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Transcriptomic analysis of glomeruli following podocyte-loss of Klf4

ABSTRACT: Transcriptomic analysis of glomeruli following podocyte-loss of Klf4

PROVIDER: PRJNA630231 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11684881.fastq.gz	Fastqsanger.gz
	SRR11684882.fastq.gz	Fastqsanger.gz
	SRR11684883.fastq.gz	Fastqsanger.gz
	SRR11684884.fastq.gz	Fastqsanger.gz
	SRR11684885.fastq.gz	Fastqsanger.gz

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Transcriptomic analysis of kidney cortex following podocyte-loss of Klf4

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Isolated glomeruli from podocyte specific Pdzd8 KO mice

Project description:Isolated glomeruli from mice were analyzed. The grouping was as follows: WT mice exposed to normal diet, podocyte specific Pdzd8 KO mice exposed to normal diet, WT mice exposed to 12w high fat diet, podocyte specific Pdzd8 KO mice exposed to 12w high fat diet.

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Comparison of Glomerular and Podocyte mRNA Profiles in eNOS-/- Diabetic Mice Induced by Streptozotocin

Project description:We compared mRNA profiles of isolated glomeruli versus sorted podocytes between diabetic and control mice. IRG mice crossed with eNOS-/- mice were further bred with podocin-rTTA and TetON-Cre mice to permanently label podocytes before the diabetic injury. Diabetes was induced by injection of streptozotocin. mRNA profiles of isolated glomeruli and sorted podocytes from diabetic and control mice at 10 weeks after induction of diabetes were examined. Consistent with the previous reports, expression of podocyte-specific markers in the glomeruli were down-regulated in the diabetic mice compared to controls. However, these differences disappeared when mRNA levels were corrected for podocyte number per glomerulus. Interestingly, the expression of these markers was not altered in sorted podocytes from diabetic mice, suggesting that the reduced expression of podocyte markers in isolated glomeruli is likely a secondary effect of reduced podocyte number, rather than the loss of differentiation markers. Analysis of the differentially expressed genes in diabetic mice also revealed distinct up-regulated pathways in the glomeruli (mitochondrial function and oxidative stress) and podocytes (actin organization). In conclusion, our data suggest that podocyte-specific gene expression in transcriptome obtained from the whole glomeruli may not represent those of podocytes in the diabetic kidney. We compared mRNA profiles of isolated glomeruli versus sorted podocytes between diabetic and control mice.

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