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To examine functional roles, we mated Cav2.2\u2212/\u2212 mice with db/db (diabetic) mice on the C57BLKS background. Cav2.2 was localized in glomeruli including podocytes and in distal tubular cells. Diabetic Cav2.2\u2212/\u2212 mice significantly reduced urinary albumin excretion, glomerular hyperfiltration, blood glucose levels, histological deterioration and systolic blood pressure (SBP) with decreased urinary catecholamine compared to diabetic Cav2.2+/+ mice. Interestingly, diabetic heterozygous Cav2.2+/\u2212 mice also decreased albuminuria, although they exhibited comparable systolic blood pressure, sympathetic nerve activity and creatinine clearance to diabetic Cav2.2+/+ mice. Consistently, diabetic mice with cilnidipine, an N-/L-type calcium channel blocker, showed a reduction in albuminuria and improvement of glomerular changes compared to diabetic mice with nitrendipine. In cultured podocytes, depolarization-dependent calcium responses were decreased by \u03c9-conotoxin, a Cav2.2-specific inhibitor. Furthermore, reduction of nephrin by transforming growth factor-\u03b2 (TGF-\u03b2) in podocytes was abolished with \u03c9-conotoxin, cilnidipine or mitogen-activated protein kinase kinase inhibitor. 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The images or other third party material in this article are included in the article\u2019s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/"}]}, "item_6_select_64": {"attribute_name": "\u8457\u8005\u7248\u30d5\u30e9\u30b0", "attribute_value_mlt": [{"subitem_select_item": "publisher"}]}, "item_6_source_id_35": {"attribute_name": "ISSN", "attribute_value_mlt": [{"subitem_source_identifier": "2045-2322", "subitem_source_identifier_type": "ISSN"}]}, "item_6_source_id_39": {"attribute_name": "NII ISSN", "attribute_value_mlt": [{"subitem_source_identifier": "2045-2322", "subitem_source_identifier_type": "ISSN"}]}, "item_6_text_70": {"attribute_name": "wosonly keywords", "attribute_value_mlt": [{"subitem_text_value": "CA-V 2.2; HYPERTENSIVE PATIENTS; CILNIDIPINE; MICE; INHIBITION; PODOCYTES; EXPRESSION; OVEREXPRESSION; PROTEINURIA; ARTERIOLES"}]}, "item_6_textarea_68": {"attribute_name": "wosonly abstract", "attribute_value_mlt": [{"subitem_textarea_value": "Pharmacological blockade of the N- and L-type calcium channel lessens renal injury in kidney disease patients. The significance of specific blockade of alpha 1 subunit of N-type calcium channel, Ca(v)2.2, in diabetic nephropathy, however, remains to be clarified. To examine functional roles, we mated Ca(v)2.2(-/-) mice with db/db (diabetic) mice on the C57BLKS background. Ca(v)2.2 was localized in glomeruli including podocytes and in distal tubular cells. Diabetic Ca(v)2.2(-/-) mice significantly reduced urinary albumin excretion, glomerular hyperfiltration, blood glucose levels, histological deterioration and systolic blood pressure (SBP) with decreased urinary catecholamine compared to diabetic Ca(v)2.2(+/+) mice. Interestingly, diabetic heterozygous Ca(v)2.2(+/-) mice also decreased albuminuria, although they exhibited comparable systolic blood pressure, sympathetic nerve activity and creatinine clearance to diabetic Ca(v)2.2(+/+) mice. Consistently, diabetic mice with cilnidipine, an N-/L-type calcium channel blocker, showed a reduction in albuminuria and improvement of glomerular changes compared to diabetic mice with nitrendipine. In cultured podocytes, depolarization-dependent calcium responses were decreased by.-conotoxin, a Ca(v)2.2-specific inhibitor. Furthermore, reduction of nephrin by transforming growth factor-beta (TGF-beta) in podocytes was abolished with.-conotoxin, cilnidipine or mitogen-activated protein kinase kinase inhibitor. In conclusion, Ca(v)2.2 inhibition exerts renoprotective effects against the progression of diabetic nephropathy, partly by protecting podocytes."}]}, "item_creator": {"attribute_name": "\u8457\u8005", "attribute_type": "creator", "attribute_value_mlt": [{"creatorNames": [{"creatorName": "Ohno, Shoko"}], "nameIdentifiers": [{"nameIdentifier": "106879", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Yokoi, Hideki"}], "nameIdentifiers": [{"nameIdentifier": "106880", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Mori, Kiyoshi"}], "nameIdentifiers": [{"nameIdentifier": "106881", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Kasahara, Masato"}], "nameIdentifiers": [{"nameIdentifier": "106882", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Kuwahara, Koichiro"}], "nameIdentifiers": [{"nameIdentifier": "106883", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Fujikura, Junji"}], "nameIdentifiers": [{"nameIdentifier": "106884", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Naito, Masaki"}], "nameIdentifiers": [{"nameIdentifier": "106885", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Kuwabara, Takashige"}], "nameIdentifiers": [{"nameIdentifier": "106886", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Imamaki, Hirotaka"}], "nameIdentifiers": [{"nameIdentifier": "106887", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Ishii, Akira"}], "nameIdentifiers": [{"nameIdentifier": "106888", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Saleem, Moin A."