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Cortisol overproduction results from DNA methylation of CYP11B1 in hypercortisolemia
https://doi.org/10.24517/00050650
https://doi.org/10.24517/00050650e4017e7f-b1a6-42f2-b4bf-b015e19f5621
名前 / ファイル | ライセンス | アクション |
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ME-PR-YAMAGISHI-M-11205.pdf (1.9 MB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2018-04-27 | |||||
タイトル | ||||||
タイトル | Cortisol overproduction results from DNA methylation of CYP11B1 in hypercortisolemia | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
ID登録 | ||||||
ID登録 | 10.24517/00050650 | |||||
ID登録タイプ | JaLC | |||||
著者 |
Kometani, Mitsuhiro
× Kometani, Mitsuhiro× Yoneda, Takashi× Demura, Masashi× Koide, Hiroshi× Nishimoto, Koshiro× Mukai, Kuniaki× Gomez-Sanchez, Celso E.× Akagi, Tadayuki× Yokota, Takashi× Horike, Shin-ichi× Karashima, Shigehiro× Miyamori, Isamu× Yamagishi, Masakazu× Takeda, Yoshiyu |
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著者別表示 |
米田, 隆
× 米田, 隆× 赤木, 紀之× 横田, 崇× 堀家, 慎一× 唐島, 成宙× 宮森, 勇× 山岸, 正和× 武田, 仁勇 |
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提供者所属 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 金沢大学医薬保健研究域医学系 | |||||
書誌情報 |
Scientific Reports 巻 7, 号 1, p. 11205, 発行日 2017-12-01 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 2045-2322 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1038/s41598-017-11435-2 | |||||
出版者 | ||||||
出版者 | Nature Publishing Group | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Adrenocortical hormone excess, due to primary aldosteronism (PA) or hypercortisolemia, causes hypertension and cardiovascular complications. In PA, hypomethylation of aldosterone synthase (CYP11B2) is associated with aldosterone overproduction. However, in hypercortisolemia, the role of DNA methylation of 11β-hydroxylase (CYP11B1), which catalyzes cortisol biosynthesis and is highly homologous to CYP11B2, is unclear. The aims of our study were to determine whether the CYP11B1 expression was regulated through DNA methylation in hypercortisolemia with cortisol-producing adenoma (CPA), and to investigate a possible relationship between DNA methylation and somatic mutations identified in CPA. Methylation analysis showed that the CYP11B1 promoter was significantly less methylated in CPA than in adjacent unaffected adrenal tissue and white blood cells. Furthermore, in CPA with somatic mutations in either the catalytic subunit of protein kinase A (PRKACA) or the guanine nucleotide-binding protein subunit alpha (GNAS) gene, the CYP11B1 promoter was significantly hypomethylated. In addition, DNA methylation reduced CYP11B1 promoter activity using a reporter assay. Our study results suggest that DNA methylation at the CYP11B1 promoter plays a role in the regulation of CYP11B1 expression and cortisol production in CPA, and that somatic mutations associated with CPA reduce DNA methylation at the CYP11B1 promoter. © 2017 The Author(s). | |||||
権利 | ||||||
権利情報 | Copyright © Nature Publishing Group | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 |