Lipopolysaccharide stimulates syntheses of toll-like receptor 2 and surfactant protein-A in human alveolar epithelial A549 cells through upregulating phosphorylation of MEK1 and ERK1/2 and sequential activation of NF-kappaB.

Wu TT; Chen TL; Loon WS; Tai YT; Cherng YG; Chen RM

首页> 外文期刊>Cytokine >Lipopolysaccharide stimulates syntheses of toll-like receptor 2 and surfactant protein-A in human alveolar epithelial A549 cells through upregulating phosphorylation of MEK1 and ERK1/2 and sequential activation of NF-kappaB.

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Lipopolysaccharide stimulates syntheses of toll-like receptor 2 and surfactant protein-A in human alveolar epithelial A549 cells through upregulating phosphorylation of MEK1 and ERK1/2 and sequential activation of NF-kappaB.

机译：脂多糖通过上调MEK1和ERK1 / 2的磷酸化以及NF-κB的顺序激活来刺激人肺泡上皮A549细胞中Toll样受体2和表面活性剂蛋白A的合成。

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Surfactant proteins (SPs) and toll-like receptors (TLRs) contribute to regulation of sepsis-induced acute lung injury. Lipopolysaccharide (LPS) is one of the major causes of septic shock. This study was designed to evaluate the effects of LPS on the regulation of tlr-2 and sp-a gene expression in human alveolar epithelial A549 cells and the possible mechanisms. Exposure of A549 cells to LPS increased the expressions of TLR2 and SP-A mRNA and protein in time-dependent manners. A search using a bioinformatic approach found that there are several nuclear factor kappa-B (NF-kappaB)-DNA-binding motifs in the promoter region of the tlr2 and sp-a genes. Immunoblotting analyses revealed that exposure to LPS time-dependently enhanced the translocation of NF-kappaB from the cytoplasm to nuclei. Analyses of an electrophoretic mobility shift assay further showed that LPS augmented the transactivation activity of NF-kappaB to its consensus oligonucleotides in A549cells. Sequentially, treatment of A549 cells with LPS increased phosphorylation of extracellular signal-regulated kinase (ERK)1/2, p38-mitogen-activated protein kinase (p38MAPK), and MAPK kinase-1 (MEK1). Pretreatment with PD98059, an inhibitor of ERK1/2, significantly decreased LPS-induced TLR2 and SP-A mRNA expression.

机译：表面活性剂蛋白（SPs）和toll样受体（TLRs）有助于调节败血症引起的急性肺损伤。脂多糖（LPS）是败血性休克的主要原因之一。本研究旨在评估脂多糖对人肺泡上皮A549细胞tlr-2和sp-a基因表达的调节作用及其可能的机制。 A549细胞暴露于LPS以时间依赖性方式增加了TLR2和SP-A mRNA及蛋白的表达。使用生物信息学方法进行的搜索发现，在tlr2和sp-a基因的启动子区域中存在几个核因子kappa-B（NF-kappaB）-DNA结合基序。免疫印迹分析表明，暴露于LPS时间依赖性地增强了NF-κB从细胞质到细胞核的转运。电泳迁移率变动分析的分析进一步表明，LPS在A549细胞中增强了NF-κB与其共有寡核苷酸的反式激活活性。因此，用LPS处理A549细胞会增加细胞外信号调节激酶（ERK）1/2，p38促分裂原激活蛋白激酶（p38MAPK）和MAPK激酶-1（MEK1）的磷酸化。用ERK1 / 2抑制剂PD98059预处理可显着降低LPS诱导的TLR2和SP-A mRNA表达。

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《Cytokine》 |2011年第1期|共8页
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Wu TT; Chen TL; Loon WS; Tai YT; Cherng YG; Chen RM;
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1. Lipopolysaccharide stimulates syntheses of toll-like receptor 2 and surfactant protein-A in human alveolar epithelial A549 cells through upregulating phosphorylation of MEK1 and ERK1/2 and sequential activation of NF-kappaB. [J] . Wu TT, Chen TL, Loon WS, Cytokine . 2011,第1期

机译：脂多糖通过上调MEK1和ERK1 / 2的磷酸化以及NF-κB的顺序激活来刺激人肺泡上皮A549细胞中Toll样受体2和表面活性剂蛋白A的合成。
2. Lipopolysaccharide Stimulates Surfactant Protein-A in Human Renal Epithelial HK-2 Cells through Upregulating Toll-like Receptor 4 Dependent MEK1/2-ERK1/2-NF-κB Pathway [J] . Jiao Liu, Guang Li, Wen-Jie Xie, 中华医学杂志（英文版） . 2017,第010期

机译：脂多糖通过上调Toll样受体4依赖的MEK1 / 2-ERK1 /2-NF-κB途径刺激人肾上皮HK-2细胞中的表面活性蛋白A。
3. Toll-like receptor 2-mediated sequential activation of MyD88 and MAPKs contributes to lipopolysaccharide-induced sp-a gene expression in human alveolar epithelial cells. [J] . Chuang CY, Chen TG, Tai YT, Immunobiology: Zeitschrift fur Immunitatsforschung . 2011,第6期

机译：Toll样受体2介导的MyD88和MAPKs的顺序激活有助于人肺泡上皮细胞中脂多糖诱导的sp-a基因表达。
4. INTERACTION OF LECTINS WITH EPITHELIAL CELLS OF DEEP LUNG: HUMAN ALVEOLAR CELLS IN PRIMARY CULTURE VERSUS A549 CELL LINE [C] . R Abu-Dahab, U.F. Schaefer, C.-M. Lehr International symposium on controlled release of bioactive materials;Consumer diversified products conference . 2001

机译：凝集素与深肺上皮细胞的相互作用：原代培养的人肺泡细胞对A549细胞的作用
5. Activation of host cell gene expression by respiratory syncytial virus infection of the alveolar epithelial cell line A549: A role for the redox responsive transcription factor NF-kappaB. [D] . Carpenter, Laura Rosenbalm. 2002

机译：呼吸道合胞病毒感染肺泡上皮细胞系A549激活宿主细胞基因表达：氧化还原反应性转录因子NF-κB的作用。
6. Lipopolysaccharide Stimulates Surfactant Protein-A in Human Renal Epithelial HK-2 Cells through Upregulating Toll-like Receptor 4 Dependent MEK1/2-ERK1/2-NF-κB Pathway [O] . Jiao Liu, Guang Li, Wen-Jie Xie, 2017

机译：脂多糖通过上调Toll样受体4依赖的MEK1 / 2-ERK1 /2-NF-κB途径刺激人肾上皮HK-2细胞中的表面活性蛋白A。
7. Lipopolysaccharide Stimulates Surfactant Protein-A in Human Renal Epithelial HK-2 Cells through Upregulating Toll-like Receptor 4 Dependent MEK1/2-ERK1/2-NF-κB Pathway [O] . Jiao Liu, Guang Li, Wen-Jie Xie, 2017

机译：脂多糖通过上调Toll样受体4依赖性mEK1 / 2-ERK1 / 2-NF-κB途径刺激人肾上皮HK-2细胞中的表面活性蛋白-a

Lipopolysaccharide stimulates syntheses of toll-like receptor 2 and surfactant protein-A in human alveolar epithelial A549 cells through upregulating phosphorylation of MEK1 and ERK1/2 and sequential activation of NF-kappaB.

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