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This can contribute to a reduction in the effectiveness of circulating BNP and exacerbate heart failure progression. The precise mechanisms governing the increase in proBNP remain unclear, however.\u003cbr/\u003eMethods and Results\u003cbr/\u003eWe used our recently developed, highly sensitive human proBNP assay system to investigate the mechanisms underlying the increase in plasma proBNP levels. We divided 53 consecutive patients hospitalized with heart failure into 2 groups based on their aortic plasma levels of immunoreactive BNP. Patients with higher levels exhibited more severe heart failure, a higher proportion of proBNP among the immunoreactive BNP forms secreted from failing hearts, and a weaker effect of BNP as estimated from the ratio of plasma cyclic guanosine monophosphate levels to log‐transformed plasma BNP levels. Glycosylation at threonines 48 and 71 of human proBNP contributed to the increased secretion of proBNP by attenuating its processing, and GalNAc‐transferase (GALNT) 1 and 2 mediated the glycosylation‐regulated increase in cardiac human proBNP secretion. Cardiac GALNT1 and 2 expression was suppressed by microRNA (miR)‐30, which is abundantly expressed in the myocardium of healthy hearts, but is suppressed in failing hearts.\u003cbr/\u003eConclusions\u003cbr/\u003eWe have elucidated a novel miR‐30‐GALNT1/2 axis whose dysregulation increases the proportion of inactive proBNP secreted by the heart and impairs the compensatory actions of BNP during the progression of heart failure.", "subitem_description_type": "Abstract"}]}, "item_6_description_30": {"attribute_name": "資源タイプ(コンテンツの種類)", "attribute_value_mlt": [{"subitem_description": "Article", "subitem_description_type": "Other"}]}, "item_6_description_5": {"attribute_name": "引用", "attribute_value_mlt": [{"subitem_description": "JOURNAL OF THE AMERICAN HEART ASSOCIATION. 6(2): e003601(2017)", "subitem_description_type": "Other"}]}, "item_6_link_3": {"attribute_name": "信州大学研究者総覧へのリンク", "attribute_value_mlt": [{"subitem_link_text": "Kuwahara, Koichiro", "subitem_link_url": "http://soar-rd.shinshu-u.ac.jp/profile/ja.HVchWCcp.html"}]}, "item_6_link_67": {"attribute_name": "WoS", "attribute_value_mlt": [{"subitem_link_text": "Web of Science", "subitem_link_url": "http://gateway.isiknowledge.com/gateway/Gateway.cgi?\u0026GWVersion=2\u0026SrcAuth=ShinshuUniv\u0026SrcApp=ShinshuUniv\u0026DestLinkType=FullRecord\u0026DestApp=WOS\u0026KeyUT=000413896000011"}]}, "item_6_publisher_4": {"attribute_name": "出版者", "attribute_value_mlt": [{"subitem_publisher": "WILEY"}]}, "item_6_relation_47": {"attribute_name": "PubMed", "attribute_value_mlt": [{"subitem_relation_name": [{"subitem_relation_name_text": "28188250"}], "subitem_relation_type_id": {"subitem_relation_type_id_text": "https://www.ncbi.nlm.nih.gov/pubmed/28188250", "subitem_relation_type_select": "PMID"}}]}, "item_6_relation_48": {"attribute_name": "DOI", "attribute_value_mlt": [{"subitem_relation_name": [{"subitem_relation_name_text": "10.1161/JAHA.116.003601"}], "subitem_relation_type_id": {"subitem_relation_type_id_text": "https://doi.org/10.1161/JAHA.116.003601", "subitem_relation_type_select": "DOI"}}]}, "item_6_rights_62": {"attribute_name": "権利", "attribute_value_mlt": [{"subitem_rights": "© 2017 The Authors. 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This can contribute to a reduction in the effectiveness of circulating BNP and exacerbate heart failure progression. The precise mechanisms governing the increase in proBNP remain unclear, however. \u003cbr/\u003eMethods and Results-We used our recently developed, highly sensitive human proBNP assay system to investigate the mechanisms underlying the increase in plasma proBNP levels. We divided 53 consecutive patients hospitalized with heart failure into 2 groups based on their aortic plasma levels of immunoreactive BNP. Patients with higher levels exhibited more severe heart failure, a higher proportion of proBNP among the immunoreactive BNP forms secreted from failing hearts, and a weaker effect of BNP as estimated from the ratio of plasma cyclic guanosine monophosphate levels to log-transformed plasma BNP levels. Glycosylation at threonines 48 and 71 of human proBNP contributed to the increased secretion of proBNP by attenuating its processing, and GalNAc-transferase (GALNT) 1 and 2 mediated the glycosylation-regulated increase in cardiac human proBNP secretion. Cardiac GALNT1 and 2 expression was suppressed by microRNA (miR)-30, which is abundantly expressed in the myocardium of healthy hearts, but is suppressed in failing hearts. \u003cbr/\u003eConclusions-We have elucidated a novel miR-30-GALNT1/2 axis whose dysregulation increases the proportion of inactive proBNP secreted by the heart and impairs the compensatory actions of BNP during the progression of heart failure."}]}, "item_creator": {"attribute_name": "著者", "attribute_type": "creator", "attribute_value_mlt": [{"creatorNames": [{"creatorName": "Nakagawa, Yasuaki", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "106831", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Nishikimi, Toshio", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "106832", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Kuwahara, Koichiro", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "106833", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Fujishima, Aoi", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "106834", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Oka, Shogo", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "106835", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Tsutamoto, Takayoshi", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "106836", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Kinoshita, Hideyuki", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "106837", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Nakao, Kazuhiro", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "106838", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Cho, Kosai", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "106839", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Inazumi, Hideaki", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "106840", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Okamoto, Hiroyuki", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "106841", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Nishida, Motohiro", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "106842", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Kato, Takao", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "106843", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Fukushima, Hiroyuki", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "106844", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Yamashita, Jun