Dataset related to the article "MiRNA profiling revealed enhanced susceptibility to oxidative stress of endothelial cells from bicuspid aortic valve"

<p>This record contains raw data related to the article &quot;MiRNA profiling revealed enhanced susceptibility to oxidative stress of endothelial cells from bicuspid aortic valve&quot;</p> <p>&nbsp;</p> <p><strong>Abstract</strong></p> <p>Aims</p> <p>Calcific&nbsp;<a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/aortic-valve-stenosis">aortic valve stenosis</a>&nbsp;(CAVS) is the most frequent manifestation of&nbsp;<a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/aortic-valve-disease">aortic valve disease</a>&nbsp;and the third leading cause of cardiovascular disease in the Western countries associated with significant morbidity and mortality. An active biological progression involving inflammation and&nbsp;<a href="https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/alpha-oxidation">oxidation</a>&nbsp;leading to valve endothelial damage is considered a hallmark of the early stages of valve degeneration. However, tricuspid (TAV) and&nbsp;<a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/premolar">bicuspid</a>&nbsp;(BAV)&nbsp;<a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/aortic-valve">aortic valve</a>&nbsp;deterioration are considered to differ only by shear stress. We hypothesized that&nbsp;<a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/endothelial-cell">endothelial cells</a>&nbsp;(EC) derived from BAV and TAV patients have different&nbsp;<a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/microrna">miRNA</a>&nbsp;expression patterns and thus distinct pathways could lead to endothelial damage in BAV than TAV patients.</p> <p>Methods and results</p> <p>We isolated ECs from patients with bicuspid or tricuspid aortic valve, which underwent surgery due to CAVS. MiRNA expression profile by PCR revealed eight upregulated&nbsp;<a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/microrna">miRNAs</a>&nbsp;between BAV and TAV ECs. Functional analysis identified that BAV ECs presented altered cellular response to&nbsp;<a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/oxidative-stress">oxidative stress</a>&nbsp;and DNA damage stimulus&nbsp;<em>via</em>&nbsp;<a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/protein-p53">p53</a>&nbsp;and alteration in the intrinsic apoptotic&nbsp;<a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/signal-transduction">signaling pathway</a>.&nbsp;<a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/gpx3">GPX3</a>&nbsp;and SRXN1&nbsp;<a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/messenger-rna">mRNA</a>&nbsp;were express at lower levels in BAV compared to TAV ECs, leading to an increment of&nbsp;<a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/double-stranded-dna">DNA double-strand</a>&nbsp;breaks. BAV ECs had a sustained&nbsp;<a href="https://www.sciencedirect.com/topics/medicine-and-dentistry/programmed-cell-death">apoptosis</a>&nbsp;activation when compared to TAV ECs. This difference was exacerbated by oxidative stress stimulus leading to a reduced survival rate but completely reverted by miR-328-3p inhibition.</p> <p>Conclusion</p> <p>The present data showed molecular differences in oxidative stress susceptibility, DNA damage magnitude, and apoptosis induction between ECs derived from BAV and TAV patients.</p>