E-MTAB-2409 - 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

Status
Released on 2 May 2014, last updated on 3 June 2014
Organism
Homo sapiens
Samples (6)
Array (1)
Protocols (6)
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.
Experiment types
transcription profiling by array, cellular modification design, co-expression, replicate design
Contact
Citation
The long non-coding HOTAIR is modulated by cyclic stretch and WNT/?-CATENIN in human aortic valve cells and is a novel repressor of calcification genes. Carrion K, Dyo J, Patel V, Sasik R, Mohammed S, Hardiman G, Nigam V.
MIAME
PlatformsProtocolsFactorsProcessedRaw
Files
Investigation descriptionE-MTAB-2409.idf.txt
Sample and data relationshipE-MTAB-2409.sdrf.txt
Raw data (1)E-MTAB-2409.raw.1.zip
Processed data (1)E-MTAB-2409.processed.1.zip
Array designA-GEOD-10558.adf.txt
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