作者: Dimitrios Papadopoulos , Georgios Scheiner-Bobis
DOI: 10.1016/J.BBAMCR.2017.05.006
关键词:
摘要: Tight junctions (TJ) between brain endothelial cells are essential for formation and maintenance of the blood-brain barrier (BBB). Although loss BBB integrity is associated with several neuropathological disorders, treatments that augment or stabilise scarce. Here we show physiological concentrations dehydroepiandrosterone sulfate (DHEAS) stimulate expression TJ proteins zonula occludens-1 (ZO-1) claudin-3 in brain-derived cell line bEnd.3 promote neighbouring cells, demonstrated by augmented transendothelial resistance across monolayers. Silencing androgen receptor siRNA does not prevent DHEAS-induced stimulation ZO-1 expression, indicating conversion DHEAS into testosterone required its actions. Suppression Gnα11 prevents actions, pointing towards a G-protein-coupled as being mediator effects. These results consistent idea DHEAS, acting hormone own right, supports BBB. The current findings might help developing new strategies prevention treatment neurological disorders defects.