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首页> 外文期刊>Cellular Signalling >Induction of cyclooxygenase-2 by lipopolysaccharide in canine tracheal smooth muscle cells: involvement of p42/p44 and p38 mitogen-activated protein kinases and nuclear factor-kappa B pathways
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Induction of cyclooxygenase-2 by lipopolysaccharide in canine tracheal smooth muscle cells: involvement of p42/p44 and p38 mitogen-activated protein kinases and nuclear factor-kappa B pathways

机译：脂多糖在犬气管平滑肌细胞中诱导环氧合酶-2：p42 / p44和p38丝裂原激活的蛋白激酶和核因子-κB通路的参与

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Lipopolysaccharide (LPS) was found to induce inflammatory responses in the airways and exerted as a potent stimulus for PG synthesis. This study was to determine the mechanisms of LPS-enhanced cyclooxygenase (COX)-2 expression associated with PGE(2) Synthesis in tracheal smooth muscle cells (TSMCs). LPS markedly increased the expression of COX-2 and release of PGE(2) in a time- and concentration-dependent manner, whereas COX- I remained unaltered. Both the expression of COX-2 and the generation of PGE(2) in response to LPS were attenuated by a tyrosine kinase inhibitor genistein, a phosphatidylcholine-phospholipase C inhibitor D609, a phosphatidylinositol-phospholipase C inhibitor U73122, protein kinase C inhibitors, GF109203X and staurosporine, removal of Ca2+ by addition of BAPTA/AM plus EGTA, and phosphatidylinositol 3-kinase (PI3-K) inhibitors, LY294002 and wortmannin. Furthermore, LPS-induced NF-kappaB activation correlated with the degradation Of IkappaB-alpha, COX-2 expression, and PGE(2) synthesis, was inhibited by transfection with dominant negative mutants of NIK and IKK-alpha, but not by IKK-beta. LPS-induced COX-2 expression and PGE(2) Synthesis were completely inhibited by PD98059 (an inhibitor of MEK1/2) and SB203580 (an inhibitor of p38 MAPK inhibitor), but these two inhibitors had no effect on LPS-induced NF-kappaB activation, indicating that NF-kappaB is activated by LPS independently of activation of p42/p44 MAPK and p38 MAPK pathways in TSMCs. Taken together, these findings suggest that the increased expression of COX-2 correlates with the release of PGE(2) from LPS-challenged TSMCs, at least in part, independently mediated through MAPKs and NF-kappaB signalling pathways. LPS-mediated responses were modulated by PLC, Ca2+, PKC, tyrosine kinase, and PI3-K in these cells. (C) 2002 Elsevier Science Inc. All rights reserved. [References: 50]
机译：发现脂多糖（LPS）在气道中引起炎症反应，并作为PG合成的有效刺激物。这项研究是要确定与气管平滑肌细胞（TSMCs）中PGE（2）合成相关的LPS增强的环氧合酶（COX）-2表达的机制。 LPS以时间和浓度依赖性方式显着增加COX-2的表达和PGE（2）的释放，而COX-1则保持不变。酪氨酸激酶抑制剂染料木黄酮，磷脂酰胆碱-磷脂酶C抑制剂D609，磷脂酰肌醇-磷脂酶C抑制剂U73122，蛋白激酶C抑制剂，GF109203X减弱了COX-2的表达和响应LPS的PGE（2）的生成。和星形孢菌素，通过添加BAPTA / AM和EGTA以及磷脂酰肌醇3-激酶（PI3-K）抑制剂LY294002和渥曼青霉素来去除Ca2 +。此外，LPS诱导的NF-kappaB激活与IkappaB-α，COX-2表达和PGE（2）合成的降解相关，被NIK和IKK-alpha的显性负突变体转染抑制，但IKK- Beta。 LPS诱导的COX-2表达和PGE（2）合成被PD98059（MEK1 / 2的抑制剂）和SB203580（p38 MAPK抑制剂的抑制剂）完全抑制，但是这两种抑制剂对LPS诱导的NF- kappaB激活，表明NF-κB被LPS激活，与TSMC中p42 / p44 MAPK和p38 MAPK途径的激活无关。综上所述，这些发现表明，COX-2的表达增加与LPS挑战的TSMC释放PGE（2）有关，至少部分是通过MAPK和NF-κB信号通路独立介导的。在这些细胞中，LPS介导的反应受到PLC，Ca2 +，PKC，酪氨酸激酶和PI3-K的调节。 （C）2002 Elsevier Science Inc.保留所有权利。 [参考：50]

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