{"created":"2023-06-20T16:47:09.958776+00:00","id":18795,"links":{},"metadata":{"_buckets":{"deposit":"7ff94158-f4d1-4569-8e5b-3e31555d77b4"},"_deposit":{"created_by":3,"id":"18795","owners":[3],"pid":{"revision_id":0,"type":"depid","value":"18795"},"status":"published"},"_oai":{"id":"oai:kindai.repo.nii.ac.jp:00018795","sets":["14:2667:4374"]},"author_link":["31758","31759"],"item_8_biblio_info_21":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2017","bibliographicIssueDateType":"Issued"},"bibliographicPageEnd":"6","bibliographicPageStart":"1","bibliographic_titles":[{"bibliographic_title":"科学研究費助成事業研究成果報告書 (2016)"}]}]},"item_8_description_33":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"研究成果の概要（和文）：hADSCを、溶存酸素濃度を指標として低酸素培養することにより、新規のhADSCの亜集団を同定した。この時、解糖系が亢されることが認められた。このとき、これらの集団では、低酸素応答因子HIF非依存的なNotchシグナルの活性化が引き起こされていた。Notchシグナルは解糖系亢進に関与するトランスポーター等の発現上昇、解糖系抑制に関与する酵素群の発現抑制に関与することを見出した。また、Notchシグナルはp53シグナル経路の抑制、NF-κBによるGLUT3, TPIの発現上昇に関与していることを明らかにした。同時に、上記の亜集団から、上述の表現型を強く示すさらなる細胞集団の絞り込みに至った。\n研究成果の概要（英文）：Human adipose tissue-derived multilineage progenitor cells (hADMPCs) are attractive for cell therapy and tissue engineering because of their multipotency and ease of isolation without serial ethical issues. Here, we show that Notch signaling is required for glycolysis regulation under hypoxic conditions. Our results demonstrate that 5% O2 dramatically increased the glycolysis rate, improved the proliferation efficiency, prevented senescence, and maintained the multi potency of hADMPCs. Hypoxia significantly increased the level of activated Notch1 and expression of its downstream gene, HES1. Furthermore, Hypoxia markedly increased glucose consumption and lactate production, which decreased back to normoxic levels on treatment with a g-secretase inhibitor. We also found that HES1 was involved in induction of GLUT3, TPI, and PGK1 in addition to reduction of TIGAR and SCO2 expression. These results clearly suggest that Notch signaling regulates glycolysis under hypoxic conditions. ","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：2014～2016;   課題番号：26501007;   研究分野：幹細胞生物学・皮膚科学;   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-26501007/"}]}]},"item_8_text_10":{"attribute_name":"著者 役割","attribute_value_mlt":[{"subitem_text_value":"研究代表者/連携研究者"}]},"item_8_text_7":{"attribute_name":"著者(英)","attribute_value_mlt":[{"subitem_text_language":"en","subitem_text_value":"MORIYAMA, Hiroyuki"},{"subitem_text_language":"en","subitem_text_value":"MORIYAMA, Mariko"}]},"item_8_text_8":{"attribute_name":"著者 所属","attribute_value_mlt":[{"subitem_text_value":"近畿大学薬学総合研究所; 准教授"},{"subitem_text_value":"近畿大学・薬学総合研究所・准教授"}]},"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":"森山, 博由"},{"creatorName":"モリヤマ, ヒロユキ","creatorNameLang":"ja-Kana"}],"nameIdentifiers":[{},{}]},{"creatorNames":[{"creatorName":"森山, 麻里子"},{"creatorName":"モリヤマ, マリコ","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":"2017-11-01"}],"displaytype":"detail","filename":"26501007seika.pdf","filesize":[{"value":"231.9 kB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"26501007seika.pdf","url":"https://kindai.repo.nii.ac.jp/record/18795/files/26501007seika.pdf"},"version_id":"4f837b80-12ed-427a-bd64-631855f68c03"}]},"item_keyword":{"attribute_name":"キーワード","attribute_value_mlt":[{"subitem_subject":"間葉系幹細胞","subitem_subject_scheme":"Other"},{"subitem_subject":"分化能","subitem_subject_scheme":"Other"},{"subitem_subject":"Notchシグナル","subitem_subject_scheme":"Other"},{"subitem_subject":"解糖系","subitem_subject_scheme":"Other"},{"subitem_subject":"代謝","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":"幹細胞機能亢進を制御するＮｏｔｃｈ／解糖系経路解明による新規間葉系幹細胞創製","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"幹細胞機能亢進を制御するＮｏｔｃｈ／解糖系経路解明による新規間葉系幹細胞創製"},{"subitem_title":"Isolation of a novel human-mesenchymal stem cells based on the mechanism of Notch/ glycolytic pathway.","subitem_title_language":"en"}]},"item_type_id":"8","owner":"3","path":["4374"],"pubdate":{"attribute_name":"公開日","attribute_value":"2017-11-01"},"publish_date":"2017-11-01","publish_status":"0","recid":"18795","relation_version_is_last":true,"title":["幹細胞機能亢進を制御するＮｏｔｃｈ／解糖系経路解明による新規間葉系幹細胞創製"],"weko_creator_id":"3","weko_shared_id":3},"updated":"2023-06-20T21:49:38.096479+00:00"}