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首页> 外文期刊>Prostaglandins and Other Lipid Mediators >p38 kinase/cytosolic phospholipase A2/cyclooxygenase-2 pathway: a new signaling cascade for lipopolysaccharide-induced interleukin-1beta and interleukin-6 release in differentiated U937 cells.
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p38 kinase/cytosolic phospholipase A2/cyclooxygenase-2 pathway: a new signaling cascade for lipopolysaccharide-induced interleukin-1beta and interleukin-6 release in differentiated U937 cells.

机译：p38激酶/胞质磷脂酶A2 /环氧合酶2途径：脂多糖诱导的U937细胞中脂多糖诱导的IL-1β和IL-6释放的新信号传导级联。

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p38 Mitogen-activated protein kinase (p38 MAPK) activation is essential for lipopolysaccharide (LPS)-induced pro-inflammatory cytokines expression. Although the regulation results from combined effect of both transcription and translation levels, the precise mechanism by which p38 regulates still remains to be elucidated. Our previous work showed cytosolic phospholipase A(2) (cPLA(2)), a substrate of p38, was involved in this regulation. Further investigations were carried out to study the possible mechanisms of the interleukin expression modulated by cPLA(2) in LPS-treated differentiated U937 cells. p38 MAPK inhibitor SB203580 suppressed interleukin-1beta (IL-1beta) and interleukin-6 (IL-6) release, as well as the activation of cPLA(2). Transfection of cPLA(2) antisense oligonucleotides or pre-treatment with cPLA(2) inhibitor AACOCF3 abolished IL-1beta and IL-6 release in a dose-dependent manner. These implied a potential role of cPLA(2) in LPS-induced p38 pathways on interleukin release. As a downstream enzyme of cPLA(2), cyclooxygenase-2 (COX-2) was down-regulated by SB203580 and/or AACOCF(3), which precisely matched the levels of IL-1beta and IL-6. Treatment with the COX-2 inhibitor (NS-398) or COX-2 antisense oligonucleotides also diminished IL-1beta and IL-6 release. Given these findings, the p38 MAPK/cPLA(2)/COX-2 pathway was proposed to be implicated in the LPS-induced IL-1beta and interleukin-6 production in differentiated U937 cells.
机译：p38丝裂原激活的蛋白激酶（p38 MAPK）激活对于脂多糖（LPS）诱导的促炎性细胞因子表达至关重要。尽管调节是由转录和翻译水平的共同作用引起的，但p38调节的确切机制仍有待阐明。我们以前的工作表明，胞质磷脂酶A（2）（cPLA（2）），p38的底物，参与了这一调控。进行了进一步的研究，以研究由cPLA（2）调控的LPS处理的分化U937细胞中白介素表达的可能机制。 p38 MAPK抑制剂SB203580抑制白介素1β（IL-1beta）和白介素6（IL-6）的释放以及cPLA（2）的激活。转染cPLA（2）反义寡核苷酸或使用cPLA（2）抑制剂AACOCF3进行预处理，以剂量依赖性方式消除了IL-1beta和IL-6的释放。这些暗示cPLA（2）在白介素释放的LPS诱导的p38途径中的潜在作用。作为cPLA（2）的下游酶，SB203580和/或AACOCF（3）下调了环氧合酶2（COX-2），使其与IL-1beta和IL-6的水平精确匹配。用COX-2抑制剂（NS-398）或COX-2反义寡核苷酸处理也可以减少IL-1beta和IL-6的释放。鉴于这些发现，有人提出p38 MAPK / cPLA（2）/ COX-2途径与分化的U937细胞中LPS诱导的IL-1beta和白介素6产生有关。

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