Abstract：
:The blood-brain barrier (BBB) plays an important role in controlling the passage of molecules from the blood to the extracellular fluid environment of the brain. An immortalised rat brain endothelial cell line (GPNT) was used to investigate the mechanisms underlying dexamethasone-induced decrease in paracellular permeability. Following treatment with 1 microM dexamethasone there was a decrease in transmonolayer paracellular permeability mainly to sucrose, fluorescein and dextrans of up to 20 KDa. According to pore theory, these differences in permeability were consistent with a decrease in the number of pores between brain endothelial cells. This effect was accompanied by a concentration of filamentous actin and cortactin to the cell periphery. Concomitantly, the continuity of the tight junctional protein ZO-1 at the cell borders was improved and was associated with an increase in both ZO-1 and occludin expression. By contrast, the expression and distribution of adherens junctional proteins such as beta-catenin and p100/p120 remained unchanged. These observations suggest that glucocorticoids induce a more differentiated BBB phenotype in cultured brain endothelial cells through modification of tight junction structure.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Romero IA,Radewicz K,Jubin E,Michel CC,Greenwood J,Couraud PO,Adamson Pdoi
10.1016/s0304-3940(03)00348-3keywords:
subject
Has Abstractpub_date
2003-06-26 00:00:00pages
112-6issue
2eissn
0304-3940issn
1872-7972pii
S0304394003003483journal_volume
344pub_type
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