著者 Nakamura, Yoki| Morioka, Norimitsu| Abe, Hiromi| Zhang, Fang Fang| Hisaoka-Nakashima, Kazue| Liu, Keyue| Nishibori, Masahiro| Nakata, Yoshihiro|
発行日 2013-08-21
出版物タイトル PLOS ONE
8巻
8号
資料タイプ 学術雑誌論文
著者 大熊 佑| 劉 克約| 和気 秀徳| 春間 純| 吉野 正| 大塚 愛二| 高橋 英夫| 森 秀治| 西堀 正洋| 伊達 勲|
発行日 2013-08-01
出版物タイトル 岡山医学会雑誌
125巻
2号
資料タイプ 学術雑誌論文
JaLCDOI 10.18926/AMO/47262
フルテキストURL 65_6_369.pdf
著者 Terada, Chuji| Yoshida, Aki| Nasu, Yoshihisa| Mori, Shuji| Tomono, Yasuko| Tanaka, Masato| Takahashi, Hideo K.| Nishibori, Masahiro| Ozaki, Toshifumi| Nishida, Keiichiro|
抄録 We investigated the expression and localization of high-mobility group box chromosomal protein-1 (HMGB-1) in human osteoarthritic (OA) cartilage in relation to the histopathological grade of cartilage destruction, and examined the role of HMGB-1 in the regulation of proinflammatory cytokine expression in chondrocytes. An immunohistochemical study demonstrated that total HMGB-1-positive cell ratios increase as the Osteoarthritis Research Society International (OARSI) histological grade increased. The population of cytoplasmic HMGB-1-positive chondrocytes was especially increased in the deep layers of higher-grade cartilage. The ratios and localization of receptors for advanced glycation end products (RAGE) expression by chondrocytes in Grade 2, 3, and 4 were significantly higher than those in Grade 1. In vitro stimulation with IL-1β, but not TNFα, significantly upregulated the expression of HMGB-1 mRNA by human OA chondrocytes. Both IL-1β and TNFα promoted the translocation of HMGB-1 from nuclei to cytoplasm. IL-1β and TNFα secretions were stimulated at higher levels of HMGB-1. The results of our study suggest the involvement of HMGB-1 in the pathogenesis of cartilage destruction in OA.
キーワード HMGB-1 RAGE chondrocyte osteoarthritis cartilage
Amo Type Original Article
発行日 2011-12
出版物タイトル Acta Medica Okayama
65巻
6号
出版者 Okayama University Medical School
開始ページ 369
終了ページ 377
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
著作権者 CopyrightⒸ 2011 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 22189477
Web of Science KeyUT 000298516900003
著者 西堀 正洋|
発行日 2010-12-01
出版物タイトル 岡山医学会雑誌
122巻
3号
資料タイプ 一般雑誌記事
JaLCDOI 10.18926/AMO/31987
フルテキストURL fulltext.pdf
著者 Kawabata, Masahiro| Kawabata, Teruyuki| Nishibori, Masahiro|
抄録 <p>DNA damage causes chromosomal instability leading to oncogenesis, apoptosis, and severe failure of cell functions. The DNA repair system includes base excision repair, nucleotide excision repair, mismatch repair, translesion replication, non-homologous end-joining, and recombinational repair. Homologous recombination performs the recombinational repair. The RAD51 gene is an ortholog of Esherichia coli recA, and the gene product Rad51 protein plays a central role in the homologous recombination. In mammals, 7 recA-like genes have been identified: RAD51, RAD51L1/B, RAD51L2/C, RAD51L3/D, XRCC2, XRCC3, and DMC1. These genes, with the exception of meiosis-specific DMC1, are essential for development in mammals. Disruption of the RAD51 gene leads to cell death, whereas RAD51L1/B, RAD51L2/C, RAD51L3/D, XRCC2, and XRCC3 genes (RAD51 paralogs) are not essential for viability of cells, but these gene-deficient cells exhibit a similar defective phenotype. Yeast two-hybrid analysis, co-immunoprecipitation, mutation analysis, and domain mapping of Rad51 and Rad51 paralogs have revealed protein-protein interactions among these gene products. Recent investigations have shown that Rad51 paralogs play a role not only in an early step, but also in a late step of homologous recombination. In addition, identification of alternative transcripts of some RAD51 paralogs may reflect the complexity of the homologous recombination system.</p>
