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Effect of XCT790 on Human Aortic Valve (AV) Endothelial Cells (ECs) from Patients with Healthy Tricuspid, Calcified Tricuspid, or Calcified Bicuspid Avs

ABSTRACT: Effect of XCT790 on Human Aortic Valve (AV) Endothelial Cells (ECs) from Patients with Healthy Tricuspid, Calcified Tricuspid, or Calcified Bicuspid Avs

PROVIDER: PRJNA635427 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11858800_1.fastq.gz	Fastqsanger.gz
	SRR11858800_2.fastq.gz	Fastqsanger.gz
	SRR11858801_1.fastq.gz	Fastqsanger.gz
	SRR11858801_2.fastq.gz	Fastqsanger.gz
	SRR11858802_1.fastq.gz	Fastqsanger.gz

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Effect of XCT790 on Human Aortic Valve (AV) Endothelial Cells (ECs) from Patients with Healthy Tricuspid, Calcified Tricuspid, or Calcified Bicuspid Avs

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RNA Expression Profile of Calcified Bicuspid, Tricuspid and Normal Human Aortic Valves by RNA Sequencing [BAV]

Project description:Purpose: The molecular mechanisms leading to premature development of aortic valve stenosis (AS) in individuals with a bicuspid aortic valve (BAV) are unknown. The objective of this study was to identify genes differentially expressed between calcified BAV and tricuspid valves with (TAVc) and without (TAVn) calcification using RNA sequencing (RNA-Seq). Methods: Ten human calcified BAV and nine TAVc were collected from men who underwent aortic valve replacement. Eight TAVn were obtained from men who underwent heart transplantation. mRNA levels were measured using the Illumina HiSeq 2000 system. Reads were aligned with TopHat. Cuffdiff, DESeq, edgeR, and SAMSeq were used to compare gene expression. Genes with adjusted P < 0.05 in the four methods were called differentially expressed. Pathway analysis was performed with IPA. Results: Two genes were up-regulated and none were down-regulated in BAV compared to TAVc. There were 462 genes up-regulated and 282 down-regulated in BAV compared to TAVn. Compared to TAVn, 329 genes were up- and 170 were down-regulated in TAVc. Conclusions: This is the first transcriptome study on calcified and normal aortic valves using RNA-Seq. BAV and TAVc have a highly similar expression profile. These results contribute to our molecular understanding of AS and the identification of new therapeutic targets that are urgently needed to prevent, slow the development or treat AS in patients with bicuspid and tricuspid valves.

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RNA Expression Profile of Calcified Bicuspid, Tricuspid and Normal Human Aortic Valves by RNA Sequencing [TAV]

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RNA Expression Profile of Calcified Bicuspid, Tricuspid and Normal Human Aortic Valves by RNA Sequencing

Project description:RNA Expression Profile of Calcified Bicuspid, Tricuspid and Normal Human Aortic Valves by RNA Sequencing

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MiRNA microarray analysis of human bicuspid and tricuspid aortic valve leaflet tissues

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Aortic smooth muscle cells in bicuspid valve patients

Project description:and with higher incidence if associated to bicuspid aortic valve (BAV) for unknown reasons. TAA is usually diagnosed fortuitously and the lack of effective drug therapy to delay progression and avoid dissection lies in the limited knowledge of pathophysiology. Objectives. We aimed to identify the molecular hallmarks that difference the aortic dilatation associated to bicuspid (BAV) and tricuspid aortic valve (TAV) patients while setting plasma diagnostic molecular panels valve-associated. Methods. Sporadic TAA patients and control subjects (n=91) were classified according to valve type (BAV, TAV). Vascular smooth muscle cells isolated from TAA patients’ aortas were firstly analyzed by mass spectrometry based high-throughput proteomics according to valve type. Extracellularly secreted proteins were secondly analyzed in plasma from TAA patients versus control subjects as diagnostic candidates. Results. Aneurysmal aortas from BAV patients showed a stress phenotype, weakened extracellular matrix interactions, DNA damage and affected protein homeostasis compared to TAV patients. Two plasma marker panels of sporadic TAA valveassociated were identified, showing significant correlation with aortic diameter for C1QTNF5, LAMA2, and SPARC proteins, in BAV patients, and for CP and FAP proteins, in TAV patients. Conclusions. The arterial wall of BAV patients shows a limited capacity to counteract drivers of sporadic TAA while resembling aged arteries.The molecular pathways identified here support the need of differential molecular diagnosis and therapeutic approaches for BAV and TAV patients.

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