{"created":"2023-05-15T09:41:14.290557+00:00","id":300,"links":{},"metadata":{"_buckets":{"deposit":"07ec0114-dce6-49f1-8e09-a5f66d1b156d"},"_deposit":{"created_by":11,"id":"300","owners":[11],"pid":{"revision_id":0,"type":"depid","value":"300"},"status":"published"},"_oai":{"id":"oai:kagawa-u.repo.nii.ac.jp:00000300","sets":["13:40"]},"author_link":["421"],"item_10006_date_granted_11":{"attribute_name":"学位授与年月日","attribute_value_mlt":[{"subitem_dategranted":"2018-03-24"}]},"item_10006_degree_grantor_9":{"attribute_name":"学位授与機関","attribute_value_mlt":[{"subitem_degreegrantor":[{"subitem_degreegrantor_language":"ja","subitem_degreegrantor_name":"香川大学"},{"subitem_degreegrantor_language":"en","subitem_degreegrantor_name":"Kagawa University"}],"subitem_degreegrantor_identifier":[{"subitem_degreegrantor_identifier_name":"16201","subitem_degreegrantor_identifier_scheme":"kakenhi"}]}]},"item_10006_degree_name_8":{"attribute_name":"学位名","attribute_value_mlt":[{"subitem_degreename":"博士（医学）","subitem_degreename_language":"ja"}]},"item_10006_description_7":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"Abstract\nThe kidney expresses protease-activated receptor-1 (PAR-1). PAR-1 is known as a thrombin receptor, but its role in kidney injury is not well understood. In this study, we examined the contribution of PAR-1 to kidney glomerular injury and the effects of its inhibition on development of nephropathy. Mice were divided into 3 groups: control, doxorubicin + vehicle (15 mg/kg doxorubicin and saline) and doxorubicin + Q94 (doxorubicin at 15 mg/kg and the PAR-1 antagonist Q94 at 5 mg/kg/d) groups. Where indicated, doxorubicin was administered intravenously and PAR-1 antagonist or saline vehicle by subcutaneous osmotic mini-pump. PAR-1 expression was increased in glomeruli of mice treated with doxorubicin. Q94 treatment significantly suppressed the increased albuminuria in these nephropathic mice. Pathological analysis showed that Q94 treatment significantly attenuated periodic acid–Schiff and desmin staining, indicators of podocyte injury, and also decreased glomerular levels of podocin and nephrin. Furthermore, thrombin increased intracellular calcium levels in podocytes. This increase was suppressed by Q94 and Rox4560, a transient receptor potential cation channel (TRPC)3/6 antagonist. In addition, both Q94 and Rox4560 suppressed the doxorubicin-induced increase in activities of caspase-9 and caspase-3 in podocytes. These data suggested that PAR-1 contributes to development of podocyte and glomerular injury and that PAR-1 antagonists have therapeutic potential.","subitem_description_language":"en","subitem_description_type":"Abstract"}]},"item_10006_dissertation_number_12":{"attribute_name":"学位授与番号","attribute_value_mlt":[{"subitem_dissertationnumber":"甲第679号"}]},"item_10006_relation_15":{"attribute_name":"関連サイト","attribute_value_mlt":[{"subitem_relation_type":"isVersionOf","subitem_relation_type_id":{"subitem_relation_type_id_text":"https://doi.org/10.1016/j.jphs.2017.09.002","subitem_relation_type_select":"DOI"}},{"subitem_relation_type":"isIdenticalTo","subitem_relation_type_id":{"subitem_relation_type_id_text":"https://dl.ndl.go.jp/pid/11122655","subitem_relation_type_select":"URI"}}]},"item_10006_relation_22":{"attribute_name":"PubMed番号","attribute_value_mlt":[{"subitem_relation_type_id":{"subitem_relation_type_id_text":"29110957","subitem_relation_type_select":"PMID"}}]},"item_10006_relation_28":{"attribute_name":"論文ID（NAID）","attribute_value_mlt":[{"subitem_relation_type_id":{"subitem_relation_type_id_text":"500001069838","subitem_relation_type_select":"NAID"}}]},"item_10006_rights_13":{"attribute_name":"権利","attribute_value_mlt":[{"subitem_rights":"Copyright ©2017 The Authors. Production and hosting by Elsevier B.V. on behalf of Japanese Pharmacological