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s / Atherosclerosis 263 (2017) e111ee282 e133 parameters. In our research we examined three distinctive endothelial microvesicles populations, expressing CD105+ or CD31+, CD42bor CD144, CD42bmarkers. We also looked at CD62e expression in all three populations. Results: There was significant positive correlation with systolic blood pressure and diastolic blood pressure and total cholesterol concentration, especially with microvesicles, expressing CD62e. Conclusions: CD62e is an endothelial activation marker, synthesized by activated endothelium. CD62e positive microvesicles are strongly associated with endothelial activation and disease progression. Data show, that increased microvesicle count contribute to atherosclerosis risk factors. Research is being continued to evaluate diagnostic value of endothelial microvesicle count in atherosclerosis. PO070. CIGARETTE SMOKE AQUEOUS EXTRACT AFFECTS ENDOTHELIUM, MONOCYTES AND THEIR INTERACTION Silvia Castiglioni, Silvia Stella Barbieri, Alberto Corsini, Stefano Bellosta. Department of Pharmacological and Biomolecular Sciences, Universit a degli Studi di Milano, Milan, Italy Aim: Cigarette smoke causes vascular endothelial cells (ECs) dysfunction, a key event in atherogenesis. We recently demonstrated that cigarette smoke condensate (CSC), which contains the hydrophobic components of cigarette smoke, stimulates the expression of adhesion molecules by ECs and the release of chemotactic factors by human monocytes (HM) that in turn cause a change in EC morphology. In the present study, we investigated the effects of the Aqueous Extract (AE) of cigarette smoke, which contains hydrophilic components of both the condensate and the gas phase, on HM and EC interaction in the atherosclerotic process. Methods: ECs were incubated with 10% AE or medium conditioned by HM alone (CHM) or exposed to AE (CMAE) and the effects evaluated by RT-PCR, immunocytochemistry or cell chemotaxis. Results: Our data show that AE has a dual behavior: on one hand, it induces morphological changes in ECs causing the shrinking of their cytoplasm (-55% vs control) and increasing the expression of adhesion molecules VCAM-1 and ICAM-1 (+3-fold vs control, qRT-PCR) and of the NF-kB promoter activity (+2-fold vs control, luciferase assay). HM exposed to AE increase also pro-inflammatory cytokines expression that in turn promotes HM chemotaxis (Boyden chamber assay). On the other hand, AE increases also the expression of genes with anti-inflammatory properties such as IL-10 and KLF2 in HM and ECs respectively. Conclusions: AE causes pro-inflammatory effects on HM and ECs, by affecting cell morphology and adhesion molecules and cytokines expression, that are not adequately counteracted by AE effects on IL-10 and KLF-2 expression. PO071. VALIDATION OF A LC/MSMS METHOD FOR SIMULTANEOUS QUANTIFICATION OF 9 NUCLEOTIDES IN BIOLOGICAL MATRIXES AND ITS APPLICATIONS IN CARDIOVASCULAR DISEASES Melissa Cortese, C edric Delporte, Damien Dufour, Caroline Noyon, Alexandre Rousseau, Jean N eve, Bernard Robaye, Karim Zouaoui Boudjeltia, Pierre Van Antwerpen. 1 Laboratory of Organic Pharmaceutical Chemistry, Faculty of Pharmacy, Universit e Libre de Bruxelles, Brussels, Belgium; 2 Laboratory of Experimental Medicine, CHU de Charleroi, A. V esale Hospital, Universit e Libre de Bruxelles, Montigny-leTilleul, Belgium; 3 Institute of Interdisciplinary Research in Human and Molecular Biology, Faculty of Sciences, Universit e Libre de Bruxell, Gosselies,