The molecular mechanisms of platelets activation in patients with cerebrovascular disease
| Autor: | A. B. Laskovets, O. V. Sirotkina, T. V. Vavilova, D. V. Karelov, A. A. Topanova, V.V. Goldobin |
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| Rok vydání: | 2015 |
| Předmět: |
Blood Platelets
Male Platelet Aggregation Primary Cell Culture Gene Expression General Biochemistry Genetics and Molecular Biology Gene Frequency Von Willebrand factor von Willebrand Factor RNA Precursors medicine Humans Platelet Platelet activation Stroke Alleles Aspirin Polymorphism Genetic biology business.industry Coronary Thrombosis Platelet Glycoprotein GPIb-IX Complex General Medicine Middle Aged medicine.disease Thrombosis Adenosine Diphosphate Case-Control Studies Immunology biology.protein Platelet aggregation inhibitor Female business Platelet Aggregation Inhibitors medicine.drug |
| Zdroj: | Biomeditsinskaya Khimiya. 61:606-612 |
| ISSN: | 2310-6905 2310-6972 |
| DOI: | 10.18097/pbmc20156105606 |
| Popis: | 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.Tserebrovaskuliarnye zabolevaniia zanimaiut vtoroe mesto sredi prichin smertnosti naseleniia i iavliaiutsia odnoĭ iz naibolee vazhnykh mediko-sotsial'nykh problem. Pri povrezhdenii stenki sosuda éndotelial'nye kletki sekretiruiut soderzhashchiĭsia v nikh faktor Villebranda, kotoryĭ sviazyvaetsia so svoim retseptorom na poverkhnosti trombotsita – glikoproteinom GP Ib-V-IX. Izvestny polimorfizmy Thr145Met i T(-5)C gena GP Iba, kotorye sviazany s riskom razvitiia arterial'nykh trombozov, pokazany otlichiia v ékspressionnom profile trombotsitov patsientov s razlichnym techeniem ishemicheskoĭ bolezni serdtsa. Tsel'iu dannogo issledovaniia iavilos' opredelenie roli trombotsitarnogo retseptora dlia faktora Villebranda v aktivatsii trombotsitov u bol'nykh s tserebrovaskuliarnymi zabolevaniiami. V issledovanie byli vkliucheny 123 patsienta s tserebrovaskuliarnymi zabolevaniiami i 97 zdorovykh dobrovol'tsev, u kotorykh byli proanalizirovany: kolichestvo retseptora dlia faktora Villebranda metodom protochnoĭ tsitometrii, nalichie polimorfizmov Thr145Met i T(-5)C GP Iba metodom PTsR s posleduiushchim restriktsionnym analizom, uroven' ékspressii gena GP Iba metodom PTsR v real'nom vremeni i ADP-indutsirovannaia agregatsiia po Bornu. Nami pokazano, chto: 1) polimorfnyĭ allel' 145Met GP Iba chashche vstrechaetsia u patsientov, perenesshikh ishemicheskiĭ insul't na fone makroangiopatii sosudov golovnogo mozga; 2) v aktivirovannykh trombotsitakh pre-mRNK gena GP Iba preobrazuetsia v zreluiu mRNK, i étot protsess blokiruetsia priemom antiagregantnykh preparatov atsetilsalitsilovoĭ kisloty. |
| Databáze: | OpenAIRE |
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