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Peroxisome Proliferator‐Activated Receptor α Ligands Increase Lectin‐Like Oxidized Low Density Lipoprotein Receptor‐1 Expression in Vascular Endothelial Cells
Author(s) -
HAYASHIDA KAZUTAKA,
KUME NORIAKI,
MINAMI MANABU,
KATAOKA HIROHARU,
MORIMOTO MASAFUMI,
KITA TORU
Publication year - 2001
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2001.tb03965.x
Subject(s) - downregulation and upregulation , peroxisome proliferator activated receptor , receptor , nuclear receptor , peroxisome , transcription factor , chemistry , peroxisome proliferator activated receptor alpha , microbiology and biotechnology , biology , biochemistry , gene
A bstract : Lectin‐like oxidized low density lipoprotein receptor‐1 (LOX‐1) is a receptor for atherogenic oxidized LDL expressed in vascular endothelial cells, smooth muscle cells, and macrophages. Peroxiosme proliferator‐activated receptors (PPARs) include subfamilies PPARα and PPARγ, which are expressed in endothelial cells and involved in transcriptional regulation of a large number of genes that affect lipoprotein and fatty acid metabolism as well as inflammation. We therefore explored the effects of PPARα and PPARγ ligands on expression of LOX‐1. Treatment of cultured bovine aortic endothelial cells (BAECs) with PPARα ligands (fenofibrate and WY14643) remarkably upregulated LOX‐1 expression, which was detected by western and northern blot analyses. LOX‐1 promoter‐reporter gene assay showed that PPARα ligands activate transcription of the LOX‐1 gene. PPARγ ligands, in contrast, did not significantly affect LOX‐1 expression in BAECs. PPARα appears to be a key regulator in promoting LOX‐1 expression in BAECs. Upregulated expression of LOX‐1 may modulate the catabolism of oxidized LDL and atherosclerotic progression.