Romero, I.A.; Radewicz, K.; Jubin, E.; Michel, C.C.; Greenwood, J.; Couraud, P.O. and Adamson, P.
|DOI (Digital Object Identifier) Link:||http://dx.doi.org/10.1016/S0304-3940(03)00348-3|
|Google Scholar:||Look up in Google Scholar|
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.
|Item Type:||Journal Article|
|Keywords:||Blood–brain barrier; Brain endothelium; Permeability; Dexamethasone; Glucocorticoids; Cell junctions|
|Academic Unit/Department:||Science > Life, Health and Chemical Sciences
|Interdisciplinary Research Centre:||Biomedical Research Network (BRN)|
|Depositing User:||Ignacio A Romero|
|Date Deposited:||23 Aug 2007|
|Last Modified:||14 Jan 2016 16:41|
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