Oxidized low-density lipoprotein-induced periodontal inflammation is associated with the up-regulation of cyclooxygenase-2 and microsomal prostaglandin synthase 1 in human gingival epithelial cells
Oxidized low-density lipoprotein-induced periodontal inflammation is associated with the up-regulation of cyclooxygenase-2 and microsomal prostaglandin synthase 1 in human gingival epithelial cells
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DOI：
10.1016/j.bbrc.2011.09.002
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发表时间：
2011-10-07
影响因子：
3.1
通讯作者：
Itabe, Hiroyuki
中科院分区：
文献类型：
--
作者：
Nagahama, Yu;Obama, Takashi;Itabe, Hiroyuki
牙周炎以慢性牙龈组织炎症为特征，炎症介质如IL-8和前列腺素E-2 （PGE(2)）与疾病进展有关。先前我们发现氧化修饰的低密度脂蛋白（oxLDL）存在于龈沟液中。在本研究中，我们利用Ca9-22细胞和原代人口腔角质形成细胞（HOK）进一步研究了oxLDL在牙龈上皮细胞炎症反应中的作用。用oxLDL处理Ca9-22细胞和HOK诱导IL-8和PGE(2)生成酶环氧化酶-2和微粒体PGE(2)合成酶-1的上调。由oxLDL诱导的这些反应被核因子κ B （nf - κ B）抑制剂显著抑制。然而，与巨噬细胞的结果不同，oxLDL并没有导致这两种细胞中CD36表达的增加。这些结果表明，oxLDL通过激活nf - κ B通路引发牙龈上皮细胞炎症反应。这些数据表明牙周病与脂质代谢相关疾病（包括动脉粥样硬化）之间存在机制联系。(C) 2011爱思唯尔公司版权所有。
Periodontitis is characterized by chronic gingival tissue inflammation, and inflammatory mediators such as IL-8 and prostaglandin E-2 (PGE(2)) are associated with disease progression. Previously we showed that oxidatively modified low-density lipoprotein (oxLDL) was present in gingival crevicular fluid. In this study, the role of oxLDL in the gingival epithelial cell inflammatory response was further investigated using Ca9-22 cells and primary human oral keratinocytes (HOK). Treatment of Ca9-22 cells and HOK with oxLDL induced an up-regulation of IL-8 and the PGE(2)-producing enzymes, cyclooxygenase-2 and microsomal PGE(2) synthase-1. These responses induced by oxLDL were significantly suppressed by a nuclear factor-kappa B (NF-kappa B) inhibitor. However, unlike the result in macrophages, oxLDL did not lead to an increase in CD36 expression in these two cells. These results suggest that oxLDL elicits gingival epithelial cell inflammatory responses through an activation of the NF-kappa B pathway. These data suggest a mechanistic link between periodontal disease and lipid metabolism-related disorders, including atherosclerosis. (C) 2011 Elsevier Inc. All rights reserved.