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HNF3α targets Nckap1l and promotes renal fibrosis following ischemia-reperfusion injury [CUT&TAG]

ABSTRACT: HNF3α targets Nckap1l and promotes renal fibrosis following ischemia-reperfusion injury [CUT&TAG]

PROVIDER: PRJNA1148649 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30260239_1.fastq.gz	Fastqsanger.gz
	SRR30260239_2.fastq.gz	Fastqsanger.gz
	SRR30260240_1.fastq.gz	Fastqsanger.gz
	SRR30260240_2.fastq.gz	Fastqsanger.gz

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HNF3α targets Nckap1l and promotes renal fibrosis following ischemia-reperfusion injury [CUT&TAG]

Project description:Ischemia-reperfusion injury-induced acute kidney injury is a major cause of chronic kidney disease, lacking effective interventions. We found elevated HNF3α (also known as FOXA1) expression in CKD patients, which correlated with collagen deposition, serum creatinine, and urea levels. Conditional knockout of HNF3α in renal tubular epithelial cells protected against IRI-induced renal fibrosis in vivo. To explore the mechanisms by which HNF3α promotes renal fibrosis, we analyse the genome-wide target sites of HNF3α using CUT&Tag sequencing.

2025-03-01 | GSE274963 | GEO

HNF3α targets Nckap1l and promotes renal fibrosis following ischemia-reperfusion injury

Project description:Ischemia-reperfusion injury-induced acute kidney injury is a major cause of chronic kidney disease, lacking effective interventions. We found elevated HNF3α expression in CKD patients, which correlated with collagen deposition, serum creatinine, and urea levels. Conditional knockout of HNF3α in renal tubular epithelial cells protected against IRI-induced renal fibrosis in vivo. To explore the mechanisms by which HNF3α promotes renal fibrosis, we transfected TKPTS cells with Hnf3a overexpression plasmids or control plasmids, and then performed transcriptome sequencing.

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HNF3α targets Nckap1l and promotes renal fibrosis following ischemia-reperfusion injury

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Differential Ly6C Expression after Renal Ischemia-Reperfusion Identifies Unique Macrophage Populations

Project description:Macrophages are a heterogeneous cell type implicated in injury, repair, and fibrosis after AKI, but the macrophage population associated with each phase is unclear.results of this study in a renal ischemia-reperfusion injury model allow phenotype and function to be assigned to CD11b+/Ly6C+ monocyte/macrophage populations in the pathophysiology of disease after AKI. we used a renal bilateral ischemia-reperfusion injury mouse model to identify unique monocyte/macrophage populations by differential expression of Ly6C in CD11b+Â cells and to define the function of these cells in the pathophysiology of disease on the basis of microarray gene signatures and reduction strategies Macrophage populations were sorted by Flow Cytometry into low and intermediate populations by Itgam(Cd11b) and Ly6c markers. The cells obtained in 5 weeks sham, 5 weeks IR, 9 day sham, and 9 day IR with 6 samples per group (3 int and 3 low). Cells were sorted in 350ul of RLT lysing buffer and kept at -80c until RNA extraction.Sample amplification, fragmentation, hybridization,washing and scanning were performed according to validated Affymetrix protocol in a CLIA certified lab.

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