{"created":"2023-07-25T08:11:24.413273+00:00","id":11593,"links":{},"metadata":{"_buckets":{"deposit":"f52a4321-ca81-4444-9528-027c5e32629e"},"_deposit":{"created_by":3,"id":"11593","owners":[3],"pid":{"revision_id":0,"type":"depid","value":"11593"},"status":"published"},"_oai":{"id":"oai:ir.kagoshima-u.ac.jp:00011593","sets":[]},"author_link":["74426","74427","55439"],"item_8_alternative_title_18":{"attribute_name":"別言語のタイトル","attribute_value_mlt":[{"subitem_alternative_title":"Spatiotemporal spread of inflammation caused by HMGB1 nuclear DNA-binding protein"}]},"item_8_alternative_title_19":{"attribute_name":"タイトルよみ","attribute_value_mlt":[{"subitem_alternative_title":"カクナイ DNA ケツゴウ タンパク HMGB1 ニヨル エンショウ ノ ジクウテキ ヒロガリ"}]},"item_8_date_6":{"attribute_name":"作成日","attribute_value_mlt":[{"subitem_date_issued_datetime":"2013-06-06"}]},"item_8_description_4":{"attribute_name":"要約(Abstract)","attribute_value_mlt":[{"subitem_description":"2011-2012年度科学研究費助成事業(科学研究費補助金(若手研究(B))研究成果報告書　課題番号：23790447　研究代表者：大山陽子(鹿児島大学・医学部・歯学部附属病院・特任教授)","subitem_description_type":"Other"},{"subitem_description":"遺伝子転写やDNA安定化など核内で作用すると考えられていた核蛋白が、ひとたび細胞壊死やマクロファージからの分泌などにより細胞外へ放出されると、一転して組織の炎症を惹起し増幅させるという全く新しい核蛋白作用の概念がもたらされている。我々はその代表的核蛋白であるHigh Mobility Group Box-1 Protein(HMGB1)が肉芽腫炎症の一つのメディエーターであり、炎症の慢性化、遷延化の惹起、ひいては臓器不全をも引き起こすことを明らかにしている。\n本研究では、さらなる肉芽腫炎症発展メカニズムの解明を目指すべく結晶誘発性肉芽腫性腎炎動物モデルを用い検証を行った。\n＝腎肉芽腫炎症におけるHMGB1の臓器障害メカニズムとその制御機構＝\n肉芽腫治療を考慮した際に、その炎症性メディエーターであるHMGB1制御は必要不可欠である。HMGB1抑制を観点に、通常の腎炎モデルに加えHMGB1過剰投与群も作成し、下記の検\n討を行った。\n① HMGB1受容体であるRAGE(Receptor for Advanced Glycation Endproducts)、Toll-like receptor (TLR) 2、4の発現およびHMGB1過剰投与下におけるそれら発現の変化\n② 腎炎動物モデルを用い、抗HMGB1抗体投与群を作成。生食投与群をコントロールとして腎機能、炎症性サイトカインの測定、および病理組織像など多角的な検証による抗HMGB1\n抗体の肉芽腫性炎症治療薬としての可能性の探求\n③ 本肉芽腫炎症におけるThrombomodulin(TM)関与の有無\n④ 本肉芽腫炎症における活性酸素の関与およびその炎症惹起機構の検討\n今回の研究結果より、HMGB1受容体、ならびにTMは肉芽腫炎症の治療のターゲットとなる可能性が示された。","subitem_description_type":"Other"},{"subitem_description":"High-mobility group box-1 protein (HMGB1) was originally described as a nuclear DNA-binding protein that facilitates gene transcription by stabilizing nucleosome formation. HMGB1 can also be released or secrete extracellularly from cells as a result of cellular necrosis or activated macrophages/monocytes in response to inflammatory stimuli respectively, and acts as a pro-inflammatory cytokine or alarm signal for tissue damage. We have revealed that HMGB1 can trigger a potent inflammatory response and accelerates granulomatous inflammation leading to severe tissue injury. In this study, we tried to disclose further mechanism of HMGB1- associated granulomatous inflammation. From a point of view that controlling HMGB1 is essential for treatment of granulomatous nephritis, we studied experiments using a granulomatous nephritis animal model to investigate follows;\n１． The relationship between degrees of the nephritis and HMGB1 receptors expression\n２． The effect of anti-HMGB1 antibody\n３． TM association of the nephritis\n４． Reactive oxygen species association of the nephritis\nWe have found that receptors of HMGB1 and TM could be a target for inhibiting granulomatous nephritis.","subitem_description_type":"Other"}]},"item_8_full_name_2":{"attribute_name":"著者よみ","attribute_value_mlt":[{"nameIdentifiers":[{}],"names":[{"name":"オオヤマ, ヨウコ"}]}]},"item_8_full_name_3":{"attribute_name":"別言語の著者","attribute_value_mlt":[{"nameIdentifiers":[{}],"names":[{"name":"OYAMA, Yoko"}]}]},"item_8_publisher_23":{"attribute_name":"公開者・出版者","attribute_value_mlt":[{"subitem_publisher":"鹿児島大学"}]},"item_8_subject_15":{"attribute_name":"NDC","attribute_value_mlt":[{"subitem_subject":"491.6","subitem_subject_scheme":"NDC"}]},"item_8_text_24":{"attribute_name":"公開者よみ","attribute_value_mlt":[{"subitem_text_value":"カゴシマ ダイガク"}]},"item_8_text_25":{"attribute_name":"公開者別名","attribute_value_mlt":[{"subitem_text_value":"Kagoshima University"}]},"item_8_text_41":{"attribute_name":"科研費番号 ","attribute_value_mlt":[{"subitem_text_value":"23790447"}]},"item_8_version_type_14":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_970fb48d4fbd8a85","subitem_version_type":"VoR"}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"大山, 陽子"}],"nameIdentifiers":[{},{}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2016-10-31"}],"displaytype":"detail","filename":"23790447.pdf","filesize":[{"value":"226.1 kB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"23790447.pdf","url":"https://ir.kagoshima-u.ac.jp/record/11593/files/23790447.pdf"},"version_id":"009e5d16-2509-42d1-b842-2744cda3b5d6"}]},"item_keyword":{"attribute_name":"キーワード","attribute_value_mlt":[{"subitem_subject":"High mobility group box-1 protein","subitem_subject_scheme":"Other"},{"subitem_subject":"RAGE","subitem_subject_scheme":"Other"},{"subitem_subject":"TLR2","subitem_subject_scheme":"Other"},{"subitem_subject":"TLR4","subitem_subject_scheme":"Other"},{"subitem_subject":"Thrombomodulin","subitem_subject_scheme":"Other"},{"subitem_subject":"Reactive oxygen species","subitem_subject_scheme":"Other"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"jpn"}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"research report","resourceuri":"http://purl.org/coar/resource_type/c_18ws"}]},"item_title":"核内DNA結合蛋白HMGB1による炎症の時空的拡がり","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"核内DNA結合蛋白HMGB1による炎症の時空的拡がり"}]},"item_type_id":"8","owner":"3","path":["83"],"pubdate":{"attribute_name":"公開日","attribute_value":"2013-10-01"},"publish_date":"2013-10-01","publish_status":"0","recid":"11593","relation_version_is_last":true,"title":["核内DNA結合蛋白HMGB1による炎症の時空的拡がり"],"weko_creator_id":"3","weko_shared_id":3},"updated":"2024-01-29T08:29:06.255183+00:00"}