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  1. 広島大学の刊行物
  2. Hiroshima Journal of Medical Sciences
  3. 62巻3号

Induction of Timp1 in Smooth Muscle Cells during Development of Abdominal Aortic Aneurysms

https://hiroshima.repo.nii.ac.jp/records/2013683
https://hiroshima.repo.nii.ac.jp/records/2013683
fd6559b7-587a-4653-97a6-b20192c969bd
名前 / ファイル ライセンス アクション
HiroshimaJMedSci_62_63.pdf HiroshimaJMedSci_62_63.pdf (540.2 KB)
Item type デフォルトアイテムタイプ_(フル)(1)
公開日 2023-03-18
タイトル
タイトル Induction of Timp1 in Smooth Muscle Cells during Development of Abdominal Aortic Aneurysms
言語 en
作成者 Bumdelger, Batmunkh

× Bumdelger, Batmunkh

en Bumdelger, Batmunkh

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Kokubo, Hiroki

× Kokubo, Hiroki

en Kokubo, Hiroki

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Kamata, Ryo

× Kamata, Ryo

en Kamata, Ryo

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Fujii, Masayuki

× Fujii, Masayuki

en Fujii, Masayuki

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Ishida, Mari

× Ishida, Mari

en Ishida, Mari

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Ishida, Takafumi

× Ishida, Takafumi

en Ishida, Takafumi

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Yoshizumi, Masao

× Yoshizumi, Masao

en Yoshizumi, Masao

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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
権利情報
権利情報 (c) Hiroshima University Medical Press.
主題
主題Scheme Other
主題 Abdominal aortic aneurysm
主題
主題Scheme Other
主題 Mmp9
主題
主題Scheme Other
主題 Timp1
主題
主題Scheme Other
主題 TNF-α
主題
主題Scheme NDC
主題 490
内容記述
内容記述 Abdominal aortic aneurysm (AAA) is known to develop mainly by the increased diameter of aorta through metalloproteinases (MMPs). Although activities of MMPs are tightly regulated by the presence of tissue inhibitor of MMPs (TIMPs) and imbalances between MMPs and TIMPs may serve to fragility of arterial wall, little is known about TIMPs behavior in aneurysmal formation. Here, we utilized a murine experimental AAA model, and found that by immunohistochemical analysis, Timp1 as and Timp1 mRNA levels was also revealed in aortic tissue in AAA by RT-PCR. In cultured vascular smooth muscle cells (SMCs), Tumor Necrosis Factor (TNF)-α significantly activated both Mmp9 and Timp1 expression, and they were blocked by Jun kinase inhibitor (SP600125) in a dose-dependent manner. Interestingly, a proteasome inhibitor (MG132), which is known as an agent for inhibition of the nuclear factor-kappa B (NF-kB), significantly inhibited the TNF-α-induced expression of Timp1, whereas MG132, which also works as an activator of c-Jun/AP-1 pathway, strongly increased Mmp9. Taken together, inflammatory cytokines, including TNF-α, may simultaneously induce MMPs and TIMPs for the remodeling of the medial layer, leading to the increased diameter of the aorta, the aneurysm.
言語 en
出版者
出版者 Hiroshima University Medical Press
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 departmental bulletin paper
出版タイプ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
収録物識別子
収録物識別子タイプ ISSN
収録物識別子 0018-2052
収録物識別子
収録物識別子タイプ NCID
収録物識別子 AA00664312
開始ページ
開始ページ 63
書誌情報 Hiroshima Journal of Medical Sciences
Hiroshima Journal of Medical Sciences

巻 62, 号 3, p. 63-67, 発行日 2013-09
旧ID 35413
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