{"created":"2023-07-27T06:51:25.112260+00:00","id":44836,"links":{},"metadata":{"_buckets":{"deposit":"27b8ebb5-a759-46a4-be63-4c74267c47aa"},"_deposit":{"created_by":18,"id":"44836","owners":[18],"pid":{"revision_id":0,"type":"depid","value":"44836"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00044836","sets":["2812:2813:2828"]},"author_link":["2881","20436"],"item_9_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2006-03","bibliographicIssueDateType":"Issued"},"bibliographicPageStart":"6p.","bibliographicVolumeNumber":"2004-2005","bibliographic_titles":[{"bibliographic_title":"平成17(2005)年度 科学研究費補助金 基盤研究(C) 研究成果報告書"},{"bibliographic_title":"2005 Fiscal Year Final Research Report","bibliographic_titleLang":"en"}]}]},"item_9_creator_33":{"attribute_name":"著者別表示","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{}],"nameIdentifiers":[{},{},{},{}]}]},"item_9_description_21":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"血管傷害モデルにおいて、HO-1は酸化ストレスにより誘導される細胞傷害/細胞死を抑制することが明らかにされた。同時に、HO-1による細胞保護作用は、HO-1の発現量や発現の局在、さらに発現時間などにより精密に調節されている可能性が示唆された。特に、細胞接着に依存する細胞ではHO-1の過剰発現が細胞接着因子の発現低下と細胞死を誘導する可能性も明らかにされた。\n末梢血単球の内、CCR2 CD16^<bright>亜群が恒常的にHO-1を産生し、血管内皮の機能維持に重要な役割を果たしていることが明らかにされた。さらに、急性炎症性疾患ではこれらの単球亜群が増加、過度の炎症による組織/臓器傷害の抑制に関与していることが示唆された。\n蛋白尿を伴う糸球体傷害では、尿中蛋白量に比例して尿細管によるHO-1 mRNA発現が誘導された。種々の腎疾患の中でも、病態の差異に応じてHO-1 mRNAの局在は特徴的なパターンを示した。腎疾患におけるHO-1 mRNA発現の局在とその程度を評価することにより、新たな視点で病態解析が可能となった。\n慢性気道炎症では呼気中CO濃度が増加することが知られている。原発性肺高血圧症や二次性肺高血圧症症例での肺組織を用いた検討では、肺胞マクロファージのみでなく、気道壁や毛細血管内のマクロファージにおいてもHO-1蛋白発現が認められた。このことから、気道炎症を伴う種々疾患においても多様なレベルでHO-1が炎症の制御に関わっていることが示された。\nステロイド投与により単球表面のHb・Hp受容体(CD163)発現が著しく増強することが明らかにされた。また、CD163発現を増強した単球はHb・Hpの取り込みが亢進、IL-10のみでなく、HO-1の産生が有意に増加した。これらの事実は、血管傷害のみでなく、気管支喘息や慢性気管支炎などの気道炎症性疾患に対しても、従来想定されていなかった機序での抗炎症効果を示すものとして極めて興味深い。現在、この点について研究を継続中である。","subitem_description_type":"Abstract"},{"subitem_description":"It was shown in a vascular injury model that HO-1 inhibits cell injury/death induced by oxidative stress. At the same time, it is suggested that the cytoprotective effect of HO-1 is strictly dependent on the level, location and duration of the enzyme activity. In particular, anchorage dependent cells, such as endothelial cells, are highly sensitive to overexpression of HO-1, which lead to the loss of adhesion molecules and apoptosis.\nAmong circulating monocytes, C16<bright> CCR2- subpopulation is shown to produce HO-1 in vivo, playing critical role in protecting the functions of endothelial cells. Furthermore, this particular subpopulation of monocytes increases during acute inflammatory illnesses, suggesting that they play significant anti-inflammatory roles by preventing excessive tissue/organ damage.\nHO-1 mRNA expression within renal tubular epithelium increased in association with urinary protein levels in various glomerular injuries. However, the distribution of HO-1 mRNA varied amo ng illnesses of different pathogenesis, indicating that the pattern of HO-1 mRNA expression reflect distinct mechanisms of tissue injury in different kidney diseases.\nIt has been shown recently that CO in expiratory air reflects inflammation of the airway. Increased levels of HO-1 protein expression were detected within in lung tissue of primary pulmonary hypertension. Major HO-1 producers were alveolar macrophages, and macrophages within capillary lumen, bronchial wall and airway. These results indicate that macrophages play anti-inflammatory roles by producing HO-1/CO within the airway at different levels.\nSteroid administration induced rapid and significant increase of CD163, receptors for hemoglobin/haptoglobin complex, on manocyte surfaces. These monocytes with high CD163 levels rapidly uptake Hb/Hp complex, and subsequently produced HO-1 and IL-10. These results indicate that monocyte HO-1 production is important not only for the protection of vascular endothelial cells, but unexpectedly for the maintenance of airway function. Further investigation is being performed to resolve these issues.","subitem_description_type":"Abstract"}]},"item_9_description_22":{"attribute_name":"内容記述","attribute_value_mlt":[{"subitem_description":"研究課題/領域番号:16591014, 研究期間(年度):2004-2005","subitem_description_type":"Other"},{"subitem_description":"出典：「ヘムオキシゲナーゼ1産生制御による単球機能の調節と炎症治療戦略の開発」研究成果報告書　課題番号16591014\n  (KAKEN：科学研究費助成事業データベース（国立情報学研究所）)\n　　　本文データは著者版報告書より作成","subitem_description_type":"Other"}]},"item_9_identifier_registration":{"attribute_name":"ID登録","attribute_value_mlt":[{"subitem_identifier_reg_text":"10.24517/00051175","subitem_identifier_reg_type":"JaLC"}]},"item_9_publisher_17":{"attribute_name":"公開者","attribute_value_mlt":[{"subitem_publisher":"金沢大学医薬保健研究域医学系"}]},"item_9_relation_28":{"attribute_name":"関連URI","attribute_value_mlt":[{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/search/?qm=40210281"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/search/?qm=40210281","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-16591014/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-16591014/","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-16591014/165910142005kenkyu_seika_hokoku_gaiyo/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-16591014/165910142005kenkyu_seika_hokoku_gaiyo/","subitem_relation_type_select":"URI"}}]},"item_9_version_type_25":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_ab4af688f83e57aa","subitem_version_type":"AM"}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2018-06-22"}],"displaytype":"detail","filename":"HO-PR-YACHIE-A-kaken 2006-6p.pdf","filesize":[{"value":"337.7 kB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"HO-PR-YACHIE-A-kaken 2006-6p.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/44836/files/HO-PR-YACHIE-A-kaken 2006-6p.pdf"},"version_id":"19bdaa10-a3bc-4def-9f90-38d244edf70d"}]},"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":"ヘムオキシゲナーゼ1産生制御による単球機能の調節と炎症治療戦略の開発","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"ヘムオキシゲナーゼ1産生制御による単球機能の調節と炎症治療戦略の開発"},{"subitem_title":"Development of novel anti-inflammatory therapy through regulation of heme oxygenase-1 production by monocytes","subitem_title_language":"en"}]},"item_type_id":"9","owner":"18","path":["2828"],"pubdate":{"attribute_name":"公開日","attribute_value":"2018-06-22"},"publish_date":"2018-06-22","publish_status":"0","recid":"44836","relation_version_is_last":true,"title":["ヘムオキシゲナーゼ1産生制御による単球機能の調節と炎症治療戦略の開発"],"weko_creator_id":"18","weko_shared_id":-1},"updated":"2023-07-27T14:31:30.001664+00:00"}