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RNA-seq results of the kidney of male kidney-specific G9a knockout mice after acute kidney injured

ABSTRACT: RNA-seq results of the kidney of male kidney-specific G9a knockout mice after acute kidney injured

PROVIDER: PRJNA760905 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15724269_1.fastq.gz	Fastqsanger.gz
	SRR15724269_2.fastq.gz	Fastqsanger.gz
	SRR15724270_1.fastq.gz	Fastqsanger.gz
	SRR15724270_2.fastq.gz	Fastqsanger.gz
	SRR15724271_1.fastq.gz	Fastqsanger.gz

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RNA-seq results of the kidney of male kidney-specific G9a knockout mice after acute kidney injured

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Project description:In this study, we aimed to evaluate the effect of M2-like macrophages in the injured kidney on kidney cancer progression. As an acute kidney injury to chronic kidney disease model, we used unilateral ischemia-reperfusion injury (uIRI). And we inoculated RenCa cells, which are murine kidney cancer cell line, into renal subcapsule 14 days after uIRI (uIRI-Can) and compared uIRI-Can to RenCa cells inoculated into sham-operated renal subcapsule (Sham-Can) 20 days after inoculation. To identify gene characteristics of M2-like macrophages that are commonly detected both in the uIRI kidney cortex and uIRI-Can, we sorted Ly6Clow macrophages from 4 groups, uIRI kidney cortex, sham kidney cortex, uIRI-Can, and Sham-Can, and conducted RNA-Seq. This study revealed the characteristic gene expression of M2-like macrophages which were commonly detected in the injured kidney cortex and kidney cancer progressed on the injured kidney. And this could be a future therapeutic target of macrophage-targeted therapy.

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Project description:The G9a mediates mono- and dimethylation of Lys9 of histone H3 at specific gene loci, which is associated with transcriptional repression. ZNF644 and WIZ contain multiple zinc finger motifs that recognize consensus DNA sequences.

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Expression data from injured murine kidney

Project description:Renal recovery following injury relies on cellular regeneration. In the mouse kidney following injury, injured epithelial cells undergoes de-differentiate, proliferate and re-differentiate into functional cells, following a a tightly controlled genetic programme where specific sets of genes are up-regulated. We used microarrays to detail the global programme of gene expression underlying cellular regeneration following injury with or without a HDAC inhibitor, m4PTB, treatment and identified distinct classes of up-regulated genes during this process. Male BALB/c mice underwent 26 minute unilateral ischemia-reperfusion (IR) with contralateral nephrectomy treated with vehicle or 100 mg/kg m4PTB 24 h after inducing renal injury, and kidneys harvested for RNA extraction 12 h later. We sought to obtain kidneys within a similar degree of injury in order to carefully evaluate the effect of m4PTB on expression profiles. To that end, we selected kidneys according to three different criteria of injury: (1) level of serum creatinine at Day1, (2) the level of blood urea nitrogen (BUN) (3) Kim1 expression by qPCR at Day1.5 using haevested kidneys

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Combined double knockout of Ezh2 and G9a leads to expression change in murine retinal ganglion cells

Project description:Purpose: The goal of this study is to evaluate H3K27me3 histone marks in retinal ganglion cells in Ezh2 (Math5Cre, Ezh2-/-) and combined G9a-Ezh2 (Math5Cre; G9a+/-Ezh2-/-) knockout mutant mice at P1. Both Ezh2 and G9a are major epigenetic silencing machineries. Ezh2 mediates the trimethylation of lysine 27 on histone 3. Emerging evidences show an interdependence between Ezh2 and G9a to facilitate K27 trimethylation. Methods: P1 retinal ganglion cells were collected and chromatin immunoprecipitation was performed with EZ- CHIP kit from Millipore. Library preparation was done with Rubicon Genomics Thruplex DNAseq. Results: Here, we find a pool of common K27me3 target genes of Ezh2 and G9a in double knockout that leads to dysfunction in double mutant RGCs. Conclusion: This study provides the first Chip-seq analysis of K27me3 in murine RGCs. Our data supports that an interaction between Ezh2 and G9a is also evident in murine retinal ganglion cells. This work should be a framework for further study of retinal ganglion cells and retinal diseases.

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