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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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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.

2024-05-14 | GSE254076 | GEO

Effect of depletion of NR4A3 on vascular calcification [CUTtag_H3K18LA]

2024-05-14 | GSE254075 | GEO

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

2024-05-14 | GSE254077 | GEO

Effect of depletion of NR4A3 on vascular calcification [CUTtag_H3K18LA]

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

| PRJNA1068787 | ENA

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

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

| PRJNA1068785 | ENA

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.

2015-11-07 | E-GEOD-74755 | biostudies-arrayexpress

Downregulation of HDAC9 by β-hydroxybutyrate suppresses vascular calcification in chronic kidney disease

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.

2021-11-01 | GSE186772 | GEO

Paraspeckle protein NONO attenuates vascular calcification by inhibiting BMP2 transcription

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.

2024-01-10 | GSE252244 | GEO

Ursolic acid-induced DECR1 degradation via NF-κB/NLRP3 pathway inihibits vascular calcification

Project description:In this study, we repoort the protective effect of ursolic acid (UA) on vascular calcification in chronic kidney disease. To elucidate the molecular mechanism underlying the anti-vascular calcification effect of UA, we performed RNA-seq to identify the gene expresion under UA treatmment.

2024-09-13 | GSE276910 | GEO

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

Project description:Vascular calcification, the ectopic deposition of calcium in blood vessels, develops in association with various metabolic diseases and atherosclerosis. Because it often causes stiffness and remodeling of the blood vessels, vascular calcification increases morbidity and mortality. Both miRNA and mRNA microarrays (Series GSE74755) were performed with rat VSMCs and reciprocally regulated pairs of miRNA and mRNA were selected after bioinformatic analysis.

2019-12-31 | GSE130486 | GEO

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