{"created":"2023-06-20T16:46:36.642645+00:00","id":18123,"links":{},"metadata":{"_buckets":{"deposit":"43ac8c03-92c0-4122-8a4b-25018eee48c2"},"_deposit":{"created_by":29,"id":"18123","owners":[29],"pid":{"revision_id":0,"type":"depid","value":"18123"},"status":"published"},"_oai":{"id":"oai:kindai.repo.nii.ac.jp:00018123","sets":["14:2667:4296"]},"author_link":["3356","3960"],"item_8_biblio_info_21":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2016","bibliographicIssueDateType":"Issued"},"bibliographicPageEnd":"4","bibliographicPageStart":"1","bibliographic_titles":[{"bibliographic_title":"科学研究費助成事業研究成果報告書 (2015)"}]}]},"item_8_description_33":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"研究成果の概要（和文）：非侵襲的な変形性膝関節症（OA）の治療においては、破壊責任分子経路の同定とこれに介入する方法を確立する必要がある．本研究では細胞内にストレスを伝達し軟骨に組織破壊的変化をもたらす分子としてRho/ROCK経路とそれを取り巻く分子経路に着目した。活性酸素によるストレスはRho/ROCK、TAK1の活性化を誘導し、軟骨基質の発現抑制と滑膜炎症変化を誘導した。一方でRac、Nrf2の活性化は軟骨基質の発現、抗ストレス分子の発現を誘導した。これらの分子はいずれもストレス応答経路として重要であり、薬理的介入は新規のOA治療戦略として有望である。\n研究成果の概要（英文）：Despite advances in diagnosis, surgery and epidemiological understandings, any effective treatment to prevent or/and cure from osteoarthritis (OA) have not been discovered. Here we searched the effector molecules potentially playing a central role in the stress transduction that can activate OA changes, and found that small-GTPase Rho and Rac had an opposite effect in the cartilage matrix maintenance. We also found that the activity of TGFb-activated kinase 1(TAK1) could be regulated by Rho/ROCK, and the TAK1 activity induced expression of a tissue degeneration factor Cox-2 in the synovial fibroblast cells. Finally, we examined a defensive role of anti-stress molecule Nrf2 against the stress-mediated OA change and demonstrated that Nrf2 was important to maintain chondrocyte matrix. Our findings provide the basis for new biologic and pharmacological approaches to the prevention and treatment of OA.","subitem_description_type":"Abstract"}]},"item_8_description_36":{"attribute_name":"内容記述","attribute_value_mlt":[{"subitem_description":"研究種目：基盤研究(C);  研究期間：2013～2015;   課題番号：25462388;   研究分野：整形外科;   科研費の分科・細目：","subitem_description_type":"Other"}]},"item_8_description_37":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"subitem_description":"Research Paper","subitem_description_type":"Other"}]},"item_8_description_41":{"attribute_name":"フォーマット","attribute_value_mlt":[{"subitem_description":"application/pdf","subitem_description_type":"Other"}]},"item_8_publisher_14":{"attribute_name":"出版者 名前","attribute_value_mlt":[{"subitem_publisher":"近畿大学"}]},"item_8_relation_11":{"attribute_name":"著者 外部リンク","attribute_value_mlt":[{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-25462388/"}]}]},"item_8_text_10":{"attribute_name":"著者 役割","attribute_value_mlt":[{"subitem_text_value":"研究代表者"},{"subitem_text_value":"研究分担者"}]},"item_8_text_7":{"attribute_name":"著者(英)","attribute_value_mlt":[{"subitem_text_language":"en","subitem_text_value":"FUKUDA, Kanji"},{"subitem_text_language":"en","subitem_text_value":"TERAMURA Takeshi"}]},"item_8_text_8":{"attribute_name":"著者 所属","attribute_value_mlt":[{"subitem_text_value":"近畿大学医学部; 教授"},{"subitem_text_value":"近畿大学医学部附属病院; 助教"}]},"item_8_text_9":{"attribute_name":"著者所属(翻訳)","attribute_value_mlt":[{"subitem_text_value":"Kindai University"}]},"item_8_version_type_12":{"attribute_name":"版","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_be7fb7dd8ff6fe43","subitem_version_type":"NA"}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"福田, 寛二"},{"creatorName":"フクダ, カンジ","creatorNameLang":"ja-Kana"}],"nameIdentifiers":[{},{}]},{"creatorNames":[{"creatorName":"寺村, 岳士"},{"creatorName":"テラムラ, タケシ","creatorNameLang":"ja-Kana"}],"nameIdentifiers":[{},{}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2016-10-14"}],"displaytype":"detail","filename":"25462388seika.pdf","filesize":[{"value":"277.9 kB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"25462388seika.pdf","url":"https://kindai.repo.nii.ac.jp/record/18123/files/25462388seika.pdf"},"version_id":"4dcacb1c-184b-403e-b985-5ceca299e793"}]},"item_keyword":{"attribute_name":"キーワード","attribute_value_mlt":[{"subitem_subject":"変形性関節症","subitem_subject_scheme":"Other"},{"subitem_subject":"活性酸素","subitem_subject_scheme":"Other"},{"subitem_subject":"Rhoキナーゼ","subitem_subject_scheme":"Other"},{"subitem_subject":"TAK1","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":"ストレス応答分子としてのRhoファミリータンパク質の機能と関節変性反応への関与","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"ストレス応答分子としてのRhoファミリータンパク質の機能と関節変性反応への関与"},{"subitem_title":"Function of stress effector molecules in the catabolic reactions of chondrocytes and roles in OA progression/repression.","subitem_title_language":"en"}]},"item_type_id":"8","owner":"29","path":["4296"],"pubdate":{"attribute_name":"公開日","attribute_value":"2016-10-14"},"publish_date":"2016-10-14","publish_status":"0","recid":"18123","relation_version_is_last":true,"title":["ストレス応答分子としてのRhoファミリータンパク質の機能と関節変性反応への関与"],"weko_creator_id":"29","weko_shared_id":-1},"updated":"2023-06-20T22:08:27.861406+00:00"}