The MAP kinase pathway mediates transcytosis induced by TNF-α in an in vitro blood-brain barrier model

Abstract : Cerebral capillary endothelial cells constitute the blood-brain barrier (BBB). In these highly specialized cells, transcellular transports rarely occur, and the presence of tight junctions between them leads to a low paracellular permeability. In order to understand the functions of this barrier, an in vitro model of the BBB has been developed and consists in a co-culture of primary cerebral capillary endothelial cells and glial cells. When these endothelial cells are subjected to an inflammatory agent, such as tumor necrosis factoralpha (TNF-α), in vitro BBB permeability is increased, as indicated by the increase in holotransferrin transcytosis. However, no significant change in the paracellular permeability is observed. In order to understand the molecular mechanisms that underlie these transcytosis processes, we investigated the implication of the mitogen-activated protein kinase (MAPK) signalling pathway, as TNF-α is known to activate this kinase family. In the present study, an increase in the activation of p42–44 MAPK is observed after TNF-α treatment. Holotransferrin transcytosis as well as p42–44 MAPK activation are inhibited after addition of a p42–44 MAPK pathway inhibitor (UO126) during TNF-α challenge. These data suggest that the MAPK pathway is involved in the transcytosis regulation in endothelial cells from an in vitro BBB model.
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European Journal of Neuroscience, Wiley, 2005, 22, p. 835-844
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Contributeur : Wilfried Déplanques <>
Soumis le : lundi 6 décembre 2010 - 09:12:28
Dernière modification le : samedi 7 avril 2018 - 14:40:02

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  • HAL Id : hal-00543167, version 1

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Florence Miller, Laurence Fenart, Valérie Landry, Caroline Coisne, Roméo Cecchelli, et al.. The MAP kinase pathway mediates transcytosis induced by TNF-α in an in vitro blood-brain barrier model. European Journal of Neuroscience, Wiley, 2005, 22, p. 835-844. 〈hal-00543167〉

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