}], "nameIdentifiers": [{"nameIdentifier": "106889", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Numata, Tomohiro"}], "nameIdentifiers": [{"nameIdentifier": "106890", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Mori, Yasuo"}], "nameIdentifiers": [{"nameIdentifier": "106891", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Nakao, Kazuwa"}], "nameIdentifiers": [{"nameIdentifier": "106892", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Yanagita, Motoko"}], "nameIdentifiers": [{"nameIdentifier": "106893", "nameIdentifierScheme": "WEKO"}]}, {"creatorNames": [{"creatorName": "Mukoyama, Masashi"}], "nameIdentifiers": [{"nameIdentifier": "106894", "nameIdentifierScheme": "WEKO"}]}]}, "item_files": {"attribute_name": "\u30d5\u30a1\u30a4\u30eb\u60c5\u5831", "attribute_type": "file", "attribute_value_mlt": [{"accessrole": "open_date", "date": [{"dateType": "Available", "dateValue": "2018-10-31"}], "displaytype": "detail", "download_preview_message": "", "filename": "srep27192.pdf", "filesize": [{"value": "2.7 MB"}], "format": "application/pdf", "future_date_message": "", "is_thumbnail": false, "licensefree": "This work is licensed under a Creative Commons Attribution 4.0 International License. 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Ablation of the N-type calcium channel ameliorates diabetic nephropathy with improved glycemic control and reduced blood pressure
http://hdl.handle.net/10091/00021006
c594f1e2-0d48-4c79-8d22-af2d10bfde36
名前 / ファイル | ライセンス | Actions | |
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This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
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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 | ||||||
タイトル | Ablation of the N-type calcium channel ameliorates diabetic nephropathy with improved glycemic control and reduced blood pressure | |||||
言語 | ||||||
言語 | eng | |||||
キーワード | ||||||
主題 | Diabetic nephropathy | |||||
キーワード | ||||||
主題 | Hypertension | |||||
資源タイプ | ||||||
資源 | http://purl.org/coar/resource_type/c_6501 | |||||
タイプ | journal article | |||||
著者 |
Ohno, Shoko
× Ohno, Shoko× Yokoi, Hideki× Mori, Kiyoshi× Kasahara, Masato× Kuwahara, Koichiro× Fujikura, Junji× Naito, Masaki× Kuwabara, Takashige× Imamaki, Hirotaka× Ishii, Akira× Saleem, Moin A.× Numata, Tomohiro× Mori, Yasuo× Nakao, Kazuwa× Yanagita, Motoko× Mukoyama, Masashi |
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信州大学研究者総覧へのリンク | ||||||
Kuwahara, Koichiro | ||||||
http://soar-rd.shinshu-u.ac.jp/profile/ja.HVchWCcp.html | ||||||
出版者 | ||||||
出版者 | NATURE PUBLISHING GROUP | |||||
引用 | ||||||
内容記述タイプ | Other | |||||
内容記述 | SCIENTIFIC REPORTS. 6: 27192(2016) | |||||
書誌情報 |
SCIENTIFIC REPORTS 巻 6, p. 27192, 発行日 2016-06-07 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Pharmacological blockade of the N- and L-type calcium channel lessens renal injury in kidney disease patients. The significance of specific blockade of α1 subunit of N-type calcium channel, Cav2.2, in diabetic nephropathy, however, remains to be clarified. To examine functional roles, we mated Cav2.2−/− mice with db/db (diabetic) mice on the C57BLKS background. Cav2.2 was localized in glomeruli including podocytes and in distal tubular cells. Diabetic Cav2.2−/− mice significantly reduced urinary albumin excretion, glomerular hyperfiltration, blood glucose levels, histological deterioration and systolic blood pressure (SBP) with decreased urinary catecholamine compared to diabetic Cav2.2+/+ mice. Interestingly, diabetic heterozygous Cav2.2+/− mice also decreased albuminuria, although they exhibited comparable systolic blood pressure, sympathetic nerve activity and creatinine clearance to diabetic Cav2.2+/+ mice. Consistently, diabetic mice with cilnidipine, an N-/L-type calcium channel blocker, showed a reduction in albuminuria and improvement of glomerular changes compared to diabetic mice with nitrendipine. In cultured podocytes, depolarization-dependent calcium responses were decreased by ω-conotoxin, a Cav2.2-specific inhibitor. Furthermore, reduction of nephrin by transforming growth factor-β (TGF-β) in podocytes was abolished with ω-conotoxin, cilnidipine or mitogen-activated protein kinase kinase inhibitor. In conclusion, Cav2.2 inhibition exerts renoprotective effects against the progression of diabetic nephropathy, partly by protecting podocytes. | |||||
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 | ISSN | |||||
収録物識別子 | 2045-2322 | |||||
PubMed | ||||||
関連識別子 | ||||||
識別子タイプ | PMID | |||||
関連識別子 | https://www.ncbi.nlm.nih.gov/pubmed/27273361 | |||||
関連名称 | ||||||
関連名称 | 27273361 | |||||
DOI | ||||||
関連識別子 | ||||||
識別子タイプ | DOI | |||||
関連識別子 | https://doi.org/10.1038/srep27192 | |||||
関連名称 | ||||||
関連名称 | 10.1038/srep27192 | |||||
権利 | ||||||
権利情報 | This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ | |||||
著者版フラグ | ||||||
値 | publisher | |||||
WoS | ||||||
Web of Science | ||||||
http://gateway.isiknowledge.com/gateway/Gateway.cgi?&GWVersion=2&SrcAuth=ShinshuUniv&SrcApp=ShinshuUniv&DestLinkType=FullRecord&DestApp=WOS&KeyUT=000377663900001 |