作者: Yoji Taba , Toshiyuki Sasaguri , Megumi Miyagi , Takeo Abumiya , Yoshikazu Miwa
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摘要: Ligands for peroxisome proliferator-activated receptor gamma, such as the thiazolidinedione class of antidiabetic drugs and 15-deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)), modulate various processes in atherogenesis. In search cells that generate prostaglandin D(2) (PGD(2)), metabolic precursor 15d-PGJ(2), we identified PGD(2) from culture medium endothelial cells. To study how production is regulated cells, investigated role fluid shear stress metabolism PGD(2). Endothelial expressed mRNA lipocalin-type synthase (L-PGDS) both vitro vivo. Loading laminar using a parallel-plate flow chamber markedly enhanced gene expression L-PGDS, with maximal effect being obtained at 15 to 30 dyne/cm(2). The began increase within 6 hours after loading reached level 18 24 hours. contrast, did not alter levels PGI(2) thromboxane A(2) synthase. parallel released 15d-PGJ(2) into medium. These results demonstrate promotes by stimulating L-PGDS suggest possibility gamma ligand produced vascular wall response blood flow.