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Effect of 15-deoxy-delta12,14-prostaglandin J2 on IL-1beta-induced expression of epithelial neutrophil-activating protein-78 in human endothelial cells.

作者信息

Imaizumi Tadaatsu, Kumagai Mika, Hatakeyama Masaharu, Tamo Wakako, Yamashita Koji, Yoshida Hidemi, Munakata Hirofumi, Satoh Kei

机构信息

Department of Vascular Biology, Institute of Brain Science, Hirosaki University School of Medicine, 5 Zaifu-cho, Hirosaki 036-8562, Japan.

出版信息

Prostaglandins Leukot Essent Fatty Acids. 2003 Nov;69(5):323-7. doi: 10.1016/s0952-3278(03)00145-5.

DOI:10.1016/s0952-3278(03)00145-5
PMID:14580366
Abstract

Epithelial neutrophil-activating peptide-78 (ENA-78) is a member of CXC chemokines. It is produced by endothelial cells stimulated with interleukin-1 (IL-1), along with other CXC chemokines such as IL-8 and growth-related oncogene protein-alpha (GRO-alpha). IL-1-induced ENA-78 production by endothelial cells may be important for the regulation of neutrophil activation. 15-Deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)) is a natural ligand for peroxisome proliferator-activated receptor-gamma (PPAR-gamma) and affects the expression of various genes. We examined the effect of 15d-PGJ(2) on the expression of ENA-78 in cultured endothelial cells stimulated with IL-1beta. 15d-PGJ(2) inhibited the IL-1beta-induced expression of ENA-78, but not the expression of IL-8 or GRO-alpha in response to IL-1. Ciglitazone, another agonist for PPAR-gamma, had no effect on the expression of ENA-78, suggesting that 15d-PGJ(2) may inhibit the expression of ENA-78 in a PPAR-gamma-independent manner. 15d-PGJ(2) may modulate inflammatory reactions by regulating the balance of CXC chemokines in endothelial cells.

摘要

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