Chia Nan University of Pharmacy & Science Institutional Repository:Item 310902800/28536
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    標題: CXCL1 Regulation in Human Pulmonary Epithelial Cells by Tumor Necrosis Factor
    作者: Shieh, Jiunn-Min
    Tsai, Yih-Jeng
    Tsou, Chih-Jen
    Wu, Wen-Bin
    貢獻者: 通識教育中心
    關鍵字: Chemokine
    CXCL1
    JNK
    Gro alpha
    TNF
    Signaling
    Release
    Secretion
    日期: 2014
    上傳時間: 2015-05-06 21:19:48 (UTC+8)
    出版者: Karger
    摘要: Background/Aims: The chemokine CXCL1 has been reported to be expressed in lung airway epithelium and non-small cell lung cancer biopsy specimens. In this study, we investigated the effects of TNF-alpha, an abundant cytokine detected in inflammation and various cancers, on CXCL1 release by human A549 lung carcinoma epithelial cells. Methods: CXCL1 expression was determined by ELISA and RT-PCR. TNF-alpha signaling was examined by western blotting. Monocyte migration was assayed by a Transwell migration system. Results: TNF-alpha stimulated CXCL1 release and mRNA expression, and this release was inhibited by inhibitors of JNK, p38 MAPK, PI-3K/Akt and AP-1 transcription factor. INF-alpha treatment was followed by JNK, p38 MAPK and PI3K/Akt activation. However, only the JNK inhibitor could reduce the CXCL1 mRNA level, suggesting that JNK is required mainly for CXCL1 mRNA synthesis, whereas p38 MAPK and PI-3K/Akt might be responsible for CXCL1 secretion. Dexamethasone (dex) and TGF-beta reduced CXCL1 secretion, with dex upregulating the expression of MAP kinase phosphatase-1 and TGF-beta causing smad2/3 activation and nuclear translocation. A functional analysis showed that the released CXCL1 enhanced monocyte migration and could be abolished by a CXCL1 neutralizing antibody and CXCR antagonist. Conclusion: We demonstrate that TNF-alpha induces CXCL1 expression through the JNK, p38 MAPK and PI-3K/Akt signaling pathways in human pulmonary epithelial cells. Copyright (C) 2014 S. Karger AG, Basel
    關聯: Cellular Physiology and Biochemistry, v.34 n.4, pp.1373-1384
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