Browsing by Author "Meng Xiao Jie"

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    C-reactive protein induces high-mobility group box-1 protein release through activation of p38MAPK in macrophage RAW264.7 cells
    (2008-05-01) Ko ichi Kawahara; Kamal Krishna Biswas; Masako Unoshima; Takashi Ito; Kiyoshi Kikuchi; Yoko Morimoto; Masahiro Iwata; Salunya Tancharoen; Yoko Oyama; Kazunori Takenouchi; Yuko Nawa; Noboru Arimura; Meng Xiao Jie; Binita Shrestha; Naoki Miura; Toshiaki Shimizu; Kentaro Mera; Shin ichiro Arimura; Noboru Taniguchi; Hideo Iwasaka; Sonshin Takao; Teruto Hashiguchi; Ikuro Maruyama; Kagoshima University; Oita University Faculty of Medicine; Mahidol University
    Background: C-reactive protein (CRP) is widely used as a sensitive biomarker for inflammation. Increasing evidence suggests that CRP plays a role in inflammation. High-mobility group box-1 (HMGB1), a primarily nuclear protein, is passively released into the extracellular milieu by necrotic or damaged cells and is actively secreted by monocytes/macrophages. Extracellular HMGB1 as a potent inflammatory mediator has stimulated immense curiosity in the field of inflammation research. However, the molecular dialogue implicated between CRP and HMGB1 in delayed inflammatory processes remains to be explored. Methods and results: The levels of HMGB1 in culture supernatants were determined by Western blot analysis and enzyme-linked immunosorbent assay in macrophage RAW264.7 cells. Purified CRP induced the release of HMGB1 in a dose- and time-dependent fashion. Immunofluorescence analysis revealed nuclear translocation of HMGB1 in response to CRP. The binding of CRP to the Fcγ receptor in RAW264.7 cells was confirmed by fluorescence-activated cell sorter analysis. Pretreatment of cells with IgG-Fc fragment, but not IgG-Fab fragment, efficiently blocked this binding. CRP triggered the activation of p38MAPK and ERK1/2, but not Jun N-terminal kinase. Moreover, both p38MAPK inhibitor SB203580 and small interfering RNA significantly suppressed the release of HMGB1, but not the MEK1/2 inhibitor U-0126. Conclusion: We demonstrated for the first time that CRP, a prominent risk marker for inflammation including atherosclerosis, could induce the active release of HMGB1 by RAW264.7 cells through Fcγ receptor/p38MAPK signaling pathways, thus implying that CRP plays a crucial role in the induction, amplification, and prolongation of inflammatory processes, including atherosclerotic lesions. © 2008 Elsevier Inc. All rights reserved.
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    HMGB1: A new marker for estimation of the postmortem interval
    (2010-01-01) Kiyoshi Kikuchi; Ko ichi Kawahara; Kamal Krishna Biswas; Takashi Ito; Salunya Tancharoen; Naoto Shiomi; Yoshiro Koda; Fumiyo Matsuda; Yoko Morimoto; Yoko Oyama; Kazunori Takenouchi; Naoki Miura; Noboru Arimura; Yuko Nawa; Shinichiro Arimura; Meng Xiao Jie; Binita Shrestha; Masahiro Iwata; Kentaro Mera; Hisayo Sameshima; Yoshiko Ohno; Ryuichi Maenosono; Yutaka Tajima; Hisaaki Uchikado; Terukazu Kuramoto; Kenji Nakayama; Minoru Shigemori; Yoshihiro Yoshida; Teruto Hashiguchi; Ikuro Maruyama; Division of Laboratory and Vascular Medicine; Kagoshima University Faculty of Medicine; Kagoshima University; Omuta City General Hospital; Saiseikai Shiga Hospital; Kurume University School of Medicine; Mahidol University
    Estimation of the postmortem interval (PMIPMIPMI) is one of the most important tasks in forensic medicine. Numerous methods have been proposed for the determination of the time since death by chemical means. High mobility group box-1 (HMHMGB1), a nonhistone DNADNADNA-binding protein is released by eukaryotic cells upon necrosis. Postmortem serum levels of HMGB1 of 90 male Wistar rats stored at 4, 14 and 24 °C since death were measured by enzyme-linked immunosorbent assay. The serum HMHMGB1 level showed a time-dependent increase up to seven days at 4 °C. At 14 °C, the HMGB1 level peaked at day 3, decreased at day 4, and then plateaued. At 24 °C, the HMHMGB1 level peaked at day 2, decreased at day 3, and then plateaued. Our findings suggest that HMGB1 is related to the PMIPMIPMI in rats.