in podocytes exacerbated GN development. Global gene expression profile in mouse glomeruli using RNAseq analysis indicates a transcriptomic signature of GN related to immune system, extracellular matrix, and cytoskeleton gene dysregulation at the onset of the disease. Furthermore, glomeruli with podocyte Epac1 deletion display altered mitochondrion and metabolic processes in nephritic mice. Consistently, mechanistic analysis demonstrates that Epac1 activation increases human podocyte mitochondrial function to cope with extra energy demand in stress condition. Of particular importance, Epac1 increases aerobic glycolysis to ameliorate podocyte viability and motility. Therefore, the metabolic flexibility mediated by Epac1 constitutes a protective mechanism against podocyte injury. Altogether these data highlight the potential of Epac1 as a therapeutic approach for CKD treatment.

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