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  1. 20 医学系研究科・医学部
  2. 20A 学術誌論文
  3. 20A1 雑誌掲載論文

Stromal interaction molecule 1 haploinsufficiency causes maladaptive response to pressure overload

http://hdl.handle.net/10295/00006319
http://hdl.handle.net/10295/00006319
940b41cd-cdac-46f6-b004-735b66267d80
名前 / ファイル ライセンス アクション
iA_2022_126.pdf iA_2022_126.pdf (4.5 MB)
Item type 学術雑誌論文 / Journal Article(1)
公開日 2023-02-25
タイトル
タイトル Stromal interaction molecule 1 haploinsufficiency causes maladaptive response to pressure overload
言語 en
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
アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
作成者 Ohba, Takayoshi

× Ohba, Takayoshi

en Ohba, Takayoshi

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Watanabe, Hiroyuki

× Watanabe, Hiroyuki

en Watanabe, Hiroyuki

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Murakami, Manabu

× Murakami, Manabu

en Murakami, Manabu

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Iino, Kenji

× Iino, Kenji

en Iino, Kenji

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Adachi, Takeshi

× Adachi, Takeshi

en Adachi, Takeshi

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Baba, Yoshihiro

× Baba, Yoshihiro

en Baba, Yoshihiro

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Kurosaki, Tomohiro

× Kurosaki, Tomohiro

en Kurosaki, Tomohiro

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Ono, Kyoichi

× Ono, Kyoichi

en Ono, Kyoichi

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Ito, Hiroshi

× Ito, Hiroshi

en Ito, Hiroshi

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内容記述
内容記述タイプ Abstract
内容記述 Stromal interaction molecule 1 (STIM1), an endo/sarcoplasmic reticulum Ca2+ sensor, has been shown to control a Ca2+- dependent signal that promotes cardiac hypertrophy. However, whether STIM1 has adaptive role that helps to protect against cardiac overload stress remains unknown. We hypothesized that STIM1 deficiency causes a maladaptive response to pressure overload stress. We investigated STIM1 heterozygous KO (STIM1(+/)-) mice hearts, in which STIM1 protein levels decreased to 27% of wild-type (WT) with no compensatory increase in STIM2. Under stress-free conditions, no significant differences were observed in electrocardiographic and echocardiographic parameters or blood pressure between STIM1(+/)-and WT mice. However, when STIM1(+/)-mice were subjected to transverse aortic constriction (TAC), STIM1(+/-) mice had a higher mortality rate than WT mice. The TAC-induced increase in the heart weight to body weight ratio (mean mg/g +/- standard error of the mean) was significantly inhibited in STIM1(+/-) mice (WT sham, 4.12 +/- 0.14; WT TAC, 6.23 +/- 0.40; STIM1(+/-) sham, 4.53 +/- 0.16; STIM1(+/-) TAC, 4.63 +/- 0.08). Reverse transcription- polymerase chain reaction analysis of the left ventricles of TAC-treated STIM1(+/-) mice showed inhibited induction of cardiac fetal genes, including those encoding brain and atrial natriuretic proteins. Western blot analysis showed upregulated expression of transient receptor potential channel 1 (TRPC1) in TAC-treated WT mice, but suppressed expression in TAC-treated STIM1(+/-) mice. Taken together, the hearts of STIM1 haploinsufficient mice had a superficial resemblance to the WT phenotype under stress-free conditions; however, STIM1 haploinsufficient mice showed a maladaptive response to cardiac pressure overload.
言語 en
出版タイプ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
書誌情報 en : PLOS ONE

巻 12, 号 11, 発行日 2017
収録物識別子
収録物識別子タイプ ISSN
収録物識別子 1932-6203
出版者
出版者 Public Library of Science
言語 en
関連情報
関連タイプ isIdenticalTo
識別子タイプ DOI
関連識別子 https://doi.org/10.1371/journal.pone.0187950
権利情報
権利情報 © 2017 Ohba et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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