The molecular mechanisms of platelets activation in patients with cerebrovascular disease

   


1. National Research Centre “Kurchatov institute”, B.P. Konstantinov Petersburg Nuclear Physics Institute, Gatchina, Russia; Federal Almazov North-West Medical Research Centre, St. Petersburg, Russia; Mechnikov North-Western State Medical University, St. Petersburg, Russia
2. Mechnikov North-Western State Medical University, St. Petersburg, Russia
3. National Research Centre “Kurchatov institute”, B.P. Konstantinov Petersburg Nuclear Physics Institute, Gatchina, Russia; St.Petersburg State Polytechnical University, St. Petersburg, Russia
4. Federal Almazov North-West Medical Research Centre, St. Petersburg, Russia; Mechnikov North-Western State Medical University, St. Petersburg, Russia
Type: Experimental study
DOI: 10.18097/PBMC20156105606      UDK: 577.217.5      PubMed Id: 26539867
Year: 2015 vol: 61  issue:5  pages: 606-612
Abstract: Cerebrovascular disease is a main cause of mortality and one of the big medical problems. After the vascular wall’s damage the endothelial cells secrete the von Willebrand factor which then connects with its platelet’s receptor GP Ib-V-IX. There are two polymorphisms Thr145Met and T(-5)C of the GP Iba gene associated with arterial thrombosis development. Also the difference in platelets’ genes expressions was shown in patients with various clinical course of ischemic heart disease. The aim of this study was to investigate the role of platelet’s receptor for von Willebrand factor in platelets’ activation in patients with cerebrovascular disease. 123 patients with cerebrovascular disease and 97 healthy donors were included into the study. We analyzed the level of receptor for von Willebrand factor on platelet’s membrane by flow cytometry, Thr145Met and T(-5)C GP Iba polymorphiams by PCR-RFLP, the GP Iba gene expression by RT-PCR and ADP-induced platelet aggregation by Born method. We have shown: 1) the 145Met GP Iba allele prevalence in patients with atherotrombotic stroke development due to macroangiopathy; 2) the pre-mRNA transform into the mature mRNA in activated platelets and this process may be stopped by the antiplatelet therapy by acetylsalicylic acid.
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Reference: Sirotkina O.V., Laskovets A.B., Goldobin V.V., Topanova A.A., Karelov D.V., Vavilova T.V., The molecular mechanisms of platelets activation in patients with cerebrovascular disease, Biomeditsinskaya khimiya, 2015, vol: 61(5), 606-612.
This paper is also available as the English translation:10.1134/S1990750815010102
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