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MiRNA expression profile in calcium oxalate (CaOx) nephrocalcinosis model.

ABSTRACT: miRNA expression profile in calcium oxalate (CaOx) nephrocalcinosis model.

PROVIDER: PRJNA776020 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16617200.fastq.gz	Fastqsanger.gz
	SRR16617201.fastq.gz	Fastqsanger.gz
	SRR16617202.fastq.gz	Fastqsanger.gz
	SRR16617203.fastq.gz	Fastqsanger.gz
	SRR16617204.fastq.gz	Fastqsanger.gz

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miRNA expression profile in calcium oxalate (CaOx) nephrocalcinosis model.

Project description:Microarray analysis was used to assess the expression levels of miRNAs in six pairs of kidney tissues of calcium oxalate (CaOx) nephrocalcinosis mouse model and normal mouse kidney tissues.The animals used in the experiment were male 6-8 weeks old C57BL/6J mice. To establish a CaOx nephrocalcinosis mouse model, each mouse was intraperitoneally injected with saline or glyoxylate acid (Gly) (75 mg/kg/d, 200 μl) from day 1 to day 7. Animals were euthanized after 7 days, and kidney samples were collected at the time of euthanasia.

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Single cell gene expression from the kidneys of calcium oxalate (CaOx) nephrocalcinosis mice model.

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Project description:Microarray analysis was used to assess the expression levels of mRNAs in kidney tissues of calcium oxalate (CaOx) nephrocalcinosis mouse model and normal mouse kidney tissues.The animals used in the experiment were male 6-8 weeks old wild type and NLPR3 knock out C57BL/6J mice. To establish a CaOx nephrocalcinosis mouse model, each mouse was intraperitoneally injected with saline or glyoxylate acid (Gly) (75 mg/kg/d, 200 μl) from day 1 to day 7. Animals were euthanized after 7 days, and kidney samples were collected at the time of euthanasia.

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EZH2-mediated macrophage-to-myofibroblast transition contributes to calcium oxalate crystal-induced kidney fibrosis

Project description:Long-term nephrocalcinosis leads to kidney injury, fibrosis, and even chronic kidney disease (CKD). Reports have proved macrophages can transition into myofibroblasts(MMT), leading to collagen deposition and fibrosis in CKD. However, the effect of MMT in calcium oxalate (CaOx) crystal-induced kidney fibrosis remains unclear. This study demonstrated that histone methyltransferase EZH2-mediated MMT contributes to CaOx crystal-induced fibrosis. We identified abundant MMT cells by immunofluorescence and flow cytometry in kidney tissues of patients with CaOx-related CKD, CaOx nephrocalcinosis mouse model, and CaOx-treated RAW264.7 macrophage cells. A high level of MMT cell infiltration was associated with a decline in the glomerular filtration rate in CaOx nephrocalcinosis patients. Clodronate Liposomes-mediated macrophage depletion attenuates calcium oxalate crystal-induced fibrosis in mice. Subsequently, transcriptomic and single-cell sequencing revealed that EZH2 was highly expressed in kidneys with CaOx deposition, especially in macrophages. Further study demonstrated that EZH2 inducible knock-out or pharmacological inhibition by GSK-126 attenuated MMT and renal fibrosis in vivo and in vitro. Mechanistically, ChIP and transcriptomic sequencing showed that EZH2 inhibition reduced the enrichment of H3K27me3 on the DUSP23 gene promoter and elevated DUSP23 expression. The Co-IP and molecular docking analysis showed that DUSP23 mediated the dephosphorylation of pSMAD3 (S423/425), the key regulator of MMT. In addition, DUSP23 over-expression could alleviate SMAD3-mediated MMT. Thus, our study found that EZH2 promotes kidney fibrosis by meditating MMT via the DUSP23/SMAD3 pathway in nephrocalcinosis.

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Project description:Single cell gene expression from the kidneys of calcium oxalate (CaOx) nephrocalcinosis mice model.

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