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ÖZSAVCI, DERYA

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ÖZSAVCI

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End date: 2009 × Start date: 2001 ×

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    Flow cytometric assay of platelet glycoprotein receptor numbers in hypercholesterolemia
    (TAYLOR & FRANCIS INC, 2002) ÖZSAVCI, DERYA; Ozsavci, D; Yardimci, T; Demirel, GY; Demiralp, E; Uras, F; Onder, E
    In this study, platelet glycoprotein (Gp) receptor numbers were measured by a flow cytometric assay using Cytoquant Gp in seven hypercholesterolemic and five normal subjects. Thrombin receptor agonist peptide (TRAP) was used to activate platelets. In hypercholesterolemia the Gp receptor numbers per resting platelet were found to be: 38 629 +/- 8538 (GpIIb/IIIa), 22 269 +/- 5628 (GpIb), 37 037 +/- 9810 (GpIIIa), 224 +/- 504 (CD62-P). After activation, receptor numbers were determined to be: 56 399 +/- 9003 (GpIIb/ IIIa), 10 970 +/- 5319 (GpIb), 50 715 +/- 7904 (GpIIIa), 1222 +/- 687 (P-selectin). In the normal group before the activation, receptor numbers were: 43 828 +/- 8862 (GpIIb/ IIIa), 22 166 +/- 3847 (GpIb), 42 351 +/- 1049 (GpIIIa), 62 +/- 139 (CD62-P), After activation, receptor numbers were determined to be: 60 573 +/- 4294 (GpIIb/ IIIa), 13 003 +/- 4118 (GpIb), 52 067 +/- 1039 (GpIIIa), 3608 +/- 1508 (CD62-P). In hypercholesterolemic subjects, GpIIb/ IIIa and GpIIIa receptor numbers on activated platelets increased significantly, whereas P-selectin numbers remained unchanged. However, the GpIb levels decreased significantly. In the control group, after activation, GpIIb/ IIIa and P-selectin receptors increased significantly, GpIIIa receptor numbers did not change significantly, whereas GpIb receptor numbers decreased significantly. When the GpIIb/ IIIa, GpIb, GpIIIa receptor numbers of the control group and hypercholesterolemic group were compared before and after activation, no significant changes were observed (P>0.05). But P-selectin receptor numbers were significantly decreased in hypercholesterolemic patients compared to normals following TRAP activation (P<0.05). In this study, the effect of hypercholesterolemia on platelet function was observed. The striking observation about present study was the marked decrease in P-selectin expression after activation in the hypercholesterolemics compared to normals. This finding suggests some sort of platelet dysfunction in these individuals.
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    Do platelet apoptosis, activation, aggregation, lipid peroxidation and platelet-leukocyte aggregate formation occur simultaneously in hyperlipidemia?
    (PERGAMON-ELSEVIER SCIENCE LTD, 2005) ŞENER, AZİZE; Sener, A; Ozsavci, D; Oba, R; Demirel, Y; Uras, F; Yardimci, KT
    Objectives: The circulating lipoproteins may cause some abnormalities in platelet composition and function in hypercholesterolemia. The aim Of this Study was to investigate whether platelet apoptosis, platelet activation, platelet aggregation, platelet-leukocyte aggregate (PLA) formation and lipid peroxidation occur simultaneously in hyperlipidemia. Design and methods: Expression of GpIIb/IIIa (CD41a), P-selectin (CD62-P), platelet-bound fibrinogen (antifibrinogen), platelet membrane phosphatidylserine (PS), platelet-monocyte aggregates (mono-PLA) and platelet-neutrophil aggregates (neut-PLA) was measured in eight hyperlipidemic and eight normal subjects using flow cytometry. ADP (10 mu M) was used to activate platelets. Furthermore, ADP induced platelet aggregation responses, platelet malondialdehyde (MDA) and glutathione (GSH) levels were determined. Results: Before platelet activation, platelet CD62-P, anti Fibrinogen, annexin-V, mono-PLA, neut-PLA and platelet MDA levels as well as platelet aggregation responses in the hyperlipidemics were significantly higher than those in the controls (P < 0.01, P < 0.01, P < 0.01, P < 0.001, P < 0.001, P < 0.01, P < 0.001, respectively), whereas GpIIb/IIIa expression and GSH levels were not different significantly (P > 0.05). In the control group, CD62-P, antifibrinogen and annexin-V levels increased significantly after ADP activation (P < 0.05, P < 0.05, P < 0.01, respectively). In hyperlipidemic Subjects, annexin-V expression increased significantly after activation (P < 0.01), whereas expression of GpIIb/ IIIa, CD62-P and anti fibrinogen remained unchanged (P > 0.05). The levels of total cholesterol (T-CHO), low density lipoprotein cholesterol (LDL-C), serum fibrinogen (S-FGN) and high density lipoprotein cholesterol (HDL-C) in patients were found to be correlated with platelet CD62-P, anti Fibrinogen, annexin-V, mono-PLA and MDA. Conclusions: In conclusion, it seems that in hyperlipidemia, some platelets are in an activated state in circulation, and that increased lipid peroxidation, early apoptosis, platelet-leukocytes aggregate formation and platelet aggregation altogether accompany this process. (C) 2005 The Canadian Society of Clinical Chemists. All rights reserved.
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    Apo A-I binding to platelets detected by flow cytometry
    (2001) ÖZSAVCI, DERYA; Ozsavci, D.; Yardimci, T.; Demirel, G. Y.; Uras, F.; Hekim, N.; Ulutin, O. N.
    Lipoprotein-platelet interactions are very important in atherosclerosis and thrombosis. Several studies have been carried out on specific binding of various lipoproteins to platelets. But there is considerable disagreement about the details of these binding sites. Although low-density lipoprotein (LDL) receptors of several cells have been studied extensively, there is little datum about high-density lipoprotein (HDL) receptors. Apolipoprotein (apo) A-I may play a major role in the determination of the specificity of HDL receptors. In this study, binding of apo A-I to platelets was investigated by using a flow cytometric method. Citrated blood samples were obtained from five healthy and seven hypercholesterolemic subjects. Apo A-I antibody was incubated with the citrated whole blood before and after activation with ADP or thrombin receptor agonist peptide (TRAP). Then fluorescein isothiocyanate (FITC)-labeled secondary antibodies were added and analyzed on a Becton-Dickinson FACSort flow cytometer. In the hypercholesterolemic group, apo A-I binding to platelets was found to be significantly decreased after activation with TRAP (P<.05), but not after activation with ADP. In the control group, after platelet activation with ADP or TRAP, the apo A-I MFI values were not found to be significantly different from the values of resting platelets (P>.05). In this study, we demonstrated that apo A-I can bind to platelets, and this supports the hypothesis that apo A-I may play a major role in HDL binding to platelets.