Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Gliovascular and cytokine interactions modulate brain endothelial barrier in vitro | Chaitanya et al. Journal of Neuroinflammation 2011 8 162 http content 8 1 162 JIOURNAL1 OF. NEUROINFLAMMATION RESEARCH Open Access Gliovascular and cytokine interactions modulate brain endothelial barrier in vitro Ganta V Chaitanya1 Walter E Cromer2 Shannon R Wells1 Merilyn H Jennings1 P Olivier Couraud4 5 6 I z t r I r ĩ Dev m 7 D k zvf 1 zv A z- lzr-lzM 7 A i f- c rzd vr I r bv c r f zv ìk k9IAAỈ h zvl ly l bhir 2 A I rZV 7 -V h A I k k -V Z1 -V r3 V ev zd Ignacio A Romero Babette vvekSler Anat Erdreich-Epstein J Michael Mathis Alireza Minagar and J Steven Alexander1 8 Abstract The glio-vascular unit G-unit plays a prominent role in maintaining homeostasis of the blood-brain barrier BBB and disturbances in cells forming this unit may seriously dysregulate BBB. The direct and indirect effects of cytokines on cellular components of the BBB are not yet unclear. The present study compares the effects of cytokines and cytokine-treated astrocytes on brain endothelial barrier. 3-dimensional transwell co-cultures of brain endothelium and related-barrier forming cells with astrocytes were used to investigate gliovascular barrier responses to cytokines during pathological stresses. Gliovascular barrier was measured using trans-endothelial electrical resistance TEER a sensitive index of in vitro barrier integrity. We found that neither TNF-a IL-1P or IFN-g directly reduced barrier in human or mouse brain endothelial cells or ECV-304 barrier independent of cell viability metabolism but found that astrocyte exposure to cytokines in co-culture significantly reduced endothelial and ECV-304 barrier. These results indicate that the barrier established by human and mouse brain endothelial cells and other cells may respond positively to cytokines alone but that during pathological conditions cytokines dysregulate the barrier forming cells indirectly through astrocyte activation involving reorganization of junctions matrix focal adhesion or release of .
