MiRNA profiling revealed enhanced susceptibility to oxidative stress of endothelial cells from bicuspid aortic valve.

摘要: Abstract Aims Calcific aortic valve stenosis (CAVS) is the most frequent manifestation of disease and third leading cause cardiovascular in Western countries associated with significant morbidity mortality. An active biological progression involving inflammation oxidation to endothelial damage considered a hallmark early stages degeneration. However, tricuspid (TAV) bicuspid (BAV) deterioration are differ only by shear stress. We hypothesized that cells (EC) derived from BAV TAV patients have different miRNA expression patterns thus distinct pathways could lead than patients. Methods results isolated ECs or valve, which underwent surgery due CAVS. MiRNA profile PCR revealed eight upregulated miRNAs between ECs. Functional analysis identified presented altered cellular response oxidative stress DNA stimulus via p53 alteration intrinsic apoptotic signaling pathway. GPX3 SRXN1 mRNA were express at lower levels compared ECs, an increment double-strand breaks. had sustained apoptosis activation when This difference was exacerbated reduced survival rate but completely reverted miR-328-3p inhibition. Conclusion The present data showed molecular differences susceptibility, magnitude, induction