{"created":"2021-03-01T06:15:55.161546+00:00","id":9165,"links":{},"metadata":{"_buckets":{"deposit":"bcf441f3-5c7a-456e-add9-41d9f8e57134"},"_deposit":{"id":"9165","owners":[],"pid":{"revision_id":0,"type":"depid","value":"9165"},"status":"published"},"_oai":{"id":"oai:nagoya.repo.nii.ac.jp:00009165","sets":["329:330:331"]},"author_link":["25729","25730","25731","25732","25733","25734","25735","25736","25737","25738","25739","25740","25741","25742","25743","25744","25745","25746","25747","25748","25749","25750"],"item_10_alternative_title_19":{"attribute_name":"その他のタイトル","attribute_value_mlt":[{"subitem_alternative_title":"Rapid Electrical Stimulation of Contraction Modulates Gap-Junction Protein in Neonatal Rat Cultured Cardiomyocytes Involvement of Mitogen-Activated Protein Kinases and Effects of Angiotensin II-Receptor Antagonist","subitem_alternative_title_language":"en"}]},"item_10_biblio_info_6":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2005-08","bibliographicIssueDateType":"Issued"},"bibliographicIssueNumber":"4","bibliographicPageEnd":"115","bibliographicPageStart":"109","bibliographicVolumeNumber":"54","bibliographic_titles":[{"bibliographic_title":"山口医学","bibliographic_titleLang":"ja"}]}]},"item_10_description_4":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"心筋細胞間のギャップ結合の発現・分布はコネキシン蛋白の半減期が短いことにより様々な病態において直ちに変化しうる.高頻度電気刺激(RES)によるギャップ結合リモデリングへの効果はいまだ明らかにされていない.培養5日目のラット心室筋細胞に120分間3HzのRESを負荷した.RESによりCx43蛋白質および遺伝子発現量は60分後には有意に増加した.免疫染色においても同様の結果であった.心筋細胞中のangiotensin II (AngII)は15分後に約2倍に上昇した.MAPK系のリン酸化型ERKは2峰性に5分と60分で, またリン酸化型JNKも15分と60分で著明に活性化された.リン酸化型p38 MAPKは5分後に1峰性に活性化された.細胞外電位記録法により心筋細胞の興奮伝播特性の変化を解析したところ, RESにより伝導速度は有意に増加した.これらの変化はlosartanにより抑制された.RESによるCx43の発現増加はまたERK, p38の特異的阻害剤にても抑制された.RESは, 早期より心筋細胞内のAng II産生を増加し, MAPK系を活性化することによりCx43発現量を増加させた.その結果, 細胞間の刺激伝播異常を引き起こし, 不整脈基質の一つとなる可能性が示された.","subitem_description_language":"ja","subitem_description_type":"Abstract"},{"subitem_description":"BACKGROUND The expression and distribution of gap junctions in cardiac muscle can be changed readily under a variety of pathological conditions because of dynamic turnover of connexins. The effects of rapid electrical stimulation (RES) of contraction on the gap junction remodeling are not well-understood. METHODS Neonatal rat ventricular myocytes cultured for 5 days were subjected to RES at 3.0 Hz for up to 120 min. RESULTS RES resulted in a significant upregulation of Cx43. Angiotensin II content was increased significantly by RES>15 min. Phosphorylated forms of extracellular signal-regulated protein kinase (ERK), c-Jun NH_2-terminal kinases (JNK) and p38 mitogen-activated protein kinases (p38 MAPKs) were all increased dramatically by RES with peaks at 5～60 min. Propagation of excitation was visualized by extracellular potential mapping by using a multiple electrode array system. Conduction velocity was increased significantly by RES for 60 to 90 min. Treatment of myocytes with losartan prevented most of these effects of RES. RES-induced upregulation of Cx43 was also prevented by specific inhibitors for ERK and p38 MAPKs. CONCLUSIONS A short-term RES causes upregulation of Cx43 in cardiomyocytes and a concomitant increase of conduction velocity mainly through an autocrine action of Angiotensin II to activate ERK and p38 MAPKs.","subitem_description_language":"en","subitem_description_type":"Abstract"}]},"item_10_description_5":{"attribute_name":"内容記述","attribute_value_mlt":[{"subitem_description":"(小西賞受賞者)(Konishi Prize)","subitem_description_language":"ja","subitem_description_type":"Other"}]},"item_10_identifier_60":{"attribute_name":"URI","attribute_value_mlt":[{"subitem_identifier_type":"HDL","subitem_identifier_uri":"http://hdl.handle.net/2237/10933"}]},"item_10_publisher_32":{"attribute_name":"出版者","attribute_value_mlt":[{"subitem_publisher":"山口大学医学会","subitem_publisher_language":"ja"}]},"item_10_relation_43":{"attribute_name":"関連情報","attribute_value_mlt":[{"subitem_relation_type":"isVersionOf","subitem_relation_type_id":{"subitem_relation_type_id_text":"http://ci.nii.ac.jp/naid/110002774473/","subitem_relation_type_select":"URI"}}]},"item_10_rights_12":{"attribute_name":"権利","attribute_value_mlt":[{"subitem_rights":"山口大学医学会","subitem_rights_language":"ja"},{"subitem_rights":"本文データは学協会の許諾に基づきCiNiiから複製したものである","subitem_rights_language":"ja"}]},"item_10_select_15":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_select_item":"publisher"}]},"item_10_source_id_7":{"attribute_name":"ISSN","attribute_value_mlt":[{"subitem_source_identifier":"05131731","subitem_source_identifier_type":"PISSN"}]},"item_10_text_14":{"attribute_name":"フォーマット","attribute_value_mlt":[{"subitem_text_value":"application/pdf"}]},"item_1615787544753":{"attribute_name":"出版タイプ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_970fb48d4fbd8a85","subitem_version_type":"VoR"}]},"item_access_right":{"attribute_name":"アクセス権","attribute_value_mlt":[{"subitem_access_right":"open 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Takashi","creatorNameLang":"en"}],"nameIdentifiers":[{"nameIdentifier":"25746","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"YANO, Masafumi","creatorNameLang":"en"}],"nameIdentifiers":[{"nameIdentifier":"25747","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"YASUI, Kenji","creatorNameLang":"en"}],"nameIdentifiers":[{"nameIdentifier":"25748","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"KODAMA, Itsuo","creatorNameLang":"en"}],"nameIdentifiers":[{"nameIdentifier":"25749","nameIdentifierScheme":"WEKO"}]},{"creatorNames":[{"creatorName":"MATSUZAKI, Masunori","creatorNameLang":"en"}],"nameIdentifiers":[{"nameIdentifier":"25750","nameIdentifierScheme":"WEKO"}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2018-02-19"}],"displaytype":"detail","filename":"lee_2090.pdf","filesize":[{"value":"629.2 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