Novel Biphasic Role of Resolvin D1 on Expression of Cyclooxygenase-2 in Lipopolysaccharide-Stimulated Lung Fibroblasts Is Partly through PI3K/AKT and ERK2 Pathways
Novel Biphasic Role of Resolvin D1 on Expression of Cyclooxygenase-2 in Lipopolysaccharide-Stimulated Lung Fibroblasts Is Partly through PI3K/AKT and ERK2 Pathways
复制标题
resolvin D1 对脂多糖刺激的肺成纤维细胞中环氧合酶 2 表达的新双相作用部分是通过 PI3K/AKT 和 ERK2 途径实现的
DOI：
10.1155/2013/964012
复制
发表时间：
2013-01-01
影响因子：
4.6
通讯作者：
Jin, Shengwei
中科院分区：
文献类型：
--
作者：
Wu, Derong;Zheng, Shengxing;Jin, Shengwei
成纤维细胞，远非仅仅是旁观者细胞，已知在急性损伤后的炎症消退中发挥特定作用。作为内源性的“刹车信号”，溶解蛋白具有强大的抗炎和溶解作用。我们证明了COX-2蛋白的表达在LPS刺激后的6小时和48小时达到显著的峰值。PGE(2)水平在6 h达到峰值，PGD(2)水平在48 h达到峰值。然而，LPS处理后肺成纤维细胞中COX-1蛋白表达未见明显变化。外源性resolvin D1抑制了COX-2的第一个峰值表达，抑制了LPS诱导的PGE(2)的产生。相比之下，外源性resolvin D1增加了COX-2的第二峰表达，并增加了LPS诱导的PGD(2)的产生。此外，resolvin D1在6小时抑制COX-2的表达，部分是通过PI3K/AKT和ERK2信号通路。
Fibroblasts, far from being merely bystander cells, are known to play a specific role in inflammation resolution after an acute injury. As the endogenous "braking signal," resolvins possess potent anti-inflammatory and proresolution actions. We demonstrated that the expression of COX-2 protein was significantly peaked initially at 6 hours but then also at 48 hours after LPS stimulation in lung fibroblasts. PGE(2) levels also peaked at 6 hours, and PGD(2) levels were increased and peaked at 48 hours. However, no significant change in the protein expression of COX-1 was observed after treatment with LPS in lung fibroblasts. Exogenous resolvin D1 inhibited the first peak of COX-2 expression as well as the production of PGE(2) induced by LPS. In contrast, exogenous resolvin D1 increased the second peak of COX-2 expression as well as the production of PGD(2) induced by LPS. In addition, resolvin D1 inhibited COX-2 expression at 6 hours, which was partly through PI3K/AKT and ERK2 signalling pathways.