Stretch responsive miRNAs in human aortic valve interstitial cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE49558 | GEO | 2015/01/09
SECONDARY ACCESSION(S): PRJNA214242
REPOSITORIES: GEO
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Project description:miRNA-Sequencing was performed on human aortic valve interestitial cells (AVICs) exposed to 14% stretch at 1 hz or static conditions for 24h. Six static control and six samples exposed to cyclic stretch 14% for 24h
2015-01-09 | E-GEOD-49558 | biostudies-arrayexpress
Project description:AVICs were exposed to cyclic stretch to examine the role of mechanical stimuli on gene expression AVICs cultured on collagen 1 coated Bioflex were exposed to 14% stretch at 1 hz or static conditions using a Flexcell-5000
2015-01-09 | GSE47687 | GEO
Project description:AVICs were exposed to cyclic stretch to examine the role of mechanical stimuli on gene expression AVICs cultured on collagen 1 coated Bioflex were exposed to 14% stretch at 1 hz or static conditions using a Flexcell-5000 14% stretch was the experimental condition while the static condition was the control
2015-01-09 | E-GEOD-47687 | biostudies-arrayexpress
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
Project description:Investigation of whole genome gene expression level changes in hAVICs and hMVICs, compared to human dermal fibroblasts. A three chip assay using total RNA obtained from primary cultured normal valve interstital cells and human dermal fibroblasts was performed. Each chip measures the expression level of 45,033 genes from normal AVICs,MVICs and DFs.
2013-06-30 | E-GEOD-40801 | biostudies-arrayexpress
Project description:Aortic valve calcification is the most common form of valvular heart disease, but the mechanisms of calcific aortic valve disease (CAVD) are unknown. NOTCH1 mutations are associated with aortic valve malformations and adult-onset calcification in families with inherited disease. The Notch signaling pathway is critical for multiple cell differentiation processes, but its role in the development of CAVD is not well understood. The aim of this study was to investigate the molecular changes that occur with inhibition of Notch signaling in the aortic valve. Notch signaling pathway members are expressed in adult aortic valve cusps, and examination of diseased human aortic valves revealed decreased expression of NOTCH1 in areas of calcium deposition. To identify downstream mediators of Notch1, we examined gene expression changes that occur with chemical inhibition of Notch signaling in rat aortic valve interstitial cells (AVICs). We found significant downregulation of Sox9 along with several cartilage-specific genes that were direct targets of the transcription factor, Sox9. Loss of expression Sox9 has been published to be associated with aortic valve calcification. Utilizing an in vitro porcine aortic valve calcification model system, inhibition of Notch activity resulted in accelerated calcification while stimulation of Notch signaling attenuated the calcific process. Finally, the addition of Sox9 was able to prevent the calcification of porcine AVICs that occurs with Notch inhibition. In conclusion, loss of Notch signaling contributes to aortic valve calcification via a Sox9-dependent mechanism. 3 samples of aortic valve interstitial cells treated with DAPT were compared with 3 samples of aortic valve interstitial cells treated with DMSO
2011-08-25 | E-GEOD-31668 | biostudies-arrayexpress
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
Project description:Aortic valve calcification is the most common form of valvular heart disease, but the mechanisms of calcific aortic valve disease (CAVD) are unknown. NOTCH1 mutations are associated with aortic valve malformations and adult-onset calcification in families with inherited disease. The Notch signaling pathway is critical for multiple cell differentiation processes, but its role in the development of CAVD is not well understood. The aim of this study was to investigate the molecular changes that occur with inhibition of Notch signaling in the aortic valve. Notch signaling pathway members are expressed in adult aortic valve cusps, and examination of diseased human aortic valves revealed decreased expression of NOTCH1 in areas of calcium deposition. To identify downstream mediators of Notch1, we examined gene expression changes that occur with chemical inhibition of Notch signaling in rat aortic valve interstitial cells (AVICs). We found significant downregulation of Sox9 along with several cartilage-specific genes that were direct targets of the transcription factor, Sox9. Loss of expression Sox9 has been published to be associated with aortic valve calcification. Utilizing an in vitro porcine aortic valve calcification model system, inhibition of Notch activity resulted in accelerated calcification while stimulation of Notch signaling attenuated the calcific process. Finally, the addition of Sox9 was able to prevent the calcification of porcine AVICs that occurs with Notch inhibition. In conclusion, loss of Notch signaling contributes to aortic valve calcification via a Sox9-dependent mechanism.
2011-08-26 | GSE31668 | GEO
Project description:Aortic valve calcifications are often associated with calcium deposition and tissue mineralization, resulting in stiffness and dysfunction. To better understand the diversity of molecular and cellular processes for calcification in valve structures, we isolated human aortic valve interstitial cells (AVICs) and exposed them to calcification stimulation. RNA-seq revealed that in response to calcified stimuli, AVIC activates a robust ossification program, although the signaling pathways, cellular processes, and osteogenesis-related markers involved are diverse. In conclusion, this study provides a wealth of information suggesting that the pathogenesis of aortic valve calcification may be much more than previously understood.
2024-01-03 | GSE252266 | GEO
Project description:The goal of this study was to identify microRNAs that are modulated by cyclic stretch. miRNA-Seq was performed comparing samples from cultured E16.5 mouse cardiomyocytes exposed to either cyclic stretch of 16% at 1Hz for 24h or static conditions.
2020-01-22 | GSE120676 | GEO