K.", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "106845", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Wijnen, Wino J.", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "106846", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Creemers, Esther E.", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "106847", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Kangawa, Kenji", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "106848", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Minamino, Naoto", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "106849", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Nakao, Kazuwa", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "106850", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Kimura, Takeshi", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "106851", "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": "2018-10-31"}], "displaytype": "detail", "download_preview_message": "", "file_order": 0, "filename": "JAH3-6-e003601.pdf", "filesize": [{"value": "1.0 MB"}], "format": "application/pdf", "future_date_message": "", "is_thumbnail": false, "licensefree": "© 2017 The Authors. 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MiR30-GALNT1/2 Axis-Mediated Glycosylation Contributes to the Increased Secretion of Inactive Human Prohormone for Brain Natriuretic Peptide (proBNP) From Failing Hearts
http://hdl.handle.net/10091/00021003
http://hdl.handle.net/10091/00021003579d384d-dd70-45c3-98e8-d46358107a88
名前 / ファイル | ライセンス | アクション |
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JAH3-6-e003601.pdf (1.0 MB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2018-10-31 | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | MiR30-GALNT1/2 Axis-Mediated Glycosylation Contributes to the Increased Secretion of Inactive Human Prohormone for Brain Natriuretic Peptide (proBNP) From Failing Hearts | |||||
言語 | ||||||
言語 | eng | |||||
DOI | ||||||
識別子タイプ | DOI | |||||
関連識別子 | https://doi.org/10.1161/JAHA.116.003601 | |||||
関連名称 | 10.1161/JAHA.116.003601 | |||||
キーワード | ||||||
主題 | signal transduction, microRNA, natriuretic peptide | |||||
資源タイプ | ||||||
資源 | http://purl.org/coar/resource_type/c_6501 | |||||
タイプ | journal article | |||||
著者 |
Nakagawa, Yasuaki
× Nakagawa, Yasuaki× Nishikimi, Toshio× Kuwahara, Koichiro× Fujishima, Aoi× Oka, Shogo× Tsutamoto, Takayoshi× Kinoshita, Hideyuki× Nakao, Kazuhiro× Cho, Kosai× Inazumi, Hideaki× Okamoto, Hiroyuki× Nishida, Motohiro× Kato, Takao× Fukushima, Hiroyuki× Yamashita, Jun K.× Wijnen, Wino J.× Creemers, Esther E.× Kangawa, Kenji× Minamino, Naoto× Nakao, Kazuwa× Kimura, Takeshi |
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信州大学研究者総覧へのリンク | ||||||
氏名 | Kuwahara, Koichiro | |||||
URL | http://soar-rd.shinshu-u.ac.jp/profile/ja.HVchWCcp.html | |||||
出版者 | ||||||
出版者 | WILEY | |||||
引用 | ||||||
内容記述タイプ | Other | |||||
内容記述 | JOURNAL OF THE AMERICAN HEART ASSOCIATION. 6(2): e003601(2017) | |||||
書誌情報 |
JOURNAL OF THE AMERICAN HEART ASSOCIATION 巻 6, 号 2, p. e003601, 発行日 2017-02-10 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Background<br/>Recent studies have shown that plasma levels of the biologically inactive prohormone for brain natriuretic peptide (proBNP) are increased in patients with heart failure. This can contribute to a reduction in the effectiveness of circulating BNP and exacerbate heart failure progression. The precise mechanisms governing the increase in proBNP remain unclear, however.<br/>Methods and Results<br/>We used our recently developed, highly sensitive human proBNP assay system to investigate the mechanisms underlying the increase in plasma proBNP levels. We divided 53 consecutive patients hospitalized with heart failure into 2 groups based on their aortic plasma levels of immunoreactive BNP. Patients with higher levels exhibited more severe heart failure, a higher proportion of proBNP among the immunoreactive BNP forms secreted from failing hearts, and a weaker effect of BNP as estimated from the ratio of plasma cyclic guanosine monophosphate levels to log‐transformed plasma BNP levels. Glycosylation at threonines 48 and 71 of human proBNP contributed to the increased secretion of proBNP by attenuating its processing, and GalNAc‐transferase (GALNT) 1 and 2 mediated the glycosylation‐regulated increase in cardiac human proBNP secretion. Cardiac GALNT1 and 2 expression was suppressed by microRNA (miR)‐30, which is abundantly expressed in the myocardium of healthy hearts, but is suppressed in failing hearts.<br/>Conclusions<br/>We have elucidated a novel miR‐30‐GALNT1/2 axis whose dysregulation increases the proportion of inactive proBNP secreted by the heart and impairs the compensatory actions of BNP during the progression of heart failure. | |||||
資源タイプ(コンテンツの種類) | ||||||
内容記述タイプ | Other | |||||
内容記述 | Article | |||||
ISSN | ||||||
収録物識別子タイプ | PISSN | |||||
収録物識別子 | 2047-9980 | |||||
PubMed | ||||||
識別子タイプ | PMID | |||||
関連識別子 | https://www.ncbi.nlm.nih.gov/pubmed/28188250 | |||||
関連名称 | 28188250 | |||||
権利 | ||||||
権利情報 | © 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell. This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. | |||||
出版タイプ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
WoS | ||||||
表示名 | Web of Science | |||||
URL | http://gateway.isiknowledge.com/gateway/Gateway.cgi?&GWVersion=2&SrcAuth=ShinshuUniv&SrcApp=ShinshuUniv&DestLinkType=FullRecord&DestApp=WOS&KeyUT=000413896000011 |