An ADP ribosylation factor-GTPase activating protein negatively regulates the production of proinflammatory mediators in response to lipopolysaccharide

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• 作者：Abedul Haque (1)
  Abu Shadat Mohammod Noman (1)
  Naoki Koide (1)
  Erdenezaya Odkhuu (1)
  Yoshikazu Naiki (1)
  Shoji Hashimoto (1)
  Takayuki Komatsu (1)
  Tomoaki Yoshida (1)
  Takashi Yokochi (1) yokochi@aichi-med-u.ac.jp
• 关键词：ADP ribosylation factor ; GTPase activating protein (ASAP1) &#8211 ; Lipopolysaccharide (LPS) &#8211 ; NF ; κ ; B &#8211 ; Toll ; like receptor (TLR) &#8211 ; RAW 264.7 cells
• 刊名：Cancer Immunology, Immunotherapy
• 出版年：2011
• 出版时间：October 2011
• 年：2011
• 卷：60
• 期：10
• 页码：1439-1446
• 全文大小：1.7 MB
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• 作者单位：1. Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi 480-1195, Japan
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Cancer Research
  Immunology
  Oncology
  
• 出版者：Springer Berlin / Heidelberg
• ISSN：1432-0851

文摘

An ADP ribosylation factor-GTPase activating protein (ASAP1) is highly expressed in a variety of tumor cells and is involved in the cell motility, invasion, and metastasis. In order to elucidate the involvement of ASAP1 in lipopolysaccharide (LPS)-mediated inflammatory response, the effect of ASAP1 silencing on LPS-induced proinflammatory mediators production was examined by using RAW 264.7 macrophage-like cells. ASAP1 was constitutively expressed in the cells and the expression was augmented by LPS stimulation. Silencing of ASAP1 with small interfering RNA enhanced the production of tumor necrosis factor-α, interleukin 6, interferon-β, and nitric oxide in response to LPS. ASAP1 silencing augmented the activation of nuclear factor (NF)-κB and several mitogen-activated protein kinases (MAPKs). On the other hand, ASAP1 silencing did not affect the expression of IRAK4, TRAF6, and Akt as the upstream molecules of NF-κB signaling. A series of toll-like receptor ligands as well as LPS augmented the ASAP1 expression. Taken together, ASAP1 was suggested to negatively regulate LPS-induced proinflammatory mediators production through down-regulating LPS signaling. The feedback function of ASAP1 in LPS-mediated inflammatory response is discussed.