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Tumor necrosis factor-α up-regulates glucuronosyltransferase gene expression in human brain endothelial cells and promotes T-cell adhesion

✍ Scribed by Somsankar Dasgupta; Makoto Yanagisawa; Kannan Krishnamurthy; Sean S. Liour; Robert K. Yu

Publisher
John Wiley and Sons
Year
2007
Tongue
English
Weight
244 KB
Volume
85
Category
Article
ISSN
0360-4012

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✦ Synopsis

Abstract

Stimulation of human brain microvascular endothelial cells (SV‐HCECs) with tumor necrosis factor‐α (TNF‐α) up‐regulates sulfoglucuronosyl paragloboside (SGPG) synthesis in a dose‐ and time‐dependent manner. After TNF‐α exposure at a concentration of 50 ng/ml for 24 hr, we observed a seven‐ to tenfold elevation of SGPG concentration. Interleukin‐1β (IL‐1β) at a concentration of 10 ng/ml and the combined doses of TNF‐α and IL‐1β were less effective than TNF‐α alone. TNF‐α also stimulated T‐cell (Jurkat) adhesion with SV‐HCECs via SGPG‐L‐selectin recognition: this was determined by double‐label immunofluorescent staining with SGPG and L‐selectin antibodies. The number of T cells bound to SV‐HCECs after different cytokine stimulations was proportional to the SGPG concentration, and the cell attachment was inhibited by anti‐SGPG and anti‐L‐selectin antibodies, respectively. Our data unequivocally establish that inflammatory cytokines, particularly TNF‐α, stimulate the glucuronosyltransferse, GlcAT‐P, and GlcAT‐S, gene expression in brain endothelial cells and promote T‐cell adhesion via SGPG‐L‐selectin recognition, a preliminary step for onset of neuroinflammation. © 2007 Wiley‐Liss, Inc.

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