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Expression data from static and cyclic stretched porcine aortic heart valves

ABSTRACT: We explored the hypothesis that Serotonin (5HT) receptor signaling, that can be enhanced with 5HT transporter blockade with Fluoxetine (Fluox), in the aortic valve may vary based upon the biomechanical activity of the aortic valve leaflet. We used Affymetrix microarrays to study gene expression profiling of Porcine Aortic Valves (PAV) incubated under organ culture conditions for 24 hours in either a static state or with 10% cyclic stretch, simulating physiologic leaflet motion. PAV in the bioreactor with or without stretch were exposed to 5HT along or the combination 5HT plus Fluox.

ORGANISM(S): Sus scrofa

PROVIDER: GSE21663 | GEO | 2010/05/07

SECONDARY ACCESSION(S): PRJNA125899

REPOSITORIES: GEO

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Expression data from static and cyclic stretched porcine aortic heart valves

Project description:We explored the hypothesis that Serotonin (5HT) receptor signaling, that can be enhanced with 5HT transporter blockade with Fluoxetine (Fluox), in the aortic valve may vary based upon the biomechanical activity of the aortic valve leaflet. We used Affymetrix microarrays to study gene expression profiling of Porcine Aortic Valves (PAV) incubated under organ culture conditions for 24 hours in either a static state or with 10% cyclic stretch, simulating physiologic leaflet motion. PAV in the bioreactor with or without stretch were exposed to 5HT along or the combination 5HT plus Fluox. Fresh porcine aortic valves were obtained from a local abattoir. The three leaflets were excised from each valve and a rectangular section of tissue 15x10 mm was isolated from the central region of each valve cusp. These samples were randomized and assigned to one of four groups. The experimental groups were: 1) Static conditions with no agents added; 2) Cyclic stretch conditions with no agents added; 3) Static conditions with 5HT plus Fluox added; and 4) Cyclic stretch conditions with 5HT plus Fluox added.

2010-05-27 | E-GEOD-21663 | biostudies-arrayexpress

RNA-seq Analysis of Injured vs Sham Aortic Valves in Mice 48 hours Post-Injury

Project description:In order to analyze molecular changes in response to endothelial injury, the aortic valve in wild type mice was injured by inserting a thin anigoplasty guidewire into the mouse carotid artery and advancing the wire through the aortic valve opening. This procedure produced damage to the layer of valve endothelial cells surroung the outer edge of the valve leaflet. Sham surgery consisted of the same wire insertion prcoedure but the wire was not advanced to the level of the valve. The surgical procedure was performed in young (3-4 month old) and aging (16-18 month old) mice. Individual sham and injured aortic valves were collected 48 hours after surgery and submitted for sequencing (one valve per biological replicate).

2021-05-07 | GSE169034 | GEO

Expression data of human aortic valve cusps

Project description:Calcific aortic valve disease is the most common form of valvular heart disease in the Western World. Milder degrees of aortic valve calcification is called aortic sclerosis and severe calcification with impaired leaflet motion is called aortic stenosis. We used microarrays to detail the global programme of gene expression underlying cdevelopment of calcified aortic valve disease in humans.

2015-10-01 | GSE51472 | GEO

The alterations of gene expression in aortic valve from calcific aortic valve disease patients

Project description:Calcification of the aortic valve leads to increased leaflet stiffness resulting in development of calcific aortic valve disease (CAVD); however, the underlying molecular and cellular mechanisms of calcification are poorly understood. Here, we investigated gene expressions in relation to valvular calcification and promotion of CAVD progression.

2016-01-28 | GSE77287 | GEO

Differential gene expression in human valve interstitial cells of normal aortic valves and calcified aortic valves

Project description:Valve interstial cells(VICs) are the major cellular compents in the aortic valve. Under pathological circumstances, normal VICs differentiate into myofibroblasts or osteoblast-like phentotypes, which play important roles in the pathogenesis of calcified aortic valve disease. We used micrroarrary analysis to compare the global programme of gene expression in normal and calcified human aortic valve intersitial cells (VICs), in order to find out some key factors that mediate the phenotype change of VICs.

2016-10-23 | GSE88803 | GEO

Microarray-based gene expression on human aortic valves

Project description:Calcified aortic valve leaflets (CAVs) were explanted from patients with severe aortic valve stenosis undergoing aortic valve replacement at the Department of Cardiovascular Surgery, Union Hospital, affiliated to Tongji Medical College. Control non-calcified aortic valves with normal echocardiographic analyses were obtained during heart transplant procedures. RNA was extracted from valve leaflets and gene expression evaluated using the Arraystar Human mRNA Array. This study aimed to perform the expression analysis of mRNA on human aortic valves.

2020-07-26 | GSE155119 | GEO

The long non-coding HOTAIR is modulated by cyclic stretch and WNT/beta-CATENIN in human aortic valve cells and is a novel repressor of calcification genes

Project description:Aortic valve calcification is a significant and serious clinical problem for which there are no effective medical treatments. Individuals born with bicuspid aortic valves, 1-2% of the population, are at the highest risk of developing aortic valve calcification. Aortic valve calcification involves increased levels of calcification and inflammatory genes. Bicuspid aortic valve leaflets experience increased strain. The molecular mechanisms involved in the pathogenesis of calcification of BAVs are not well understood, especially the molecular response to mechanical stretch. HOTAIR is a long non-coding RNA (lncRNA) that has been implicated with cancer but has not been studied in cardiac disease. We have found that HOTAIR levels are decreased in BAVs and in human aortic interstitial cells (AVICs) exposed to cyclic stretch. Reducing HOTAIR levels via siRNA in AVICs results in increased expression of calcification genes.

2014-05-02 | E-MTAB-2409 | biostudies-arrayexpress

Microarray-based gene expression on human aortic valves

Project description:Aortic valves are collected from patients with severe aortic valve stenosis undergoing aortic valve replacement at the Institut universitaire de cardiologie et de pneumologie de Québec (IUCPQ), Quebec City, Canada. From this biobank collection, transcriptomic analyses from 240 aortic valves were performed. All valves were tricuspid and had a fibro-calcific remodeling score of 3 or 4. RNA was extracted from valve leaflets and gene expression evaluated using the Illumina HumanHT-12 v4 Expression BeadChip. The main objective of this study was to perform a large-scale expression quantitative trait loci (eQTL) mapping study on human aortic valves.

2018-03-14 | GSE102249 | GEO

Gene expression profile of calcified bicuspid, tricuspid and normal human aortic valves

Project description:The objective of this study was to identify genes differentially expressed between calcified bicuspid aortic valves (BAV) and tricuspid valves with (TAVc) and without (TAVn) aortic valve stenosis. Ten human BAV and nine TAVc were collected from male who underwent primary aortic valve replacement. Eight TAVn were obtained from male who underwent heart transplantation. mRNA levels were measured using Illumina HumanHT-12 v4 Expression BeadChip and compared between valve groups.

2016-09-22 | GSE83453 | GEO

Gene expression in aortic aneurysms associated with tricuspid and bicuspid valves

Project description:Patients with bicuspid aortic valve (BAV) have increased risk of thoracic ascending aortic aneurysm (AscAA) and dissection compared to those with a normal tricuspid aortic valve (TAV). The present study was undertaken to evaluate whether differences in gene expression exist in aortas from BAV and TAV patients with AscAA. Keywords: disease state analysis

2007-06-28 | GSE5180 | GEO

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