Item type |
学術雑誌論文 / Journal Article(1) |
公開日 |
2009-12-01 |
タイトル |
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タイトル |
ANGIOTENSIN RECEPTOR BLOCKER CANDESARTAN BINDS TO AND UPREGULATES MOLECULAR CHAPERONE HSP90 IN THE HIPPOCAMPAL CA1 NEURONS ― A POSSIBLE MECHANISM OF NEUROPROTECTION BY ANGIOTENSIN RECEPTOR BLOCKER ― |
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言語 |
en |
言語 |
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言語 |
jpn |
主題 |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
angiotensin II type 1 receptor |
主題 |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
heat shock protein 90 |
主題 |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
molecular chaperone |
主題 |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
apoptosis |
主題 |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
hippocampus |
主題 |
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言語 |
en |
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主題Scheme |
Other |
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主題 |
ischemic injury |
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 |
KOKUBUN, Kohei
SUGAWARA, Taku
ISHIDA, Ryuichi
FUJIWARA, Kazuhiko
ITOH, Hideaki
MIZOI, Kazuo
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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 |
Antihypertensive angiotensin II type 1 receptor blockers (ARBs) have neuroprotective effects that were independent of the reduction of blood pressure. We have previously shown that vulnerable hippocampal CA1 neurons underwent delayed cell death through mitochondria-dependent apoptotic pathway after global cerebral ischemia, but ARB protected these neurons from cell death. To elucidate the mechanism of neuroprotection by ARB candesartan, candesartan-specific binding proteins were first investigated using candesartan-affinity column and rat hippocampal tissue. And, the affinity of ARB and the binding protein was further examined by BIAcore binding assay. Then, the distribution and expression of the protein were characterized by immunohisotochemistry and Western blots. By affinity column study, molecular chaperone heat shock protein 90 (HSP90) was identified as a binding target of candesartan. BIAcore assay proved functional binding of candesartan to HSP90. Immunohistochemistry showed increased HSP90 expression in the hippocampal CA1 neurons as early as 1 day after candesartan treatment. Westen blots confirmed temporal changes in HSP90 expression. HSP90 maintains the stability of the proteins as a molecular chaperone and has been recently proven to inhibit apoptosis in in vitro studies. Our data suggest that HSP90 may play an important role in neuronal protection by ARB treatment through blocking mitochondria-dependent apoptosis. |
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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 |
ja : 秋田医学
巻 36,
号 1,
p. 25-33,
発行日 2009-06-01
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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 |
03866106 |
収録物識別子 |
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収録物識別子タイプ |
NCID |
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収録物識別子 |
AN00009294 |
出版者 |
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出版者 |
秋田医学会 |
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言語 |
ja |