Society.","subitem_rights_language":"en"},{"subitem_rights":"This is an open access article under the CC BY-NC-ND license.","subitem_rights_language":"en","subitem_rights_resource":"http://creativecommons.org/licenses/by-nc-nd/4.0/"}]},"item_10006_text_30":{"attribute_name":"KEID","attribute_value_mlt":[{"subitem_text_value":"28450"}]},"item_10006_version_type_18":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_fa2ee174bc00049f","subitem_version_type":"P"}]},"item_access_right":{"attribute_name":"アクセス権","attribute_value_mlt":[{"subitem_access_right":"open access","subitem_access_right_uri":"http://purl.org/coar/access_right/c_abf2"}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"Guan, Yu","creatorNameLang":"en"},{"creatorName":"管, 瑀","creatorNameLang":"ja"},{"creatorName":"グアン, ユ","creatorNameLang":"ja-Kana"}],"familyNames":[{"familyName":"Guan","familyNameLang":"en"},{"familyName":"管","familyNameLang":"ja"},{"familyName":"グアン","familyNameLang":"ja-Kana"}],"givenNames":[{"givenName":"Yu","givenNameLang":"en"},{"givenName":"瑀","givenNameLang":"ja"},{"givenName":"ユ","givenNameLang":"ja-Kana"}],"nameIdentifiers":[{"nameIdentifier":"421","nameIdentifierScheme":"WEKO"},{"nameIdentifier":"9000386307711 ","nameIdentifierScheme":"CiNii ID","nameIdentifierURI":"http://ci.nii.ac.jp/nrid/9000386307711 "}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2020-10-30"}],"displaytype":"detail","filename":"Med_A679.pdf","filesize":[{"value":"2.3 MB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"本文","objectType":"fulltext","url":"https://kagawa-u.repo.nii.ac.jp/record/300/files/Med_A679.pdf"},"version_id":"efbcf4b3-8eca-4d42-a6c3-ef3418bd0ec5"},{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2020-10-30"}],"displaytype":"detail","filename":"Med_A679_abstract.pdf","filesize":[{"value":"119.9 kB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"内容の要旨","objectType":"abstract","url":"https://kagawa-u.repo.nii.ac.jp/record/300/files/Med_A679_abstract.pdf"},"version_id":"693dd09a-98e4-4bce-8822-944f8d8a5c32"},{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2020-10-30"}],"displaytype":"detail","filename":"Med_A679_result.pdf","filesize":[{"value":"383.5 kB"}],"format":"application/pdf","licensetype":"license_note","mimetype":"application/pdf","url":{"label":"審査の結果の要旨","objectType":"other","url":"https://kagawa-u.repo.nii.ac.jp/record/300/files/Med_A679_result.pdf"},"version_id":"1483d702-9fed-422c-a86f-4a9b53a4e931"}]},"item_keyword":{"attribute_name":"キーワード","attribute_value_mlt":[{"subitem_subject":"Protease-activated receptor-1","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"Podocyte","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"Transient receptor potential cation channel","subitem_subject_language":"en","subitem_subject_scheme":"Other"},{"subitem_subject":"Kidney injury","subitem_subject_language":"en","subitem_subject_scheme":"Other"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"eng"}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"doctoral thesis","resourceuri":"http://purl.org/coar/resource_type/c_db06"}]},"item_title":"A protease-activated receptor-1 antagonist protects against podocyte injury in a mouse model of nephropathy","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"A protease-activated receptor-1 antagonist protects against podocyte injury in a mouse model of nephropathy","subitem_title_language":"en"}]},"item_type_id":"10006","owner":"11","path":["40"],"pubdate":{"attribute_name":"PubDate","attribute_value":"2018-05-31"},"publish_date":"2018-05-31","publish_status":"0","recid":"300","relation_version_is_last":true,"title":["A protease-activated receptor-1 antagonist protects against podocyte injury in a mouse model of nephropathy"],"weko_creator_id":"11","weko_shared_id":-1},"updated":"2024-10-31T08:02:32.606887+00:00"}