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Multiple sclerosis is a serious problem of medicine and one of the most frequent reasons of disabilities of young adults. EAE is a commonly used rodent model of MS. In physiological conditions the blood-brain barrier (BBB) maintains CNS homeostasis and prevents uncontrolled inflow of immune cells from the blood circuit. During the development of EAE, damaged BBB fails to protect CNS from autoreactive immune cells. In this study we try to investigate a possible role of P2X7R in pathological changes of BBB during EAE. Analyzing BBB tightness we observed decreased expression of Claudin5 (protein component of tight-junctions) in the isolated microvessels’ fraction using western blot technique. These data were confirmed by immunofluorescence staining of brain sections against Claudin5. To assess functional state of BBB we carried out immunohistochemical staining against albumin and we observed its extravasation in early phase of EAE. All these data suggest dysfunction of BBB at the early stage of the disease. In parallel we observed overexpression of P2X7R in microvessels’ fraction and noticed correlation between its expression and increased BBB permeability using antagonist of P2X7R. Supported by grant nr: 2012/05/N/NZ4/02191
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