Open AccessEffects of IgG from the serum of ischemic stroke patients on hemostasis
Author(s) -
T. Katrii,
Nataliia Raksha,
Tetiana Halenova,
Tetiana Vovk,
Olga Kravchenko,
Alexandra Kostiuk,
Olexiy Savchuk,
Alona Zlatska,
Tetiana Andriichuk,
Volodymyr Melnyk,
Ostapchenko Li
Publication year - 2021
Publication title -
journal of biological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.218
H-Index - 6
eISSN - 2284-0230
pISSN - 1826-8838
DOI - 10.4081/jbr.2021.9582
Subject(s) - hemostasis , medicine , stroke (engine) , ischemic stroke , thrombin , disease , platelet , immunology , cardiology , ischemia , mechanical engineering , engineering
Ischemic stroke is among the top diseases leading to mortality and disability in the world. The detailed investigation of the mechanisms underlying this pathology and especially mediating the tendency to relapse during the first year after stroke incident undoubtedly belongs to important tasks of modern medicine and biology. The current study aims to analyze the influence of IgG derived from the blood serum of ischemic stroke patients on some hemostasis factors. In total, 123 participants with IS, 62 with atherothrombotic ischemic stroke, 61 with cardioembolic ischemic stroke, and 57 subjects as control have been examined. The same patients have participated in the research a year after stroke. IgG from serum was isolated by affinity chromatography on protein A Sepharose column. The activity of key hemostasis factors under the influence of IgG was analyzed. Obtained results revealed that IgG of stroke patients but not healthy subjects caused the inhibition of the amidolytic activity of endogenously generated thrombin, protein C, factor Xa, and led to an increase in the degree of ADP-induced platelet aggregation. The reduction of clotting time in the test "Thrombin time" by IgG of patients at the acute phase of disease was also observed; IgG of healthy subjects mediated the opposite effect. In contrast to acute ischemic stroke IgG, IgG of patients one year after both atherothrombotic and cardioembolic ischemic stroke influenced only the activity of endogenously generated thrombin and factor Xa resulting in inhibition of their activities. It was also established that IgG of ischemic stroke patients, as well as healthy subjects, stimulated the secretion of tissue plasminogen activator by endotheliocytes.