Arteriosclerosis, Thrombosis, and Vascular Biology. 1999;19:2094-2104
© 1999 American Heart Association, Inc.
Vascular Biology |
Peroxisome Proliferator–Activated Receptor Activators Target Human Endothelial Cells to Inhibit Leukocyte–Endothelial Cell Interaction
From the Department of Medicine (S.M.J., F.P., X.-P.X., W.A.H., R.E.L., L.L.D.), the Division of Cardiology (S.M.J., F.P., L.L.D.), the Division of Endocrinology, Diabetes, and Hypertension (X.-P.X., W.A.H., R.E.L.), and the Department of Pathology (J.A.B.), University of California, Los Angeles, School of Medicine, Los Angeles.
Correspondence to Simon M. Jackson, PhD, Division of Cardiology, UCLA School of Medicine, 47-123 CHS, Box 951679, Los Angeles, CA 90095-1679. E-mail smjack{at}ucla.edu
Abstract—An early event in acute
and chronic inflammation and associated diseases such as
atherosclerosis and rheumatoid arthritis is the induced
expression of specific adhesion molecules on the surface of
endothelial cells (ECs), which subsequently bind
leukocytes. Peroxisome proliferator–activated receptors
(PPARs), members of the nuclear receptor superfamily of transcription
factors, are activated by fatty acid metabolites, peroxisome
proliferators, and thiazolidinediones and are now recognized as
important mediators in the inflammatory response. Whether PPAR
activators influence the inflammatory responses of ECs is
unknown. We show that the PPAR activators
15-deoxy-
12,14-prostaglandin J2
(15d-PGJ2), Wyeth 14643, ciglitazone, and troglitazone, but
not BRL 49653, partially inhibit the induced expression of vascular
cell adhesion molecule-1 (VCAM-1), as measured by ELISA, and monocyte
binding to human aortic endothelial cells (HAECs)
activated by phorbol 12-myristate 13-acetate (PMA) or
lipopolysaccharide. The "natural" PPAR
activator 15d-PGJ2 had the greatest potency and
was the only tested molecule capable of partially inhibiting the
induced expression of E-selectin and neutrophil-like HL60 cell binding
to PMA-activated HAECs. Intracellular adhesion molecule-1
induction by PMA was unaffected by any of the molecules tested. Both
PPAR-
and PPAR-
mRNAs were detected in HAECs by using reverse
transcription–polymerase chain reaction and a ribonuclease protection
assay; however, we have yet to determine which, if any, of the PPARs
are mediating this process. These results suggest that certain PPAR
activators may help limit chronic inflammation mediated by
VCAM-1 and monocytes without affecting acute inflammation mediated by
E-selectin and neutrophil binding.
Key Words: peroxisome proliferator–activated receptors • endothelial cells • adhesion molecules • inflammation
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