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-Induced VCAM-1 Expression in an IFN Regulatory Factor-1-Dependent Manner and Reduces Monocytic Cell Adhesion to Endothelial Cells1
,
* Department of Chemical Engineering,
Edison Biotechnology Institute, and
Department of Biomedical Sciences, College of Osteopathic Medicine, Ohio University, Athens, OH 45701
Proinflammatory cytokine (e.g., TNF-
)-induced expression of endothelial cell adhesion molecules (ECAMs) on the lumenal surface of the vascular endothelium and a consequent increase in leukocyte adhesion are key aspects of pathological inflammation. A promising therapeutic approach to diminish aberrant leukocyte adhesion is, therefore, to inhibit cytokine-induced ECAM expression at the transcription level. Several studies suggest that methimazole, a compound used clinically to treat autoimmune diseases, such as Graves’ disease, may also diminish pathological inflammation by suppressing ECAM expression. In this study we probed the hypothesis that a derivative of methimazole, phenyl methimazole (compound 10), can reduce cytokine-induced ECAM expression and consequent leukocyte adhesion. We found that compound 10 1) dramatically inhibits TNF--induced VCAM-1 mRNA and protein expression in human aortic endothelial cells (HAEC), has a relatively modest inhibitory effect on TNF- induced E-selectin expression and has no effect on ICAM-1 expression; 2) significantly reduces TNF--induced monocytic (U937) cell adhesion to HAEC under in vitro flow conditions similar to that present in vivo; 3) inhibits TNF--induced IFN regulatory factor-1 binding to VCAM-1 promoter; and 4) reduces TNF--induced IRF-1 expression in HAEC. Combined, the results indicate that phenyl methimazole can reduce TNF--induced VCAM-1 expression in an IFN regulatory factor-1-dependent manner and that this contributes significantly to reduced monocytic cell adhesion to TNF--activated HAEC.
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