| Item type |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2023-02-25 |
| タイトル |
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タイトル |
Stromal interaction molecule 1 haploinsufficiency causes maladaptive response to pressure overload |
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言語 |
en |
| 言語 |
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言語 |
eng |
| 資源タイプ |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
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資源タイプ |
journal article |
| アクセス権 |
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アクセス権 |
open access |
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アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
| 作成者 |
Ohba, Takayoshi
Watanabe, Hiroyuki
Murakami, Manabu
Iino, Kenji
Adachi, Takeshi
Baba, Yoshihiro
Kurosaki, Tomohiro
Ono, Kyoichi
Ito, Hiroshi
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| 内容記述 |
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内容記述タイプ |
Abstract |
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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. |
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言語 |
en |
| 出版タイプ |
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出版タイプ |
VoR |
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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
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| 収録物識別子 |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
1932-6203 |
| 出版者 |
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出版者 |
Public Library of Science |
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言語 |
en |
| 関連情報 |
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関連タイプ |
isIdenticalTo |
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識別子タイプ |
DOI |
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関連識別子 |
https://doi.org/10.1371/journal.pone.0187950 |
| 権利情報 |
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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. |
iA_2022_126.pdf (4.5 MB)
