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Platelet-Derived Procoagulant Microvesicles Are Elevated in Patients with Retinal Vein Occlusion (RVO). | LitMetric

Platelet-Derived Procoagulant Microvesicles Are Elevated in Patients with Retinal Vein Occlusion (RVO).

J Clin Med

Department of Haemostasis and Haemostatic Disorders, Chair of Biomedical Sciences, Medical University of Lodz, Mazowiecka 6/8, 92-215 Lodz, Poland.

Published: August 2022

AI Article Synopsis

  • The study investigates the role of platelets in retinal vein occlusion (RVO) by comparing platelet function in RVO patients (n = 35) to healthy controls (n = 35).
  • Findings showed significantly higher levels of soluble P-selectin and an increase in platelet-derived microvesicles with procoagulant properties in the RVO group, suggesting a link between these microvesicles and RVO development.
  • However, no notable differences were found in basic platelet parameters and inflammatory markers, indicating that while platelets may enhance coagulation risk in RVO, their overall hyperreactivity may not be a major contributing factor to the condition.

Article Abstract

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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9457368PMC
http://dx.doi.org/10.3390/jcm11175099DOI Listing

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