Abstract
BackgroundThe aim of this study was to characterize the hCMEC/D3 cell line, an in vitro model of the human Blood Brain Barrier (BBB) for the expression of brain endothelial specific claudins-3 and -12.FindingshCMEC/D3 cells express claudins-3 and -12. Claudin-3 is distinctly localized to the TJ whereas claudin -12 is observed in the perinuclear region and completely absent from TJs. We show that the expression of both proteins is lost in cell passage numbers where the BBB properties are no longer fully conserved. Expression and localization of claudin-3 is not modulated by simvastatin shown to improve barrier function in vitro and also recommended for routine hCMEC/D3 culture.ConclusionsThese results support conservation of claudin-3 and -12 expression in the hCMEC/D3 cell line and make claudin-3 a potential marker for BBB characteristics in vitro.
Highlights
The aim of this study was to characterize the hCMEC/D3 cell line, an in vitro model of the human Blood Brain Barrier (BBB) for the expression of brain endothelial specific claudins-3 and -12
Claudin-3 and -12 are expressed but only claudin-3 is localized at the Tight junction (TJ) in the hCMEC/D3 cell line We compared the expression of claudin-3 and claudin12 in hCMEC/D3 cells to primary human brain endothelium and other non-endothelial based cell lines
Claudin-3 levels are comparable between primary brain endothelium (PHB, lane 1) and transformed
Summary
The aim of this study was to characterize the hCMEC/D3 cell line, an in vitro model of the human Blood Brain Barrier (BBB) for the expression of brain endothelial specific claudins-3 and -12. At the blood brain barrier (BBB), claudins-1,-3, -5 and -12 have been shown to participate in the formation of TJs between brain microvascular endothelial cells in vivo [1,2,3,4]. Of these members, there has been a particular interest in claudin-5, as mice deficient for this protein showed size dependent transport restriction for molecules smaller than 800 Da. Claudin-12 is highly expressed at the TJs in murine development [3]. The loss of claudin-3 from the TJs in experimental allergic encephalomyelitis (EAE) demonstrates that it may be important for determining permeability in pathological conditions [4]
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