2018
27th European Cardiology Conference ” October, 22-24, Rome
Monica Tucureanu1,̽ Alexandru Filippi1 ̽, Cristina Ana Constantinescu1, Nicoleta Alexandru1, Daniela Rebleanu1, Letitia Ciortan1, Razvan Macarie1, Manuela Calin1, Sabina Frunza2, Agneta Simionescu1, Adriana Georgescu1, Ileana Manduteanu1
1 Institute of Cellular Biology and Pathology “Nicolae Simionescu”, Bucharest, Romania
2 Internal Medicine Clinic, Emergency Clinical Hospital, Bucharest, Romania
Diabetes contributes directly to the development of cardiovascular disorders including aortic valve disease. There is currently no drug therapy available for a dysfunctional valve and this urges the need for additional research to identify distinctive mechanisms of valve disease evolution. The aim of this time course study was to evaluate structural-functional correlations of the early and progression changes of valvular aortic lesion induced by diabetes. We evaluated plasma parameters, hemodynamic parameters (by echography-based in vivo imaging) and inflammatory, remodelling and calcification indexes in a streptozotocin-induced diabetic apolipoprotein E-deficient mouse model. The blood and aortic valves were collected at 1, 2, 4 weeks from the last streptozotocin injection. Inflammatory, remodeling and calcification indexes were calculated as fold changes in expression of investigated molecules in diabetic animals at different time points relative to controls. A correlation between pro-inflammatory, remodeling and calcific indexes, plasma parameters and functional hemodynamic parameters was displayed in a correlation matrix. The Pearson (r) correlation coefficient was determined using R software. The results showed statistical significant positive correlations between: (1) αSMA expression and remodelling index, (2) αSMA expression and aortic cusp thickness, (3) remodelling index and aortic cusp thickness, (4) inflammatory index and calcification index, (5) inflammatory index and remodelling index. Our study may help to advance the understanding of the mechanisms of aortic valve disease in the diabetic milieu in order to discover and validate new possible targets for nanobiotherapies.
Acknowledgments: This work was supported by a grant from the Competitiveness Operational Program 2014-2020, Targeted therapies for aortic valve disease in diabetes, THERAVALDIS, ID P_37_298, MySMIS code: 104362, contract number 115/13.09.2016.