{"created":"2023-06-19T10:55:04.529044+00:00","id":5587,"links":{},"metadata":{"_buckets":{"deposit":"cf2c443d-b323-4c84-beba-9a7619d2dc49"},"_deposit":{"created_by":17,"id":"5587","owners":[17],"pid":{"revision_id":0,"type":"depid","value":"5587"},"status":"published"},"_oai":{"id":"oai:kobe-c.repo.nii.ac.jp:00005587","sets":["40:1403:1404"]},"author_link":["5860","3194"],"item_10002_biblio_info_30":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2018-06-20","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"1","bibliographicPageEnd":"56","bibliographicPageStart":"45","bibliographicVolumeNumber":"65","bibliographic_titles":[{"bibliographic_title":"神戸女学院大学論集"},{"bibliographic_title":"KOBE COLLEGE STUDIES","bibliographic_titleLang":"en"}]}]},"item_10002_description_28":{"attribute_name":"要旨(日）","attribute_value_mlt":[{"subitem_description":"アルツハイマー型認知症の発症には性差が存在し、その原因として女性ホルモンのエストロゲンが神経細胞の保護効果を発揮することが示唆されている。本研究では神経細胞にアミロイドβを負荷したアルツハイマー型認知症の細胞モデルを用い、エストロゲンがエストロゲン受容体との結合を介して小胞体ストレスを修飾し、神経細胞を保護しているか否かを検討した。ラット神経系由来のＰＣ-12細胞に、アミロイドβ、または小胞体ストレス誘発剤のツニカマイシンを負荷すると、小胞体が増大するとともに Unfolded Protein Response (UPR) が活性化され、シャペロン蛋白GRP78が誘導された。さらに過剰な小胞体ストレスはアポトーシスによる神経細胞死を惹起した。女性ホルモンの17β-エストラジオールは、アミロイドβやツニカマイシンによる小胞体ストレスを抑制し、神経細胞死を減少させた。エストロゲン受容体阻害剤 ICI182,780は、このような17β-エストラジオールの小胞体量、GRP78誘導に対する効果を完全に抑制するとともに、アポトーシスに対する抑制効果も部分的に抑制した。以上より、エストロゲンはアミロイド負荷による神経細胞の小胞体ストレスに対し、エストロゲン受容体を介したストレス応答によって適応することが示唆された。過剰なストレスによる神経細胞死に対しても、部分的には神経細胞内のエストロゲン受容体を介したメカニズムにより対応する可能性が示唆された。","subitem_description_type":"Other"}]},"item_10002_description_49":{"attribute_name":"要旨（英）","attribute_value_mlt":[{"subitem_description":"Female hormones are supposed to play a pivotal role in the sex difference of Alzheimer's disease by exerting protective effects on neurons.We investigated whether estrogen, a kind of female hormones, reduces the damage of neural cells through binding to intracellular estrogen receptors using a cellular model of Alzheimer's disease.When amyloid β (5μＭ), a proposed pathogen of Alzheimer's disease, or tunicamycine (1μM), an inducer of endoplasmic reticulum (ER) stress, were applied to cultured PC-12 neural cells, the size of ER, a measure of ER stress and the expression of GRP78, an indicative protein of unfolded protein (UPR), were both increased. In this model, 17β-estradiol (1μM), the most potent estrogen, increased the GRP78 expression together with the decrease in ER size and the cell death by apoptosis, suggesting that 17β-estradiol augments the stress response of neural cells to amyloid β by activating UPR. When cells were pretreated with a competitive inhibitor of estrogen receptors, ICI182,780 (100μM), the increase in GRP78 expression and the decrease in ER size by 17β-estradiol were completely abolished. The effect of 17β-estradiol on the number of apoptotic cells was partially inhibited by ICI182,780. These results indicate that the female hormone estrogen enhances the stress response of neurons to amyloid β by activating UPR via the binding to estrogen receptors. Estrogen may exhibit a protective effect against cell death caused by amyloid β partly through the receptor mediated mechanism because the effect 17β-estradiol on apoptotic cell death was partially inhibited by