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

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

PROVIDER: PRJNA1068785 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27710503_1.fastq.gz	Fastqsanger.gz
	SRR27710503_2.fastq.gz	Fastqsanger.gz
	SRR27710504_1.fastq.gz	Fastqsanger.gz
	SRR27710504_2.fastq.gz	Fastqsanger.gz
	SRR27710505_1.fastq.gz	Fastqsanger.gz

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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 [CUT&Tag_NR4A3]

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

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Effect of depletion of NR4A3 on vascular calcification [CUTtag_H3K18LA]

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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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.

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The Pharmacological Effect and Mechanism of Lanthanum Hydroxide on Vascular Calcification Caused by Chronic Renal Failure Hyperphosphatemia

Project description:Objective: To investigate the treatment and mechanism of lanthanum hydroxide on hyperphosphate-induced vascular calcification in chronic renal failure. Methods: Develop a rat model of CKD hyperphosphatemia. Rats were randomly allocated to the model, lanthanum hydroxide, lanthanum carbonate, Calcium carbonate groups. Determination of serum biochemical indicators and the determination of pathological analysis of kidney tissue, Von Kossa staining and CT scan on the aortic vessels. The proteomic analysis of aortic tissue in Vivo. A calcified VSMCs model was established. The calcium content and ALP activity were measured. RT-PCR measures the mRNA expression level of SM22α, Runx2, BMP-2 and TRAF6. Western Blot measures the protein expression level of SM22α, Runx2, BMP-2, TRAF6 and NF-κB. Results: Through the detection of serum biochemical indicators and pathological analysis of kidney tissue, it can be summaryed that lanthanum hydroxide has the effect of delaying the progression of renal failure and protecting renal function. We found that the administration of lanthanum hydroxide delayed the development of vascular calcification induced by hyperphosphatemia in CKD. It can be concluded that lanthanum hydroxide may affect vascular calcification through the NF-κB pathway. , To deal with Lanthanum chloride (LaCl3) inhibited phosphate induced calcification, osteo-/chondrogenic transdifferentiation, and NF-κB signaling in cultured VSMCs. Lanthanum hydroxide significantly reduces the expression of Runx2, BMP-2, TRAF6 and NF-κB. Conclusion: Lanthanum hydroxide has a protective effect on the kidneys, and can delay the development of vascular calcification by reducing serum phosphorus concentration.

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