Abstract
Endothelial dysfunction or activation, elicited by oxidized low-density lipoprotein (OxLDL), has been implicated in the initiation and progression of atherosclerosis. We elucidated whether tumor necrosis factor-α (TNF-α)-induced endothelial OxLDL receptor, lectin-like OxLDL receptor-1 (LOX-1), mRNA expression is modified by peroxisome proliferator-activated receptor (PPAR) activators in cultured bovine aortic endothelial cells (BAEC). We confirmed that both PPARα and PPARγ were expressed in BAEC by reverse transcription-polymerase chain reaction analysis. Natural PPARγ ligand 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) and the thiazolidinediones, pioglitazone and troglitazone, decreased TNF-α-induced LOX-1 mRNA expression in BAEC. LOX-1 expression induced by phorbol 12-myristrate 13-acetate was also inhibited by 15d-PGJ2. In contrast, PPARα ligands, Wy14643 and fenofibric acid, did not alter TNF-α-induced LOX-1 expression. TNF-α-induced immunohistochemical staining of LOX-1 was suppressed by 15d-PGJ2 but not Wy14643. Taken together, PPARγ activators inhibit TNF-α-induced LOX-1 expression in cultured BAEC, which may beneficially influence inflammatory responses in atherosclerosis.
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