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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 expression of calcification and inflammatory genes. Bicuspid aortic valve leaflets experience increased biomechanical strain as compared to normal tricuspid aortic valves. The molecular pathogenesis involved in the 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. Our data suggest that  β -CATENIN is a stretch responsive signaling pathway that represses  HOTAIR . This is the first report demonstrating that  HOTAIR  is mechanoresponsive and repressed by WNT  β -CATENIN signaling. These findings provide novel evidence that  HOTAIR  is involved in aortic valve calcification.

plos one

The Long Non-Coding HOTAIR Is Modulated by Cyclic Stretch and WNT/β-CATENIN in Human Aortic Valve Cells and Is a Novel Repressor of Calcification Genes