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Glomerular Transcriptome from Experimental Nephrotic Syndrome Model and Treatment with PPARgamma Agonists [ADR]

ABSTRACT: Glomerular Transcriptome from Experimental Nephrotic Syndrome Model and Treatment with PPARgamma Agonists [ADR]

PROVIDER: PRJNA1207490 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31913834_1.fastq.gz	Fastqsanger.gz
	SRR31913834_2.fastq.gz	Fastqsanger.gz
	SRR31913835_1.fastq.gz	Fastqsanger.gz
	SRR31913835_2.fastq.gz	Fastqsanger.gz
	SRR31913836_1.fastq.gz	Fastqsanger.gz

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Glomerular Transcriptome from Experimental Nephrotic Syndrome Model and Treatment with PPARgamma Agonists [ADR]

Project description:Nephropathy was induced with puromycin amino-nucleoside (PAN) in Wistar rats and treated with daily treatments of Pioglitazone (Pio) and GQ-16. Nephropathy was induced in a separate group of rats with Adriamycin (ADR) in Wistar rats. Total glomerular RNA was isolated, and mRNA libraries were generated and subjected to sequencing using NovaSeq6000 SP. Injury with PAN and ADR resulted in differential expression of genes (DEGs). Many of the PAN-induced DEGs were restored with Pio and GQ16 treatments.

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Glomerular Transcriptome from Experimental Nephrotic Syndrome Model and Treatment with PPARgamma Agonists

Project description:Glomerular Transcriptome from Experimental Nephrotic Syndrome Model and Treatment with PPARgamma Agonists

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Glomerular Transcriptome from Experimental Nephrotic Syndrome Model and Treatment with PPARgamma Agonists

Project description:Nephropathy was induced with puromycin amino-nucleoside (PAN) in Wistar rats and treated with daily treatments of Pioglitazone (Pio) and GQ-16. Total glomerular RNA was isolated, and mRNA libraries were generated and subjected to sequencing using NovaSeq6000 SP. Injury with PAN resulted in 1089 DEGs compared to controls, and 26 of these DEGs were restored by both Pio and GQ-16 treatments, whereas 106 unique GQ-16 regulated DEGs and 17 unique Pio-regulated DEGs were identified (Fig. 4A). Overall, Pio and GQ-16 treatment resulted in 75 and 173 DEGs compared to PAN injury, which included 29 common and 190 distinct genes (Fig. 4A). Of the 29 common DEGs, 28 DEGs were down-regulated by both Pio and GQ-16 and only 1 DEG upregulated by both treatments, when compared to PAN (Fig. 4B). Of the 190 distinct DEGs identified between Pio and GQ-16 treatments, 41 were down-regulated and 5 up-regulated by Pio and 124 down-regulated and 20 up-regulated by GQ-16 treatment.

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Project description:Idiopathic nephrotic Syndrome (NS) is a common glomerular disease. While glucocorticoids (GC) are the primary treatment, the PPARγ agonist pioglitazone (Pio) also reduces proteinuria in patients with NS and directly protects podocytes from injury. Since both drugs reduce proteinuria, we hypothesized these effects result from overlapping transcriptional patterns. Systems biology approaches compared glomerular transcriptomes from rats with PAN-induced NS treated with GC vs. Pio and identified 29 commonly regulated genes-of-interest, primarily involved in extracellular matrix (ECM) remodeling. Correlation with clinical idiopathic NS patient datasets confirmed glomerular ECM dysregulation as a potential mechanism of injury. Cellular deconvolution in silico revealed GC- and Pio-induced amelioration of altered genes primarily within podocytes and mesangial cells. While validation studies are indicated, these analyses identified molecular pathways involved in the early stages of NS (prior to scarring) suggesting that targeting glomerular ECM dysregulation may enable a future non-immunosuppressive approach for proteinuria reduction in idiopathic NS.

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