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Cleavage under targets and release using nuclease (CUT&RUN) sequencing for HNF4A in human adult kidney and kidney organoid-derived proximal tubular cells

ABSTRACT: Cleavage under targets and release using nuclease (CUT&RUN) sequencing for HNF4A in human adult kidney and kidney organoid-derived proximal tubular cells

PROVIDER: PRJNA940180 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23680191_1.fastq.gz	Fastqsanger.gz
	SRR23680191_2.fastq.gz	Fastqsanger.gz
	SRR23680192_1.fastq.gz	Fastqsanger.gz
	SRR23680192_2.fastq.gz	Fastqsanger.gz
	SRR23680193_1.fastq.gz	Fastqsanger.gz

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Cleavage under targets and release using nuclease (CUT&RUN) sequencing for HNF4A in human adult kidney and kidney organoid-derived proximal tubular cells

Project description:We performed CUT&RUN sequencing to characterize HNF4A binding sites in human adult kidney and kidney organoid-derived proximal tubular cells.

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Project description:This study aims to identify genes regulated by Hnf4a in developing nephrons. In the mouse kidney, Osr2Cre efficiently deletes the Hnf4a flox allele and targets all nephron tubules except distal tubules. To investigate gene expression changes, we performed bulk RNA-seq on Osr2Cre-targeted cells from Hnf4a mutant and control kidneys.

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Project description:Kidney fibrosis is the underlying pathological process of chronic kidney disease, the mechanisms of which are still incompletely understood. Following a transcriptome-wide gene expression analysis of PDGF-B in murine and human kidney cells, we generated transgenic mouse lines with Pdgfb deletion in major expressing cells. Mice with Pdgfb deletion in kidney tubular epithelial cells showed significantly reduced activation and proliferation of peritubular fibroblasts and fibrosis in three models with tubular injury of different etiologies. We identified paracrine PDGF signaling as a key molecular mechanism of cellular crosstalk mediating the transition of kidney tubular injury to interstitial fibrosis via induction of profibrotic niches.

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Project description:The Hippo/YAP pathway plays a critical role in early embryonic kidney development, but its functions in the adult kidney are less well understood. Our previous work has demonstrated that tubular YAP activation induced by double knockout of the upstream Hippo kinases Mst1 and Mst2 (Mst1/2 dKO) promotes tubular injury and renal inflammation under basal conditions. However, the importance of tubular YAP activation remains to be established in injured kidneys in which many other injurious pathways are simultaneously activated. Several secreted factors were found to be increased by YAP in tubular cells, but how the transcriptional network is altered by YAP is largely unknown. Here, we show that tubular YAP was already activated at 6 h after unilateral ureteral obstruction (UUO). Tubular YAP deficiency greatly attenuated tubular cell over-proliferation, tubular injury and renal inflammation induced by UUO or cisplatin. RNA-Seq, ChIP and luciferase assay revealed that YAP promoted the transcription of the transcription factor KLF5 whereas no interaction between YAP and KLF5 was observed. Consistently, the elevated expression of KLF5 and its target genes in Mst1/2 dKO or UUO kidneys was blocked by ablation of Yap in tubular cells. Inhibition of KLF5 prevented tubular cell over-proliferation, tubular injury and renal inflammation in Mst1/2 dKO kidneys. Therefore, our results demonstrate that tubular YAP is a key player in kidney injury. YAP and KLF5 form a transcriptional cascade, in which tubular YAP activation induced by kidney injury promotes KLF5 transcription. Activation of this cascade induces tubular cell over-proliferation, tubular injury and renal inflammation

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