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RORα1 and RORα4 suppress TNF‐α‐induced VCAM‐1 and ICAM‐1 expression in human endothelial cells
Author(s) -
Migita Hideyuki,
Satozawa Noboru,
Lin Jiing-Huey,
Morser John,
Kawai Kohichi
Publication year - 2004
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(03)01502-3
Subject(s) - vcam 1 , tumor necrosis factor alpha , icam 1 , cell adhesion molecule , umbilical vein , retinoic acid , orphan receptor , microbiology and biotechnology , vascular endothelial growth inhibitor , biology , chemistry , cancer research , cell culture , transcription factor , immunology , biochemistry , vascular endothelial growth factor a , in vitro , vascular endothelial growth factor , genetics , gene , vegf receptors
Retinoic acid receptor‐related orphan receptor‐α (RORα) is a nuclear orphan receptor. Adenovirus‐mediated overexpression of RORα1 and RORα4 suppressed tumor necrosis factor‐α (TNF‐α)‐induced expression of vascular cell adhesion molecule‐1 (VCAM‐1) and intracellular adhesion molecule‐1 (ICAM‐1) in human umbilical vein endothelial cells. Overexpression of RORα1 and RORα4 also suppressed TNF‐α‐stimulated translocation of p50 and p65 to the nucleus. In contrast, dominant‐negative deletion mutants of RORα1 and RORα4 failed to suppress the induction of VCAM‐1 and ICAM‐1 and translocations of p50 and p65. These results suggest that RORα1 and RORα4 regulate the inflammatory responses via inhibition of the nuclear factor‐κB signaling pathway in endothelial cells.