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ID 116725
Title Alternative
Role of Sirt7 in Neointimal Formation
Author
Kimura, Yuichi Kumamoto University
Izumiya, Yasuhiro Osaka City University
Araki, Satoshi Kumamoto University
Yamamura, Satoru Kumamoto University
Hanatani, Shinsuke Kumamoto University
Onoue, Yoshiro Kumamoto University
Ishida, Toshifumi Kumamoto University
Arima, Yuichiro Kumamoto University
Nakamura, Taishi Kumamoto University
Yamamoto, Eiichiro Kumamoto University
Senokuchi, Takafumi Kumamoto University
Yoshizawa, Tatsuya Kumamoto University
Kim-Mitsuyama, Shokei Kumamoto University
Nakagata, Naomi Kumamoto University
Bober, Eva Max-Planck-Institute for Heart and Lung Research
Braun, Thomas Max-Planck-Institute for Heart and Lung Research
Kaikita, Koichi Kumamoto University
Yamagata, Kazuya Kumamoto University
Tsujita, Kenichi Kumamoto University
Keywords
Neointimal formation
Sirtuin
Smooth muscle cell
Content Type
Journal Article
Description
Background: Sirt7 is a recently identified sirtuin and has important roles in various pathological conditions, including cancer progression and metabolic disorders. It has previously been reported that Sirt7 is a key molecule in acute myocardial wound healing and pressure overload-induced cardiac hypertrophy. In this study, the role of Sirt7 in neointimal formation after vascular injury is investigated.
Methods and Results: Systemic (Sirt7−/−) and smooth muscle cell-specific Sirt7-deficient mice were subjected to femoral artery wire injury. Primary vascular smooth muscle cells (VSMCs) were isolated from the aorta of wild type (WT) and Sirt7−/−mice and their capacity for cell proliferation and migration was compared. Sirt7 expression was increased in vascular tissue at the sites of injury. Sirt7−/−mice demonstrated significant reduction in neointimal formation compared to WT mice. In vitro, Sirt7 deficiency attenuated the proliferation of serum-induced VSMCs. Serum stimulation-induced upregulation of cyclins and cyclin-dependent-kinase 2 (CDK2) was significantly attenuated in VSMCs of Sirt7−/−compared with WT mice. These changes were accompanied by enhanced expression of the microRNA 290-295 cluster, the translational negative regulator of CDK2, in VSMCs of Sirt7−/−mice. It was confirmed that smooth muscle cell-specific Sirt7-deficient mice showed significant reduction in neointima compared with control mice.
Conclusions: Sirt7 deficiency attenuates neointimal formation after vascular injury. Given the predominant role in vascular neointimal formation, Sirt7 is a potentially suitable target for treatment of vascular diseases.
Journal Title
Circulation Journal
ISSN
13474820
Publisher
The Japanese Circulation Society
Volume
85
Issue
12
Start Page
2232
End Page
2240
Published Date
2021-11-25
Rights
This article is licensed under a Creative Commons [Attribution-NonCommercial-NoDerivatives 4.0 International] license. https://creativecommons.org/licenses/by-nc-nd/4.0/
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DOI (Published Version)
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language
eng
TextVersion
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departments
Medical Sciences