ICI182,780. ","subitem_description_type":"Other"}]},"item_10002_identifier_registration":{"attribute_name":"ID登録","attribute_value_mlt":[{"subitem_identifier_reg_text":"10.18878/00005530","subitem_identifier_reg_type":"JaLC"}]},"item_10002_select_43":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_select_item":"publisher"}]},"item_10002_text_31":{"attribute_name":"出版者","attribute_value_mlt":[{"subitem_text_value":"神戸女学院大学研究所"}]},"item_10002_text_47":{"attribute_name":"著者所属","attribute_value_mlt":[{"subitem_text_value":"神戸女学院大学大学院 人間科学研究科 人間科学専攻 博士前期課程"},{"subitem_text_value":"神戸女学院大学 人間科学部 環境・バイオサイエンス学科 教授"}]},"item_10002_text_48":{"attribute_name":"雑誌書誌ID","attribute_value_mlt":[{"subitem_text_value":"AN00085725"}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"山本, 智美"},{"creatorName":"ヤマモト, トモミ","creatorNameLang":"ja-Kana"},{"creatorName":"YAMAMOTO, Tomomi","creatorNameLang":"en"}],"nameIdentifiers":[{"nameIdentifier":"5860","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"西田, 昌司"},{"creatorName":"ニシダ, マサシ","creatorNameLang":"ja-Kana"},{"creatorName":"NISHIDA, Masashi","creatorNameLang":"en"}],"nameIdentifiers":[{"nameIdentifier":"3194","nameIdentifierScheme":"WEKO"},{"nameIdentifier":"1000040283783","nameIdentifierScheme":"CiNii ID","nameIdentifierURI":"http://ci.nii.ac.jp/nrid/1000040283783"},{"nameIdentifier":"40283783","nameIdentifierScheme":"KAKEN-研究者検索","nameIdentifierURI":"https://nrid.nii.ac.jp/ja/nrid/1000040283783/"}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2018-07-17"}],"displaytype":"detail","filename":"201806_180-05.pdf","filesize":[{"value":"858.0 kB"}],"format":"application/pdf","license_note":"神戸女学院大学研究所","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"201806_180-05","url":"https://kobe-c.repo.nii.ac.jp/record/5587/files/201806_180-05.pdf"},"version_id":"32fd13d5-168f-4b1c-a364-0c86d2c7233f"}]},"item_keyword":{"attribute_name":"キーワード","attribute_value_mlt":[{"subitem_subject":"アルツハイマー型認知症","subitem_subject_scheme":"Other"},{"subitem_subject":"アミロイドβ","subitem_subject_scheme":"Other"},{"subitem_subject":"小胞体ストレス応答","subitem_subject_scheme":"Other"},{"subitem_subject":"17β-エストラジオール","subitem_subject_scheme":"Other"},{"subitem_subject":"アポトーシス","subitem_subject_scheme":"Other"},{"subitem_subject":"エストロゲン受容体","subitem_subject_scheme":"Other"},{"subitem_subject_scheme":"Other"},{"subitem_subject":"Alzheimer's disease","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"amyloid β","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"unfolded protein responses","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"17β-estradiol","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"apoptosis","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"estrogen receptor","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject_language":"en","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":"departmental bulletin paper","resourceuri":"http://purl.org/coar/resource_type/c_6501"}]},"item_title":"女性ホルモンとアルツハイマー型認知症Ⅲ―アミロイドβ負荷による神経細胞の細胞障害に対する17β-エストラジオールの作用機序の検討―","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"女性ホルモンとアルツハイマー型認知症Ⅲ―アミロイドβ負荷による神経細胞の細胞障害に対する17β-エストラジオールの作用機序の検討―"},{"subitem_title":"Female Hormones and Alzheimer's Disease ⅢーThe Mechanism of Protective Effects of 17β-Estradiol on the Cellular Injury of Neurons Induced by Amyloid βー","subitem_title_language":"en"}]},"item_type_id":"10002","owner":"17","path":["1404"],"pubdate":{"attribute_name":"公開日","attribute_value":"2018-07-17"},"publish_date":"2018-07-17","publish_status":"0","recid":"5587","relation_version_is_last":true,"title":["女性ホルモンとアルツハイマー型認知症Ⅲ―アミロイドβ負荷による神経細胞の細胞障害に対する17β-エストラジオールの作用機序の検討―"],"weko_creator_id":"17","weko_shared_id":-1},"updated":"2023-06-19T11:33:02.179139+00:00"}