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Effect of depletion of NR4A3 on vascular calcification [CUT&Tag_NR4A3]

ABSTRACT: Effect of depletion of NR4A3 on vascular calcification [CUT&Tag_NR4A3]

PROVIDER: PRJNA1068786 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27710244_1.fastq.gz	Fastqsanger.gz
	SRR27710244_2.fastq.gz	Fastqsanger.gz
	SRR27710245_1.fastq.gz	Fastqsanger.gz
	SRR27710245_2.fastq.gz	Fastqsanger.gz
	SRR27710246_1.fastq.gz	Fastqsanger.gz

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Effect of depletion of NR4A3 on vascular calcification [CUT&Tag_NR4A3]

Project description:Medial arterial calcification is a chronic systemic vascular disorder distinct from atherosclerosis and is commonly observed in patients with chronic kidney disease (CKD), diabetes mellitus, and aging individuals. We previously showed that orphan nuclear receptor NR4A3 is a key regulator in the progression of apolipoprotein (apo) A-IV-induced atherosclerosis; however, little is known about its role in vascular calcification. NR4A3 expression was upregulated in calcified aortic tissues from CKD mice or 1,25(OH)2VitD3 overload-induced mice, and in human calcified aorta. NR4A3 deficiency preserved VSMCs contractile phenotype, inhibited the expression of osteoblast differentiation-related genes, and reduced calcium deposition in the vasculature.

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Effect of depletion of NR4A3 on vascular calcification [CUTtag_H3K18LA]

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Effect of depletion of NR4A3 on vascular calcification [CUTtag_H3K18LA]

Project description:Effect of depletion of NR4A3 on vascular calcification [CUTtag_H3K18LA]

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Effect of depletion of NR4A3 on vascular calcification [RNA-seq]

Project description:Effect of depletion of NR4A3 on vascular calcification [RNA-seq]

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STING facilitates vascular calcification via p-STAT1/NLRP3 signal

Project description:Vascular calcification contributes to the cardiovascular morbidity and mortality of chronic kidney disease (CKD), but there is no approved treatment for vascular calcification. In this study, we report the role of STING in vascular calcification. To further investigate the molecular mechanism by which STING participates in vascular calcification, we performed high-throughput RNA-seq to identify the target gene of STING.

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mRNA expression profile in vascular smooth muscle cells (VSMCs) after inducing calcification

Project description:Vascular calcification (VC) is often associated with cardiovascular and metabolic diseases. However, the molecular mechanisms linking VC to these diseases have yet to be elucidated. Here we report that MDM2-induced polyubiquitination of histone deacetylase 1 (HDAC1) mediates VC. Loss of HDAC1 activity via either chemical inhibitor or genetic ablation enhanced VC. HDAC1 protein, but not mRNA, was reduced in cell and animal calcification models and in human calcified coronary artery. In the calcification-provoking condition, proteasomal degradation of HDAC1 preceded VC. The calcification-provoking condition induced MDM2 E3 ligase, which then resulted in HDAC1 K74 polyubiquitination. Overexpression of MDM2 enhanced VC, whereas loss of MDM2 blunted it. Decoy peptides spanning HDAC1 K74 and RG 7112, an MDM2 inhibitor, prevented VC in vivo and in vitro. These results demonstrate a previously unknown ubiquitination pathway and suggest MDM2-mediated HDAC1 polyubiquitination as a new therapeutic target in VC. Calcification was induced in rat aorta vascular smooth muscle cells with inorganic phosphate (Pi). Total RNA were extracted from the cells 3 and 6 days later. mRNA profile of the sample was compared with normal control.

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Project description:In this study, we report the protective effect of β-hydroxybutyrate (BHB) on vascular calcification in chronic kidney disease (CKD). To further investigate the mechanism underpinning the protective effect of BHB on vascular calcification, we performed high-throughput RNA-seq to identify the target gene of BHB. Our data demonstrate that BHB supplementation inhibits vascular calcification in CKD via targeting HDAC9.

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Project description:Vascular calcification is a common and life-threatening complication in patients with chronic kidney disease, in which osteogenic differentiation of vascular smooth muscle cells (VSMCs) plays an essential role. Paraspeckle protein NONO is a multifunctional protein involved in many nuclear biological processes but its role in vascular calcification and osteogenic differentiation of VSMCs remains unclear.By RNA sequencing analysis in primary mouse VSMCs with or without NONO knockout, we observed significant changes of genes important in regulating vascular function and osteogenic differentiation of VSMCs.

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