キーワード RAD51 RAD51 paralogs recA recombination DNA repair
Amo Type Review
発行日 2005-02
出版物タイトル Acta Medica Okayama
59巻
1号
出版者 Okayama University Medical School
開始ページ 1
終了ページ 9
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
論文のバージョン publisher
査読 有り
PubMed ID 15902993
Web of Science KeyUT 000227263300001
JaLCDOI 10.18926/AMO/31855
フルテキストURL fulltext.pdf
著者 Nishibori, Masahiro| Takahashi, Hide K.| Katayama, Hiroshi| Mori, Shuji| Saito, Shinya| Iwagaki, Hiromi| Tanaka, Noriaki| Morita, Kiyoshi| Ohtsuka, Aiji|
抄録 Lipopolysaccharide (LPS) is one of the major causes of septic shock. The polymyxin B-immobilized filter column (PMX) was developed for the adsorption of endotoxin by direct hemoperfusion and has been used for the treatment of LPS-induced septic shock. In this study, we demonstrated that PMX also specifically bound monocytes from the peripheral blood leukocytes of septic patients by mean of an analysis of bound cells using immunocytochemical and electron microscopic techniques. The specific removal of monocytes from septic patients may produce beneficial effects by reducing the interaction between monocytes and functionally associated cells including vascular endothelial cells.
キーワード septic shock polymixin B-immobilized column monocyte adsorptive removal
Amo Type Short Communication
発行日 2009-02
出版物タイトル Acta Medica Okayama
63巻
1号
出版者 Okayama University Medical School
開始ページ 65
終了ページ 69
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
論文のバージョン publisher
査読 有り
Web of Science KeyUT 000263730300009
JaLCDOI 10.18926/AMO/31845
フルテキストURL fulltext.pdf
著者 Wake, Hidenori| Mori, Shuji| Liu, Keyue| Takahashi, Hideo K.| Nishibori, Masahiro|
抄録 <p>Angiogenesis involves complex processes mediated by several factors and is associated with inflammation and wound healing. High mobility group box 1 (HMGB1) is released from necrotic cells as well as macrophages and plays proinflammatory roles. In the present study, we examined whether HMGB1 would exhibit angiogenic activity in a matrigel plug assay in mice. HMGB1 in combination with heparin strongly induced angiogenesis, whereas neither HMGB1 nor heparin alone showed such angiogenic activity. The heparin-dependent induction of angiogenesis by HMGB1 was accompanied by increases in the expression of tumor necrosis factor-alpha (TNF-alpha) and vascular endothelial growth factor-A120 (VEGF-A120). It is likely that the dependence of the angiogenic activity of HMGB1 on heparin was due to the efficiency of the diffusion of the HMGB1-heparin complex from matrigel to the surrounding areas. VEGF-A165 possessing a heparin-binding domain showed a pattern of heparin-dependent angiogenic activity similar to that of HMGB1. The presence of heparin also inhibited the degradation of HMGB1 by plasmin in vitro. Taken together, these results suggested that HMGB1 in complex with heparin possesses remarkable angiogenic activity, probably through the induction of TNF-alpha and VEGF-A120.</p>
キーワード angiogenesis HMGB1 heparin
Amo Type Original Article
発行日 2009-10
出版物タイトル Acta Medica Okayama
63巻
5号
出版者 Okayama University Medical School
開始ページ 249
終了ページ 262
