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19.01.2017 | Original Article | Ausgabe 6/2017

Heart and Vessels 6/2017

Patients with bicuspid and tricuspid aortic valve exhibit distinct regional microrna signatures in mildly dilated ascending aorta

Heart and Vessels > Ausgabe 6/2017
Sebastian Albinsson, Alessandro Della Corte, Azra Alajbegovic, Katarzyna K. Krawczyk, Ciro Bancone, Umberto Galderisi, Marilena Cipollaro, Marisa De Feo, Amalia Forte
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Electronic supplementary material

The online version of this article (doi:10.​1007/​s00380-016-0942-7) contains supplementary material, which is available to authorized users.
S. Albinsson and A. Della Corte contributed equally to the study.


MicroRNAs are able to modulate gene expression in a range of diseases. We focused on microRNAs as potential contributors to the pathogenesis of ascending aorta (AA) dilatation in patients with stenotic tricuspid (TAV) or bicuspid aortic valve (BAV). Aortic specimens were collected from the ‘concavity’ and the ‘convexity’ of mildly dilated AAs and of normal AAs from heart transplant donors. Aortic RNA was analyzed through PCR arrays, profiling the expression of 84 microRNAs involved in cardiovascular disease. An in silico analysis identified the potential microRNA–mRNA interactions and the enriched KEGG pathways potentially affected by microRNA changes in dilated AAs. Distinct signatures of differentially expressed microRNAs are evident in TAV and BAV patients vs. donors, as well as differences between aortic concavity and convexity in patients only. MicroRNA changes suggest a switch of SMC phenotype, with particular reference to TAV concavity. MicroRNA changes potentially affecting mechanotransduction pathways exhibit a higher prevalence in BAV convexity and in TAV concavity, with particular reference to TGF-β1, Hippo, and PI3K/Akt/FoxO pathways. Actin cytoskeleton emerges as potentially affected by microRNA changes in BAV convexity only. MicroRNAs could play distinct roles in BAV and TAV aortopathy, with possible implications in diagnosis and therapy.

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Supplementary material 3 (TIF 15933 KB)
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