Tadaatsu Imaizumi , Mika Kumagai , Masaharu Hatakeyama , Wakako Tamo , Koji Yamashita , Hidemi Yoshida , Hirofumi Munakata , Kei Satoh
{"title":"15-脱氧-delta12,14-前列腺素J2对il- 1诱导的人内皮细胞上皮中性粒细胞活化蛋白-78表达的影响。","authors":"Tadaatsu Imaizumi , Mika Kumagai , Masaharu Hatakeyama , Wakako Tamo , Koji Yamashita , Hidemi Yoshida , Hirofumi Munakata , Kei Satoh","doi":"10.1016/S0952-3278(03)00145-5","DOIUrl":null,"url":null,"abstract":"<div><div><span>Epithelial neutrophil-activating peptide-78 (ENA-78) is a member of CXC chemokines<span><span>. It is produced by endothelial cells stimulated with interleukin-1 (IL-1), along with other </span>CXC chemokines<span> such as IL-8 and growth-related oncogene protein-</span></span></span><em>α</em> (GRO-<em>α</em><span>). IL-1-induced ENA-78 production by endothelial cells may be important for the regulation of neutrophil activation. 15-Deoxy-Δ</span><sup>12,14</sup>-prostaglandin J<sub>2</sub> (15d-PGJ<sub>2</sub><span>) is a natural ligand for peroxisome proliferator-activated receptor-</span><em>γ</em> (PPAR-<em>γ</em>) and affects the expression of various genes. We examined the effect of 15d-PGJ<sub>2</sub> on the expression of ENA-78 in cultured endothelial cells stimulated with IL-1<em>β</em>. 15d-PGJ<sub>2</sub> inhibited the IL-1<em>β</em>-induced expression of ENA-78, but not the expression of IL-8 or GRO-<em>α</em><span><span> in response to IL-1. Ciglitazone, another </span>agonist for PPAR-</span><em>γ</em>, had no effect on the expression of ENA-78, suggesting that 15d-PGJ<sub>2</sub> may inhibit the expression of ENA-78 in a PPAR-<em>γ</em>-independent manner. 15d-PGJ<sub>2</sub><span> may modulate inflammatory reactions by regulating the balance of CXC chemokines in endothelial cells.</span></div></div>","PeriodicalId":94179,"journal":{"name":"Prostaglandins, leukotrienes, and essential fatty acids","volume":"69 5","pages":"Pages 323-327"},"PeriodicalIF":3.0000,"publicationDate":"2003-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Effect of 15-deoxy-Δ12,14-prostaglandin J2 on IL-1β-induced expression of epithelial neutrophil-activating protein-78 in human endothelial cells\",\"authors\":\"Tadaatsu Imaizumi , Mika Kumagai , Masaharu Hatakeyama , Wakako Tamo , Koji Yamashita , Hidemi Yoshida , Hirofumi Munakata , Kei Satoh\",\"doi\":\"10.1016/S0952-3278(03)00145-5\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div><span>Epithelial neutrophil-activating peptide-78 (ENA-78) is a member of CXC chemokines<span><span>. It is produced by endothelial cells stimulated with interleukin-1 (IL-1), along with other </span>CXC chemokines<span> such as IL-8 and growth-related oncogene protein-</span></span></span><em>α</em> (GRO-<em>α</em><span>). IL-1-induced ENA-78 production by endothelial cells may be important for the regulation of neutrophil activation. 15-Deoxy-Δ</span><sup>12,14</sup>-prostaglandin J<sub>2</sub> (15d-PGJ<sub>2</sub><span>) is a natural ligand for peroxisome proliferator-activated receptor-</span><em>γ</em> (PPAR-<em>γ</em>) and affects the expression of various genes. We examined the effect of 15d-PGJ<sub>2</sub> on the expression of ENA-78 in cultured endothelial cells stimulated with IL-1<em>β</em>. 15d-PGJ<sub>2</sub> inhibited the IL-1<em>β</em>-induced expression of ENA-78, but not the expression of IL-8 or GRO-<em>α</em><span><span> in response to IL-1. Ciglitazone, another </span>agonist for PPAR-</span><em>γ</em>, had no effect on the expression of ENA-78, suggesting that 15d-PGJ<sub>2</sub> may inhibit the expression of ENA-78 in a PPAR-<em>γ</em>-independent manner. 15d-PGJ<sub>2</sub><span> may modulate inflammatory reactions by regulating the balance of CXC chemokines in endothelial cells.</span></div></div>\",\"PeriodicalId\":94179,\"journal\":{\"name\":\"Prostaglandins, leukotrienes, and essential fatty acids\",\"volume\":\"69 5\",\"pages\":\"Pages 323-327\"},\"PeriodicalIF\":3.0000,\"publicationDate\":\"2003-11-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Prostaglandins, leukotrienes, and essential fatty acids\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0952327803001455\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Prostaglandins, leukotrienes, and essential fatty acids","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0952327803001455","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Effect of 15-deoxy-Δ12,14-prostaglandin J2 on IL-1β-induced expression of epithelial neutrophil-activating protein-78 in human endothelial cells
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-α (GRO-α). IL-1-induced ENA-78 production by endothelial cells may be important for the regulation of neutrophil activation. 15-Deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) is a natural ligand for peroxisome proliferator-activated receptor-γ (PPAR-γ) and affects the expression of various genes. We examined the effect of 15d-PGJ2 on the expression of ENA-78 in cultured endothelial cells stimulated with IL-1β. 15d-PGJ2 inhibited the IL-1β-induced expression of ENA-78, but not the expression of IL-8 or GRO-α in response to IL-1. Ciglitazone, another agonist for PPAR-γ, had no effect on the expression of ENA-78, suggesting that 15d-PGJ2 may inhibit the expression of ENA-78 in a PPAR-γ-independent manner. 15d-PGJ2 may modulate inflammatory reactions by regulating the balance of CXC chemokines in endothelial cells.