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
論文のバージョン publisher
査読 有り
PubMed ID 19893601
Web of Science KeyUT 000271132000005
JaLCDOI 10.18926/AMO/31812
フルテキストURL fulltext.pdf
著者 Liu, Rui| Mori, Shuji| Wake, Hidenori| Zhang, Jiyong| Liu, Keyue| Izushi, Yasuhisa| Takahashi, Hideo K.| Peng, Bo| Nishibori, Masahiro|
抄録 <p>Interaction between the receptor for advanced glycation end products (RAGE) and its ligands has been implicated in the pathogenesis of various inflammatory disorders. In this study, we establish an in vitro binding assay in which recombinant human high-mobility group box 1 (rhHMGB1) or recombinant human S100A12 (rhS100A12) immobilized on the microplate binds to recombinant soluble RAGE (rsRAGE). The rsRAGE binding to both rhHMGB1 and rhS100A12 was saturable and dependent on the immobilized ligands. The binding of rsRAGE to rhS100A12 depended on Ca2 and Zn2, whereas that to rhHMGB1 was not. Scatchard plot analysis showed that rsRAGE had higher affinity for rhHMGB1 than for rhS100A12. rsRAGE was demonstrated to bind to heparin, and rhS100A12, in the presence of Ca2, was also found to bind to heparin. We examined the effects of heparin preparations with different molecular sizesunfractionated native heparin (UFH), low molecular weight heparin (LMWH) 5000Da, and LMWH 3000Da on the binding of rsRAGE to rhHMGB1 and rhS100A12. All 3 preparations concentration-dependently inhibited the binding of rsRAGE to rhHMGB1 to a greater extent than did rhS100A12. These results suggested that heparin's anti-inflammatory effects can be partly explained by its blocking of the interaction between HMGB1 or S100A12 and RAGE. On the other hand, heparin would be a promising effective remedy against RAGE-related inflammatory disorders.</p>
キーワード RAGE HMGB1 S100A12 heparin inflammation
Amo Type Original Article
発行日 2009-08
出版物タイトル Acta Medica Okayama
63巻
4号
出版者 Okayama University Medical School
開始ページ 203
終了ページ 211
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
論文のバージョン publisher
査読 有り
PubMed ID 19727205
Web of Sience KeyUT 000269228400006
JaLCDOI 10.18926/AMO/30306
フルテキストURL fulltext.pdf
著者 Tsutsumi, Koji| Nishibori, Masahiro| Saeki, Kiyomi|
抄録 <p>In the presence of extracellular Ca2+, 6,7-dihydro-6,8,8, 10-tetramethyl-8H-pyrano [3, 2-g] chromone-2-carboxylic acid (EAA) had an inhibitory effect on the substance P-induced histamine release from rat peritoneal mast cells. Not only Ca2+ but also Mg2+, Sr2+ and Ba2+ were effective in enhancing the activity of EAA. Marked tachyphylaxis to EAA developed irrespective of the presence or absence of extracellular Ca2+. Cross-tachyphylaxis was observed between EAA and disodium cromoglycate (DSCG). These results indicate that the mode of action of EAA is similar, but not identical, with that of DSCG.</p>
キーワード 6 7-dihydro-6 8 8 10-tetramethyl-8H-pyrano(3 2-g) chromone-2-carboxylic acid (EAA) disodium cromoglycate histamine release alkaline-earth metal ions substance P
Amo Type Article
発行日 1984-08
出版物タイトル Acta Medica Okayama
38巻
4号
出版者 Okayama University Medical School
開始ページ 367
終了ページ 374
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
論文のバージョン publisher
査読 有り
PubMed ID 6208753
Web of Science KeyUT A1984TG25900006
著者 劉 克約| 森 秀治| 高橋 英夫| 友野 靖子| 和気 秀徳| 菅家 徹| 佐藤 康晴| 平賀 憲人| 足立 尚登| 吉野 正| 西堀 正洋|
発行日 2008-12-01
出版物タイトル 岡山医学会雑誌
120巻
3号
資料タイプ 学術雑誌論文
著者 西堀 正洋|
発行日 2001-08-31
出版物タイトル 岡山医学会雑誌
113巻
2号
資料タイプ 学術雑誌論文
著者 西堀 正洋|
発行日 1985-12-31
出版物タイトル
資料タイプ 学位論文