| Autor: |
Marcinkowska A; Department of Haemostasis and Haemostatic Disorders, Chair of Biomedical Sciences, Medical University of Lodz, Mazowiecka 6/8, 92-215 Lodz, Poland.; Department of Ophthalmology, Karol Jonscher's Municipal Medical Center, 93-113 Lodz, Poland., Wolska N; Platelet Signalling and Vascular Diseases, Institute for Clinical Chemistry and Laboratory Medicine, University Medical Center Hamburg-Eppendorf (UKE), 20246 Hamburg, Germany., Luzak B; Department of Haemostasis and Haemostatic Disorders, Chair of Biomedical Sciences, Medical University of Lodz, Mazowiecka 6/8, 92-215 Lodz, Poland., Cisiecki S; Department of Ophthalmology, Karol Jonscher's Municipal Medical Center, 93-113 Lodz, Poland., Marcinkowski K; Department of Haemostasis and Haemostatic Disorders, Chair of Biomedical Sciences, Medical University of Lodz, Mazowiecka 6/8, 92-215 Lodz, Poland., Rozalski M; Department of Haemostasis and Haemostatic Disorders, Chair of Biomedical Sciences, Medical University of Lodz, Mazowiecka 6/8, 92-215 Lodz, Poland. |
| Abstrakt: |
The etiopathogenesis of retinal vein occlusion (RVO) is multifactorial, and the contribution of platelets to RVO development has not been fully elucidated. We aimed to analyze platelet function in RVO patients (n = 35) and controls (n = 35). We found a higher (p < 0.05) level of soluble P-selectin in RVO group vs. controls. Additionally, in RVO patients, the concentration of platelet-derived microvesicles was higher (p < 0.05), and the difference between groups was deeper for the fraction of platelet-derived microvesicles with the procoagulant phenotype (p < 0.0001) and for overall procoagulant microvesicles level (p < 0.0001). The results were similar for the total RVO group and for both RVO types (central- and branched-retinal vein occlusion). We did not find differences in simple platelet parameters (platelet count, mean platelet volume, platelet distribution width, platecrit, reticulated platelets) and inflammatory markers (platelet-lymphocyte ratio, neutrophil-lymphocyte ratio). Similarly, no differences were found for platelet aggregation-stimulated byadenosine diphosphate; collagen; arachidonic acid; and in multiparametric flow cytometry evaluation of P-selectin, PAC-1, and fibrinogen binding for both unstimulated and adenosine diphosphate-, collagen-, and thrombin receptor activating peptide-stimulated platelets. Our results suggest that platelets can contribute to developing RVO by enhancing procoagulant activity through providing a procoagulation surface via platelet-derived microvesicles. The direct role of platelets’ hyperreactivity in developing RVO is less apparent, which is consistent with the complexity and multifactorial background of this disorder. |
