Background and Aims: Peripheral artery disease (PAD), the atherosclerotic disorder that affects arteries of the lower limbs, has increasing incidence worldwide, the major risk factors being dyslipidemia and diabetes mellitus (DM). Some of the key players in the atheroma formation are dysfunctional high-density lipoproteins (HDL), whose components that contribute to PAD evolution are less known. We aimed to identify alterations of HDL constituents which associate with PAD aggravation.

Background and Aims: Glucose fluctuations appear daily in human plasma and their presence was associated with an increased number of cardiovascular events, clinical manifestations of atherosclerosis. Endothelial cells (EC) are important for vascular homeostasis, their dysfunction contributing to the inception and progression of atherosclerosis. The aim of this study was to evaluate the deleterious impact of glucose fluctuations on EC and to decipher new molecular mechanism that could become therapeutic targets to ameliorate these effects.

Background and Aims: To identify microRNAs in plasma and atheroma from carotid artery stenosis (CAS) patients and correlate them with the patients’ evolution after endarterectomy (EA).

Background and Aims: We aimed to evaluate and compare the modulation induced by hypolipidemic dietary interventions (probiotics treatment or high fat-diet (HFD) withdrawal) on some epigenetic markers (miRNAs) in hyperlipidemic (HL) hamsters.

Background and Aims: HDL dysfunction besides HDL-cholesterol is an important CVD risk factor. Our aim was to investigate the mechanism of functional HDL production and cholesterol efflux in the small intestine in hyperlipidemic (HL) conditions, and to evaluate the potential of ginger extract (GIN) to stimulate these processes, which are important means to manage hepatic steatosis and atherosclerosis.

Objectives: To identify the effect of hyperglycemia on serum miRNAs associated with HDL in acute coronary syndrome (ACS) patients and to assess the effect of ACS sera on miRNAs and their processing machinery components (Dicer, Drosha, DGCR8) expression in human macrophages.

Objectives: We aimed to investigate the molecular mechanisms involved in VCAM-1 induction and secretion in human endothelial cells (HEC) incubated with glycated low density lipoproteins (gLDL).

Objectives: To investigate the mechanisms linking hyperlipidemia (HL) with the alteration of the ABC transporters and the dysfunctional HDL, which are essential for the development of atherosclerosis.

G. M. SANDA , M. DELEANU (1) , M. SIMIONESCU , A.V. SIMA (1) * 1 Institute of Cellular Biology and Pathology “Nicolae Simionescu” of the Romanian Academy, Bucharest, Romania 2 Faculty of Biotechnology, University of Agronomical Sciences and Veterinary Medicine, Bucharest, Romania *Corresponding author Anca V. Sima, Ph.D. Head, Lipidomics Department Institute of Cellular Biology and Pathology “N. Simionescu” of the Romanian Academy 8, B.P. Hasdeu Street, Bucharest 050568, Romania Phone: +40(0)21.319.4518, Fax: +40(0)21.319.4519, e-mail: anca.sima@icbp.ro

Purpose: Searching for new biomarkers to predict the progress of coronary artery disease (CAD), we studied the evolution of lipid and inflammatory parameters, along with five mi-RNAs, in plasma of CAD patients under treatment for 1 year.

The role of CETP in the development of atherosclerosis is debatable, and few data exist regarding the total impact of CETP inhibition on cholesterol efflux.Acceptor capacities of whole serum and HDL subfractions separated by HPLC were compared using 2 different cell systems. Subjects with CETP deficiency (2 homozygous, 1 compound heterozygous, and 5 heterozygous) were analyzed along with 10 normolipidemic controls. The fractional efflux from cholesterol-labeled Fu5AH hepatoma cells was determined to be SR-BI mediated. The efflux difference between control and liver X receptor (LXR) agonist-induced ABCA1-upregulated J774 macrophages was considered as a measure of ABCA1-mediated efflux.For the Fu5AH cell system, the total acceptor capacities of whole serum and HPLC-separated HDL fraction 2 obtained from the homozygous subjects were 38% and 116% higher than the corresponding values for the controls, respectively (p < 0.05). For the J774 cell system, the total acceptor capacities of whole serum and HPLC-separated HDL fractions were similar among the CETP-deficient subjects and controls.Serum from homozygous subjects with CETP-null defects exhibited enhanced acceptor capacity via an SR-BI dependent pathway, which is regulated by the middle HPLC-separated HDL fraction. Further, the cholesterol acceptor capacity of serum obtained from patients having complete and partial CETP deficiency was preserved via an ABCA1-dependent pathway.